HISTIMINE AND ALL ITS VARIED FUNCTIONS ..

[Guest guest]

Hi All...

I came across this info trying to figure out a few symptoms. But, Im

like totally shocked at the how many functtion Histimine plays a role in

the body. There are a lot of answers contained in this for someone who

might understand it .. because most of its way over my head. Ill paste

the link and then the full text below it just incase it become

inaccessable in the future.

http://lymedisease.medical-topics.com/tag/histamine/

<http://lymedisease.medical-topics.com/tag/histamine/>

Wednesday, October 21st, 2009

Chapter 2: A review of literature and research related

Introduction:

" Histamine was synthesized in 1907 and isolated from mammalian tissues

(Katzung, 1998, p. 261). It has different functions in the body,

including neurotransmission and neuromodulation, allergic and

inflammatory mediator and stimulator of gastric acid secretion. Common

food sources of histamine in red wine and strawberries (Firshein, 1996).

Organic chemical name for histamine is 2 – (4-imidazoyl) ethylamine.

E 'formed by decarboxylation of histidine amino acids through the action

of the enzyme histidine decarboxylase. Usual way of detoxifying the body

is methylation by histamine amino acid methionine (Pfeiffer, 1987).

Excessive amounts of histamine released in the blood can increase your

pulse and blood pressure dangerously low, to the point of discharge and

sometimes death. The mechanism of this phenomenon is described below.

Mast cells filled with granules containing histamine, and this is

histamine, which resides most of the tissues. Histamine binds to mast

cells (cells called basophils or functionally related) is idle. Exposure

to an antigen (allergen) causes the antigen-specific IgE antibody to

connect with mast cells (primary immune response). Results of the

restatement for the same antigen antibody signaling of mast cells to

release histamine (the secondary immune response) (Weinstein, 1987).

Actions of histamine including vascular permeability and

bronchoconstriction (Abbas, Lichtman, and Pober, 2000), which can lead

to both asthma and dangerous blood pressure lowering. Excess Mast, known

as mastocytosis can cause a variety of disorders, such as " decreased

attention and memory, and emotional changes from anger, irritability and

to a lesser extent, depression ( et al. Al, 1986, p. 437).

Histamine cerebral origin of neurons in the tuberomammillary nucleus

, located in the hypothalamus. These neurons project throughout the

nervous system including the olfactory system and spinal cord (Wada,

Inagaki, Itowi, and Yamatodani, 1991). Stimulate histaminergic neurons

of the cerebral cortex, either directly or indirectly, through

activation of serotonergic neurons (Blandina et al., 2004). Some

neuroactive substances Store histaminergic neurons as galanin, GABA,

substance P, glutamate decarboxylase, and adenosine deaminase (Blandina

et al., 2004). Brain Histamine increases wakefulness, locomotor

activity, sexual behavior, and the release of corticotropin (ACTH), and

decreases in slow wave sleep, nutrition and production of growth hormone

(Wada, Inagaki, Yamatodani and Watanabe , 1991).

To better understand the role of histamine in neurotransmission, an

introduction / review of neurotransmitters, their receptors and signal

transduction pathways downstream of receptors will be presented. A

neurotransmitter is a chemical that the purpose of communication between

two nerve cells called neurons. It is synthesized in neurons (histamine

is an exception), travels to the end of the neuron (axon), is released

into the extracellular space between two neurons (synapses), and then

binds to a receptor on neurons in the 'Tray entry ', usually the

dendrite. After the neurotransmitter activates the receptor, soon out of

the receiver and is taken by the release of the original axons, called

the 'reuptake'. The action of neurotransmitters is specific and local,

or paracrine. This is in contrast with the hormones that are released in

other body organs, usually scattered all tissues, and affect all cells

have receptors that hormonal (endocrine system). However, some

neurotransmitters are also hormones, as mentioned above, histamine is

one of them.

There are three classic types of neurotransmitters: peptides, small

protein fragments, acetylcholine, and amino acids / amino acid

derivatives. There are many different neurotransmitter peptides, and

some of them to interact with histamine, vitamin C, or both. Some

examples of the interactions described above are described below.

Acetylcholine acts very similar to an amino acid / neurotransmitter

amino acid derivatives, but is much more hydrophobic and lipids (fats)

online. Acetylcholine neurotransmission can be excitatory or inhibitory,

depending on the receptor binds a. Acetylcholine plays an important role

for memory and learning. The amino acids that can act as

neurotransmitters are glycine, gamma-amino butyric acid (GABA),

glutamate and aspartate. GABA, glycine and charged amino acids are

neutral and inhibitory neurotransmitters, ie, in general, inhibits

neurotransmission in neurons throughout the valley. Glutamate and

aspartate are amino acids, and both are major excitatory

neurotransmitter, even if they have an inhibitory receptor, then.

The amino acid derivative are neurotransmitters dopamine,

norepinephrine, serotonin and histamine. Both dopamine and

norepinephrine are formed by a common pathway: phenylalanine -> tyrosine

-> L-dopa -> dopamine -> norepinephrine -> epinephrine. The first two

molecules, phenylalanine and tyrosine, are both in good faith, amino

acids, and the last four molecules are amino acid derivatives. Dopamine

is an inhibitory neurotransmitter, but often this occurs through

activation of descending pathways, which eventually inhibitor. Two main

functions carried out the regulation of dopamine in the hypothalamus,

and maintenance of fine motor control, Parkinson's disease results from

excessive loss of dopaminergic neurons in the reception. Excessive

levels of dopamine can cause psychosis, and all classical antipsychotic

medications inhibit dopamine neurotransmission. Dopamine is often called

the hormone of sexual pleasure as drugs like heroin, cocaine, nicotine,

marijuana and acting for the release of dopamine in the synapse.

Norepinephrine can be excitatory or inhibitory, again depending on the

receptor binds a. It plays an important role in attention and emotion.

Epinephrine plays no important neurotransmitter in the brain. Serotonin,

also known as 5-hydroxytryptamine, is formed from tryptophan path ->

5-Hydroxytryptophan -> 5-hydroxytryptamine. As in the dopamine /

norepinephrine route, the first molecule in the street, tryptophan, an

amino acid true. Serotonin is similar to norepinephrine in the sense

that it can be excitatory or inhibitory. Serotonin appears to be

involved in the biochemical and behavioral functions, including

neuroendocrine control, sleep, appetite and temperature regulation. His

complex relationship with neuroendocrine systems has led many experts to

call for serotonin, a key neurotransmitter ',' or 'master hormone.

'However, as discussed in detail later, histamine can be equal or

greater of serotonin in the neuroendocrine influence.

As mentioned above, histamine is formed directly from the amino acid

histidine. Histamine is unique among amino acid derivatives as a

neurotransmitter is released by an axon, and is not taken after his

release from the axon neurotransmission has been completed. It is always

excited, and ironically that emotion can lead to major depression, as

discussed below. Parts of many physiological functions histamine with

serotonin, including the four functions above (neuroendocrine control,

sleep, appetite and temperature regulation). Interestingly, serotonin is

often with the histamine released during allergic reactions. Such as

norepinephrine, histamine plays a role in arousal, and, as

acetylcholine, which plays a role in learning and memory. Histamine is

also involved in psychosis, such as dopamine and, although low levels of

histamine, which are often the culprits, while elevated levels of

dopamine appear to cause psychosis. Since histamine is always excited

and functionally related neurotransmitter amino acids glutamate and

aspartate. In summary, histamine plays biochemical functions that are

shared by most other neurotransmitters, and in turn influence many

functions of other neurotransmitters.

Neurotransmitter receptors are on the receiving end of neurotransmitters

signal (usually the dendrites of the cell), and inserted into the fat

layer of the cell as the plasma membrane. Often there are different

types of receptors for each neurotransmitter. There are two types of

GABA receptors, called GABA, and GABA, both are inhibitors. Only one

glycine receptor, and as mentioned above is inhibitory. There are four

main receptors for both glutamate and aspartate; is interesting that the

ratio of two amino acids, four receivers, three of which define each

ionotropic and metabotropic. Ionotropic receptors called

N-methyl-D-aspartate (NMDA), AMPA and Kiana. The three are all

ionotropic excitatory. The group has three subgroups of metabotropic

receptors, two inhibitors and one is exciting.

There are three types of acetylcholine receptors. Two of them are called

muscarinic cholinergic receptors, and given the M1 and M2 abbreviations.

M1 receptors are excited, and M2 receptors are inhibitory. The third

type of acetylcholine receptor called nicotinic cholinergic receptors,

and excitement. There are two receptors for the neurotransmitter

dopamine, known as D1 and D2, are inhibitors. The norepinephrine

neurotransmitter receptors are the most complicated of all, and,

possibly, glutamate / aspartate. The two main types of receptors in the

brain, norepinephrine, alpha (a) and beta (. These are divided into A1

and A2 receptors, B1 and B2 receptors. A1 and B1 receptors are both

excited, and the A2 and B2 receptors are both inhibitors.

There are four main types of 5-hydroxytryptamine (5-HT or serotonin)

receptors of neurotransmitters. There are several other, but are not

well characterized, or have overlapping function with the four major

types of receptors. The 5-HT1A receptor is more abundant in the central

nervous system (CNS), and is the only inhibitory neurotransmitter of the

four. The 5-HT2A, 5-HT3 and 5-HT4 receptors are excited. As with

histamine, there are four receptors, called H1, H2, H3 and H4. The H1,

H2 and H4 receptors are excitatory. The H3 receptor is inhibitory, ie it

inhibits the release of histamine itself.

Neurotransmitters are the message of the first communication in the

brain. However, the neurotransmitter that the message is delivered to

specific receptors on the cell membrane has to remain within the cell.

The process by which this occurs is called " signal transduction " and

there are two different signal transduction to be achieved. During the

debate on glutamate / aspartate, spoke of the terms ionotropic and

metabotropic. All recipients of the actions of neurotransmitters a

reporting mechanism similar with both ionotropic receptors, o.

Ionotropic metabotropic ion channels form between the extracellular and

intracellular fluid, and are permeable to specific ions, such as

potassium (K +), chlorine (Cl-) and calcium (Ca2 +). Metabotropic

receptors transmit their signal to the cell of the brain so much more

complicated, using a variety of small organic molecules, proteins and

fatty acids at times. Some receptors are ion channels and the two

metabolic WARNING.

Ion channel receptors for the neurotransmitter can be excitatory or

inhibitory. K + channels that are very happy to achieve this goal the

reduction of potassium conductance across the plasma membrane, and vice

versa (inhibition of K + channels to increase conductivity). Excitatory

receptors in K + channel comprises M1, metabotropic subgroup I, 5-HT2A,

5-HT4, A1, B1, and both H1 and H2. K + channel inhibitory receptors

includes M2, D2, GABA, 5-HT 1A and A2. Ca2 + channels are excitatory

postsynaptic if (the classical position of the dendritic receptor), are

inhibitory presynaptic (axons). Ca2 + channel excitatory receptors can

often be more positively charged ions (cations) to enter the channel.

Excitatory nicotinic cholinergic receptor Ca2 + channel include NMDA,

AMPA, and 5-HT3. Ca2 + channel inhibitors are D2 receptors, GABA,

metabotropic subgroups II and III and A2. Cl-conductance Cl-channels are

always increasing and inhibition as GABA and glycine. Sodium (Na +) and

channels are receptor inhibitors increase Na + conductance of the

receptor in the brain of this is B2.

As seen above, there is a considerable amount of redundancy in the

functions of the receptor channels of ions. Metabolic receptors are no

exception, too. There are two main pathways of signal transduction in

the brain: the inositol triphosphate / diacylglycerol (IP3/DAG) way, and

adenosine monophosphate (cAMP) path. There are several roads that branch

off from these two main streets, and there are significant communication

or interference between the two main streets. The road is always IP3/DAG

excitement. The excitatory receptors are upstream of IP3 and DAG are M1,

metabotropic subgroup I, 5-HT2A, A1, H1 and H4. Functionally, the path

field is more complicated. Can be excitatory or inhibitory, and to

complicate matters further, by increasing or decreasing levels of cAMP

may be excitatory or inhibitory. Excitatory receptors that increase cAMP

levels are B1 and H2. Receptor inhibitors that increase cAMP levels are

D1 and B2. Receptor inhibitors that reduce levels of cAMP include M2,

D2, subgroups II and III metabotropic 5-HT 1A and A2.

There are dozens of different small molecules and proteins that are

involved in both major pathways of signal transduction, and only major,

well-defined and protein molecules will be mentioned. Structurally, the

field is relatively simple form. The standard route is via cAMP and

norepinephrine receptor B1. The norepinephrine binds to receptors B1

— although in a pattern of inhibition bind to 2 receptors (cAMP

would remain high). The B1 receptor in turn activates a protein called

modulation " monsters " (Chen, et. Al, 1999) for the G-stimulants

communicates with a receiver B2 'inhibitory protein Gi'. The GS-protein

in turn activates an enzyme called adenylate cyclase (Menkes, Rasenick,

Wheeler and Bitensky, 1983). Then cyclase produces cAMP, and increasing

their level within the cell. Elevated levels of cAMP then activates an

important enzyme, protein kinase A (PKA), which amends a number of other

proteins (substrates) (Walaas & Greengard, 1991). PKA modified proteins

through a mechanism known as phosphorylation, in which the enzyme

transfer a group of high-energy phosphate bottom (substrate) of the

protein. Importantly, PKA activity is reduced in depression (Shelton,

Maine, and Sulser, 1996).

A protein substrate of PKA that phosphorylates the protein is rightly

called cAMP response element binding (CREB), this is achieved then moves

PKA in the cell nucleus (Hagiwara et al., 1993). In this model, cAMP

pathway, CREB binds to a specific DNA sequence upstream of a gene called

brain-derived neurotrophic factor (BDNF), and increases the expression

of BDNF mRNA (Zafra et al., 1992). The central dogma of molecular

biology states that DNA is transcribed into messenger RNA (mRNA), which

is translated (expressed) in proteins (Lewin, 1994). In other words,

CREB binds upstream of the BDNF gene, production of an enzyme complex to

transcribe the DNA into mRNA of BDNF, and that the mRNA is translated

into the mature BDNF protein.

BDNF then begins several positive features, including support for the

survival and maturation (differentiation) of brain neurons (Hyman et

al., 1994), particularly serotonin (5-HT) neurons (Mamounas, Blue, and

Siuciak Altar, 1995). The effect of this is an example of positive

feedback, if at the end of the track helps to perpetuate the beginning

of the runway. By contrast, stress levels can significantly reduce BDNF

(, Makino, Kvetnansky, & Post, 1995). In conclusion, norepinephrine

/ CAMP / PKA pathway usually has a very positive role in mental health,

except when overstimulation in manic patients (Young et al., 1993). As

mentioned above, the histamine H2 receptor is coupled to the path field,

and receptor activation increases cAMP levels.

The IP3/DAG path is much more complicated than the path of cAMP. This is

because there is no main street, but two. Some might argue that is an

understatement to call IP3/DAG a " path " as the sole means of membrane

receptors divided into two distinct paths from the beginning, becoming a

way IP3, and the other to become the DAG way. The model system in this

way is 5 hybrid HT2A receptor pathway. The 5-hydroxytryptamine (5-HT,

serotonin) binds to its receptor 2A, the activation of another protein

called G-GQ, which is different from that in the process of

norepinephrine receptor. Gq activates phospholipase C (PLC). And " the

enzyme that initiates the divergence of the serotonin signal by

splitting sugar lipid phosphatidylinositol 4,5-bisphosphate (PIP2) in

the above 1,4,5-triphosphate (IP3) and diacylglycerol (DAG) (De Chaffoy

de Courcelles et al. 1985).

Signal DAG activates protein kinase C (PKC) (Nishizuka, 1986). PKC

performs a wide range of functions. It plays a role in long-term changes

of gene expression in the brain, neuron firing, and neurotransmitter

release (Stabel and , 1991). One of the most important functions

of PKC is phosphorylated microtubule associated protein 2 (map2) (Hoshi

et al., 1988). Interestingly, PKA also appears to phosphorylate map2

(Sloboda, Rudolph, Rosenbaum & Greengard, 1975). This is one of the ways

in which the field and ways IP3/DAG interact with each other.

However, a more important interaction is that map2 phosphorylation

inhibits microtubule assembly (on et al., 1980). The microtubules

form a large part of the framework of the cell cytoskeleton.

Microtubules are formed by polymerization (multimerization) of tubulin

dimers (two tubulin proteins attached). Tubulin dimers then stimulate

adenylate cyclase, the enzyme found in cAMP pathway (Hatta, Ozawa,

Saito, and Ohshika, 1995). Thus, the DAG path animal, or derivatives, in

the camp. Many neurological and psychiatric researchers were puzzled for

years that antidepressants that affect both norepinephrine and

serotonin, the reuptake biochemical results had to be very similar. The

discovery of lead in cAMP DAG through elegantly solves this paradox, the

previous theory.

The IP3 path is less clear than the path DAG. After its founding, IP3

binds to a receptor that release of intracellular calcium ions (Ca2 +).

Ca2 + has many important actions within the cell. In this model, Ca2 +

activates two important proteins, calmodulin (CAM) and calcineurin.

These two proteins downstream of IP3 do not always have positive effects

on welfare, as is standard for the field and the way DAG proteins. CaM

activates a group of enzymes known as kinases, calmodulin (CaM K). K CaM

can interact with the route to influence the transcription of

cAMP-mediated CREB. As mentioned above, CREB-mediated transcription has

a positive effect on brain function. Some CAM K activate CREB (

et al., 1998); other CaM K inhibit CREB (Hook & Means, 2001). As the Cam

K, calcineurin can activate or inhibit CREB (Schwaninger et al., 1995;

Bito, Deisseroth and Tsien, 1996). The H1 histamine receptors are linked

to IP3/Ca2 + way, the DAG / PKC path (Wada, Inagaki, Yamatodani and

Watanabe, 1991).

One of the main ways the brain communicates with the rest of the body is

through the hypothalamic-pituitary-adrenal (HPA). Within this area of

activity, the nervous system (brain) regulates the body's endocrine

system (hormone) system, and vice versa. The immune system interacts

with the HPA axis to some extent. This axis is the primary regulator of

most activities of the body. Different types of stress can increase

levels of one of the most important hormones of the HPA, the peptide

corticotropin releasing hormone (CRH) (Koob, 1999). CRH stimulates the

secretion of adrenocorticotropic hormone (ACTH). ACTH stimulates the

secretion of a class of steroid hormones called glucocorticoids (Axelrod

& Reisin, 1984), of which cortisol is the most important. Later, after

stressors is gone, there is a negative feedback loop that returns to

normal HPA axis activity. However, when the HPA axis is prolonged

over-stimulation due to chronic stress, the negative feedback loop can

not ( et al., 1992). Glucocorticoids can have both positive and

negative. Has anti-inflammatory actions (Lewin, 1994), but can also

suppress immune function properly. As mentioned below, histamine plays a

role in stimulating the HPA axis.

Vitamin C has a very interesting story. Over two hundred years ago, he

noticed that some fruit could help prevent a connective tissue disease

known as scurvy waste in the oceans bound sailors. However, the factor

antiscorbutric fruits (like lemons and limes), was not identified until

the 20th century. It was then that vitamin C was isolated in 1928 by the

adrenal gland by chemist Nobel laureate Albert Szent-Györgyi, and the

name of ascorbic acid (Grunewald, 1993). Subsequently was isolated from

fruit (lemons) in 1932 (Haas, 1992), and soon after was synthesized in

1933 (, 1996). Vitamin C is found mainly in fruits and vegetables

(Haas, 1992). " The best known sources of vitamin C are citrus –

oranges, lemons, limes, tangerines and grapefruits " (Haas, 1992, p.

142). Peppers The best vegetable sources of vitamin C are blackcurrant

and red first (Reavley, 1998). Vitamin C was the best selling

nutritional supplements for decades, in 1993 sales were EUR 117 million

(Firshein, 1996). It is better to use powder (Vayda, 1994). Ascorbate,

sodium ascorbate, and Ester-C is more tolerant of ascorbic acid (Vayda,

1994), presumably because of its non-acidic chemicals (ascorbic acid and

" sometimes the irritation of the stomach).

Vitamin C has a molecular weight of 176. 1. Its chemical formula is

C6H6O8. The chemical name is 2,3-enediol-L-acid gulono (Koenig, 1996).

Vitamin C is a chemical known as organic ketolactone, and has two

hydrogen atoms dissociated. " In the physiological pH of ascorbic acid is

almost entirely in its anionic " (Levine and Morita, 1985, p. 5). This

molecule has a hydrogen atom and a hydrogen atom is connected loosely

coupled ascorbic acid. Analogues of vitamin C 100% biological activity

include L-dehydroascorbic acid, L-ascorbic acid-6-palmitate, and

L-ascorbic acid-5, 6-diacetate (Koenig & Elmadfa, 1996).

Dehydroascorbate ascorbic acid differs from the absence of two ionizable

hydroxyl groups (Rose, 1988). A hydroxyl group containing one oxygen and

one hydrogen atom. When the two hydrogen atoms are split with their

relationship oxygen atoms, the molecule was reorganized and the oxygen

atoms each acquire a double bond with the rest of the molecule

Dehydroascorbate. Technically, not an acid Dehydroascorbate because he

can not lose more hydrogen atoms in solution. It is relatively

hydrophobic compared with ascorbic acid, and therefore can be

transported through the membranes of fat cells. Dehydroascorbate

Antiscorbutric properties but not the antioxidant properties (,

1996). When vitamin C is oxidized to Dehydroascorbate, is transported to

neighboring cells, and then further reducing the ascorbic acid (Nualart,

et. Al, 2003).

The main function of vitamin C is the production of collagen (Reavley,

1998), by hydroxylation of proline (Grunewald, 1993). That helps to

produce the molecule that transports oxygen from hemoglobin and also

helps in iron absorption Digest (Reader's Digest Association, 1999).

Vitamin C oxidizes lysine hydroxytrimethyllysine to synthesize

nonessential amino acid carnitine (Goodman et al., 1996). Helps form

bones, cartilage, teeth, and strengthens the capillaries (Hoffer and

, 1978), and this is mainly due to its role in collagen synthesis

(Hediger, 2002). Vitamin C converts folic acid to folinic acid (Goodman

et al., 1996) and the neurotransmitter dopamine hydroxylation to form

norepinephrine (Goodman et al., 1996).

Employee of enzymes known of vitamin C for optimal activity include:

4-hydroxyphenyl pyruvate dioxygenase, G-butyrate betaine, 2-oxoglutarate

4-dioxygenase, proline hydroxylase, lysine hydroxlyase,

procollagen-proline 2-oxoglutarate 3-dioxygenase, trimethyllysine 2

– oxoglutarate dioxygenase, dopamine b-monooxygenase and peptidyl

glycine a-amidating monooxygenase (Levine and Hartzell, 1987). On the

other hand, are affected by many genes (modulation) of ascorbic acid.

Genes that are modulated by ascorbic acid are acetylcholine receptors

procollagen, pro-atrial natriuretic factor, cytochrome P450 CYP2A1 and

CYP2B1, alkaline phosphatase, osteocalcin, osteopontin, lipid binding

protein, lipoprotein lipase, the light chain myosin 2, and (myogenin

Hitomi & Tsukagoshi, 1996).

The vast majority of animals can synthesize vitamin C. D-Glucose is the

starting molecule. Glucose is metabolized through the pentose phosphate

cycle, the classification aldonolactonase and L-gamma-lactone oxidase

gulono for the production of ascorbic acid (Nishikimi and Yagi, 1996).

Primates (including humans), guinea pigs, some bats and birds lack the

enzyme gulonolactone oxidase, and therefore can not synthesize vitamin C

(Banhegyi et al., 1997). The prevailing theory of why the animals lost

the ability to synthesize vitamin C is that all these animals lived in

an ascorbic acid-rich plants for millions of years and then lost the

gene for synthesizing vitamin C, due to its uselessness ( Cameron and

ing, 1993). Genetic analysis suggests that the ability to synthesize

vitamin C was lost in primates about 45-50 million years ago (Nishikimi

and Yagi, 1996). Interestingly, this happened early in the evolution and

divergence of primates, long before primates appeared as a human being.

A conservative estimate for the body of vitamin C is " an aggregate size

of approximately 1500 mg (Kallner, 1987, p. 422), a liberal estimate is

5000 mg (Ginter, 1980). Adults lose 3-4% of their total daily vitamin C

(Goodman et al., 1996). " A glass of 8 grams of fresh orange juice

provides 124 mg of vitamin C " Digest (Reader's Digest Association, 1999,

p. 379). In a person who did not say, about 200 milligrams per day is

needed to maintain vitamin C levels (Lieberman and Bruning, 1997). The

absorption of 180 mg of vitamin C is 80-90% efficiency (Koenig &

Elmadfa, 1996). Regular vitamin C supplementation increases blood

vitamin concentrations in an average of 25-30%. Both vitamin C intake

and appears to have other biological effects identical to maintain blood

levels (Boeing & Rausch, 1996). Vitamin C supplements of 2000 mg / day

increases plasma levels of 57% (ston, 1996).

The concentration of vitamin C in the brains of other mammals is

directly proportional to the density of neurons (Rice, 2000). In the

brain, the extracellular concentration of vitamin C increases rapidly

after the activation of behavior (Katsuki, 1996). Vitamin C is not

transported into the CNS cells via a sodium co-dependent transport

mechanism (Rose, 1998). Vitamin C as ascorbic acid can not enter the

brain, but must first be oxidized to Dehydroascorbate to cross the

blood-brain barrier (Agus et al., 1997), which is reduced back to

ascorbate. Oxidized vitamin C is regenerated by a small peptide called

glutathione (Banhegyi et al., 1997), and vitamin C may regenerate

oxidized glutathione (, 1996), depending on the molecule

antioxidant is required at the time. The thioredoxin reductase enzyme

can also recycle vitamin C (May 2002), antioxidants such as alpha-lipoic

acid (Xu & Wells, 1996).

Literature Review:

Histamine plays such a varied and powerful in the brain. Histamine can

only inhibit the release of all major neurotransmitters: serotonin,

glutamate, acetylcholine, GABA, dopamine and noradrenaline (Brown,

s, & Haas, 2001). Even low levels of histamine can inhibit

neuronal activation of all serotonin receptor subtypes (Lakoski &

Aghajanian, 1983). Interestingly, histamine also the release of

noradrenaline in the brain tissue (Bugajski, 1984), and inhibition of

their release, as indicated above. Excess release may lead to

norephinephrine anxiety disorders or mania. The administration of

histamine in rats, decreased concentration of dopamine in the blood

(Willems et al., 1999). In contrast, administration of histamine in the

brains of anesthetized rats increased extracellular dopamine levels

(Galosi et al., 2001). High levels of dopamine is believed to be

associated with psychosis, such as classical antipsychotics block

dopamine receptors (Victor and Ropper, 2001). Histamine can enhance

glutamate signaling (Galosi et al., 2001); excess glutamate signaling

may be neurotoxic.

Histamine itself is a very toxic molecule. Even low doses of histamine

can kill endothelial cells in culture (Fernández-Novoa, and

Cacabelos, 2001). High levels of histamine, known as histaminemia, " the

causes of the separation of vascular endothelial cells (Clemetson, 1999,

p. 1). This can lead to heart disease and death. In humans, heart rate

and reduces histamine increases blood pressure (Katzung, 1998). This

hypotensive action of histamine can cause serious clinical consequences,

including shock and death. The symptoms of excess histamine in the blood

are: gastrointestinal disorders, headache, facial flushing, tachycardia,

bronchoconstriction, rash, and hypotension (Katzung, 1998). Histamine

can cause pain or analgesia, depending on where it is injected into the

brain (Glick and Crane, 1978).

There is strong evidence of the involvement of histamine in the physical

and mental disorders. Asthma 'may be 100-1000 times more sensitive to

histamine than normal subjects (Katzung, 1998, p. 264). Histamine may be

involved in psychiatric disease Attention Deficit Disorder (ADD) (pass

through, Bacciottini, Mannaioni, and Blandina, 2000). Central

histaminergic neuron system overactivity can play a role in age-related

memory loss anxiety (Hasenöhrl, Weth, and Huston, 1999). In contrast,

low levels of histamine, appear to decrease anxiety (Peitsaro,

Käslin, Anichtchik, and Panula, 2003). Histamine may be involved in

ethanol tolerance, in laymen's terms, histamine can support alcoholism.

The rats that were genetically bred to have low levels of histamine were

more sensitive to ethanol in normal rats (Lintunen et al., 2002). In

theory, high levels of histamine can induce tolerance to ethanol.

There is a considerable amount of evidence supporting the theory that

histamine is directly involved in the stress response induced

biochemical changes. In non-stressed rats, histamine interacts normally

with a & b-adrenergic and muscarinic cholinergic receptor. He stressed

rats, histamine interacts only with a-adrenergic, non-b-adrenergic

receptors (Bugajski, 1984). Many of the anti-anxiety drugs work by

increasing the activity of the major inhibitory neurotransmitter GABA,

or GABA receptor activation. Interestingly, GABA inhibits the release of

histamine (s, Yamatodani and Timmerman, 2000). Administration of

histidine, the amino acid precursor of histamine-induced strange

'behavior mock fight' in rats, and established that both muscarinic

cholinergic receptors, H1 and extend this behavior (Pilch, Rogoz and

Skuza, 1982).

Stress can trigger release of histamine, which in turn acts to release

the stress hormones ACTH, CRH, prolactin (PRL) and vasopressin (Brown,

s, & Haas, 2001). At rest and during stress, CRF, noradrenaline

and glucocorticoids such as cortisol and maintain CNS homeostasis of the

immune system. Alter the homeostasis of this excess histamine by

changing the immune system to a pro-inflammatory status (Chrousos,

2000). Press CRF is normally initiated by the neurotransmitters

dopamine, serotonin and norepinephrine (Tuomisto & Mannisto, 1985).

Elevated levels of histamine can act to " kidnap " the required distance

from the release of neurotransmitters CRF mentioned above, in order to

unbalance the HPA axis and, finally, the central nervous system

homeostasis. In fact, it has been shown that histamine is a potent

stimulator of the organs of the pituitary and adrenal (Bugajski & Gadek,

1983). There is also evidence that histamine plays an important role in

physiological responses to chronic stress, keep your brain in a Warning

state (Parmentier, et al., 2002) against a real or imaginary challenge.

There are two types of immune responses: Th1 and Th2. Th1 immune

response is one that is directed against the microbes. Th2 immune

response is one that is directed against otherwise harmless protein

called antigens. Excess cortisol shifts the immune response toward Th2

(Hurwitz & Morgenstern, 2001). This can initiate a vicious circle of

positive feedback, since allergic reactions can promote and maintain the

HPA axis in business, eventually leading to depression (Hurwitz &

Morgenstern, 2001). Hyperactivity of the HPA axis, in turn, leads to

overproduction of cortisol. The success of feedback is supported by the

finding that stress increases cortisol levels and high levels of

cortisol are associated with depression (Brody Preut, Schommer, and

Schurmeyer, 2002). One of the possible mechanisms for the outcome of

this is that high levels of cortisol in the brain downregulate 5-HT

receptors (de Kloet, Sybesma and Reul, 1986), and may also reduce the

availability of tryptophan ( Maes, De Ruyter, Hobin and Suy, 1987),

which is essential for the synthesis of serotonin.

Stress can release neuropeptides that can induce brain mast cells

release histamine, causing an allergic reaction Th2 (Abbas, Lichtman,

and Pober, 2000). Histamine stimulates the HPA axis, without the

activation of serotonergic and adrenergic receptors. A proposed

mechanism for the effect described above is histamine, which interacts

with prostaglandin to stimulate the HPA axis (Willems et al., 1999). The

hormone corticosterone increases the levels of histamine in the

hypothalamus, and excess histamine, which in turn increases the plasma

levels of corticosterone (Mazurkiewicz-Kwilecki, 1983), providing a

'feed-forward loop that may contribute to a HPA axis dysfunction.

Some peptides that stimulate the release of CRF HPA axis hormones can

cause a variety of behavioral abnormalities in animals. The anomalies

are the reactions of fear, aversion, increased awareness, decreased food

intake, stress induced by immobilization, and inhibition of exploration

(Koob, 1999). Histamine can cause behavioral abnormalities almost

identical, reinforcing the hypothesis that histamine is an important

stimulus of CRF release. ACTH is also released by the stimulation of

both H1 and H2 receptors (Knigge and Warberg, 1991).

As mentioned above, the release of histamine increases the levels of Ca2

+ through IP3. It seems that many mental patients have elevated Ca2 +

responses (Kusumi and Koyama, 1998). There is evidence that there is an

increase of calcium released during aging (Kurian, Chandler, Patel, and

crew, 1992), which may explain some age-related dementias. Some doctors

believe that depression can be caused by hypofunction of cAMP-mediated

cellular responses and pathways IP3/DAG domain, whereas the opposite is

true for mania (Wachtel, 1990). The correlation between low levels of

field, with depression and high levels of cAMP mania has resulted so far

in 1970 (Abdulla & Hamadah, 1970). The regulation of the enzyme

phosphodiesterase degradation of cAMP. Importantly, the

phosphodiesterase inhibitor Rolipram has antidepressant activity

(Wachtel, 1982). Thus, histamine may be involved in depression or mania,

depending on the path has a greater influence on the receiver.

The following discussion is an example of a model for regulation of the

receptor cell. Low levels of serotonin causes the brain to adapt to the

increased number of serotonin receptors, called 'up-regulation " . Many

if not all, of the downstream of small molecules and proteins in the

street are up-regulated, including the density of serotonin receptors

(Arora and Meltzer, 1989). The problem is that any changes in serotonin

levels will be amplified by way of Now Up-regulation. In theory, this

can lead to mood swings, bipolar disorder, anxiety, major depression and

maybe (Aprison, Takahashi, and tachikata, 1978), presumably due to

'burnout' path overwork. Selective inhibitors of serotonin reuptake

(SSRIs — Prozac, Zoloft, Paxil, Luvox, Celexa, Lexapro) are designed

to alleviate depression by normalizing the path to the

serotonin-regulated. They block the reuptake of serotonin in the axon,

thus keeping more in the synapse. More of serotonin in the synapses

means that more binds to receptors for serotonin. Previously receptor is

regulated until then regulated down to normal levels, and the path

through the receptor becomes down-regulated, and then normalized. The

same effect was observed with the inhibitor of norepinephrine reuptake

Effexor to camp. Since histamine can inhibit the function of serotonin

receptors can cause mental illness directly through the mechanism

described above for the route to regulation.

There is ample evidence that the street names is important in the

maintenance of synaptic plasticity (mental health). Long-term

antidepressant results in the activation of PKA (Popoli, Brunello,

, & Racagni, 2000). Several types of inhibitors of serotonin and

norepinephrine reuptake (antidepressants), increasing the level of CREB

mRNA (NIBU, Nestler and Duman, 1996). The non-pharmaceutical

antidepressant S-SAM (SAM) has stimulated the field to join the PKA, and

also increased the activation by phosphorylation map2 (Zanotti et al.,

1998). As mentioned above, the H2 receptor activated by cAMP.

Histamine stimulates neuronal firing through H1 receptors, whereas the

H2 receptor activation inhibits neuronal firing (s, Yamatodani and

Timmerman, 2000). As mentioned above, the location of the H1 receptor is

IP3/DAG. The IP3/DAG molecule PIP2 signaling pathway is significantly

higher in mania (Brown, Mallinger, Renbaum, 1993). The route of the DAG

PKC enzyme is high in mania compared with normal subjects (Friedman et

al., 1993). The administration of antidepressants decreases in vitro in

cytosolic Ca2 + release (Ca2 + activation) (Shimizu et al., 1994), and

can also inhibit protein kinase Ca 2 + pathway (Silver, Sigg, and Moyer,

1986). However, the activation of some Ca 2 +-dependent protein kinases

(eg CaM KII) increased levels of BDNF expression (Ghosh, Carnahan, and

Greenberg, 1994).

The above findings underline the theory that IP3/DAG path can be both

positive and negative synaptic plasticity, which is the mobile mental

health related. One theory is that low levels of Ca2 + release lead to

synaptic depression, whereas large Ca2 + increases the opposite effect

(Lisman, 1994). Another explanation of how the road can be unbalanced

IP3/DAG is that some neurotransmitters may stimulate signaling through

one way or another. There is some evidence to support this theory. In

one study, metabolic modified products of IP3 and DAG were measured

after stimulation with neurotransmitters different path. Serotonin is

balanced and the metabolic response DAG IP3, while the response of

histamine is a weak DAG, but a strong IP3 response metabolite (Sarri,

croutons, and Claro, 1995). As mentioned above, there is much evidence

to suggest that the DAG path promotes mental health, while the IP3

pathway can cause mental illness. Both routes mentioned above are

activated by H1 receptors.

It is possible that Ca2 + (IP3/DAG) and Camp and PKA pathways may

antagonize each other (s, Yamatodani and Timmerman, 2000). In fact,

there is much evidence suggesting a direct antagonism between cAMP and

IP3 pathways (DAG feeds via cAMP, and should not be included in the

antagonism by cAMP). As mentioned above, serotonin activates the street

through IP3 binding to its receptors 5-HT2A. Serotonin-stimulated

release of Ca2 + was significantly higher in severe depression,

melancholia, call (Kusumi, Koyama and Yamashita, 1991), although the

signal serotonin maneuver through camp is the alleged mechanism of

antidepressant action. Histamine stimulates the formation of IP3

(Bielkiewicz-Vollrath, Carpenter, Schulz, and Cook, 1987). As discussed

in the preceding paragraph, the CAM is a protein downstream of IP3. CaM

activates the enzyme phosphodiesterase that degrades cAMP (Cheung,

1970), damaging the critical path. In contrast, activation of PKA

inhibits CaMKII many (Matsushita & Nairn, 1999), as mentioned above

CaMKII are immediately downstream of the CAM in the IP3 path. In

addition, some antidepressants have been shown to inhibit the CAM

(Silver, Sigg, and Moyer, 1986).

As mentioned above, calcineurin is IP3. Calcineurin inhibition can cause

anxiety for the release, the major inhibitory neurotransmitter, GABA

(Klee, Ren & Wang, 1998). Calcineurin pathway also negatively regulates

the CREB protein, cAMP, presumably by increased degradation (Bito,

Deisseroth and Tsien, 1996). A study has shown that CREB activates

calcineurin, but that was in the pancreatic islet cells, not in the

central nervous system (Schwaninger et al., 1995). Other studies have

shown that normally inhibits the activity of PKA protein calcineurin

inactivation of PKA downstream targets (substrates) (Shenolikar & Nairn,

1991; Greengard et al., 1998). Inhibits calcineurin, an important form

of synaptic plasticity known as long-long-term potentiation (LTP), which

often leads to long-term term depression (LTD) (Winder et al., 1998).

The enzyme calcineurin and cAMP-PKA pathway antagonize each other in the

regulation of various downstream proteins that CREB (Tong, Shepherd &

Jahr, 1995; Raman, Tong & Jahr, 1996; Traynelis & Wahl, 1997). Perhaps

more important, calcineurin is activated during allergic reactions

(Abbas, Lichtman, and Pober, 2000).

The H1 receptor stimulates IP3/DAG way, and is also the receptor that is

involved in allergic reactions (Repka- & Baraniuk, 2002). The

central nervous system, activation of H1 receptors can inhibit learning

and memory (Knoche et al., 2003). Histamine injected into mice initially

resulted in hypoactivity followed by hyperactivity, these effects were

abolished by the addition of an H1 block (antagonist) (Chiavegatti,

hake, and Bernardi, 1998). H1 antagonists also inhibits

histamine-induced increase in spontaneous motor activity in rats

(Kalivas, 1982). The mutant mice that have had their hit H1-receptor

responses has eased out of aggression against intruders of animals

compared with normal mice (Yanai et al., 1998a). This suggests that the

H1 receptor is involved in aggressive behavior. H1 knockout mice had a

marked increase in serotonin levels (Yanai et al., 1998b). This effect

might simply be the serotonin system to compensate for the lack of H1

receptor stimulation. Furthermore, the effect of this might suggest that

the strength of H1 receptor activation results in low levels of

serotonin, and perhaps later anxiety and depression symptoms.

Human beings have a certain mutation of the H2 receptor " had a greater

susceptibility to schizophrenia " (Brown, s, & Haas, 2001, p. 647).

Moreover, it appears that the histamine-induced depression may be

mediated through H2 receptors, although the H2 receptor activation

increases cAMP levels. In animal models, administration of histamine

often have a depressive effect, which can be reversed by the H2 receptor

blockade, but not to block H1 receptors (Cantu and Korek, 1991).

Activation of histamine H2-receptor inhibits the normal immune response

that are regulated by vitamin C (ston, 1996). As noted above, the H2

receptor activation increases cAMP levels and activated by PKA (s,

Yamatodani, and Timmerman, 2000). Activation of PKA is the theoretical

explanation of the action of many antidepressant drugs, especially those

that block the reuptake of norepinephrine. However, the increase in cAMP

may be denied by the H2 receptor activation of GABA receptors, which

then inhibit shoot all serotonergic neurons (Lakoski & Aghajanian,

1983). As mentioned above, serotonin and their receptors play a key role

in maintaining mental health. The activation of H2-receptor inhibits

neuronal firing in general (s and Yamatodani Timmerman, 2000), by

activating GABA. Although H2 receptor increases levels of cAMP, the

final result of the H2 receptor activation is inhibition of other

neurotransmitters.

An important role of histamine is the activation of cells that produce

stomach acid. Histamine-2 (H2-receptor) antagonists are commonly used as

antacids stomach. H2 receptors are also found in the brain. Histamine

H2-receptor antagonists may slow the progression of Alzheimer's disease

(Lipnik-Stangelj, Juric and Carman-Kržan, 1998). This suggests that

in the brain, histamine H2 receptor-mediated activation can cause brain

damage. All H2-receptor antagonists in the CNS can cause adverse

reactions. The CNS-specific reactions include: " delirium, psychosis,

confusion, disorientation, hallucinations, hostility, altered mental

status, irritability, drowsiness, or agitation " (Cantu and Korek, 1991,

p. 1027). In particular, the H2 antagonist, cimetidine (Tagamet) CNS can

have serious side effects, including epileptic phenomena, delirium and

coma (Van Sweden and Kamphuis, 1984). In animal studies, H2 antagonists

also can be scary (Santos, Huston, and Bandai, 2001).

H3 histamine receptor H1 and H2 receptor regulator negative, inhibiting

the release of histamine (Bongers, Leurs, on, and Raber, 2004).

Evidence in support of the effects of histamine generation of anxiety

comes from the observation that the H3 receptor blockade increases

anxiety in animals (Bongers, Leurs, on, and Raber, 2004).

However, H3 blockers may also have antidepressant effects (Ito, 2000).

Sometimes antidepressants can increase anxiety and the H3 receptor may

play an important role in this side-effect medication. The H3 receptor

has been implicated in several mental disorders, including migraine,

disorder and attention deficit hyperactivity disorder (ADHD),

schizophrenia and Alzheimer's disease (Leurs, Bakker, Timmerman, and

Esch, 2005). Unlike the three other histamine, H3 receptor can couple to

several signal transduction pathways (pass through, et al., 2004). As

mentioned above, histamine suppresses food intake. Paradoxically, the

knockout mice H3 receptor often become obese (Takahashi, Suwa, Ishikawa,

and Kotani, 2002). The H4 receptor was discovered recently. One of his

main roles seems to be the activation of mast cells (Hofstra, Desai,

Thurmond, & Fung-Leung, 2003).

Increased histamine levels in mice results in increased use of vitamin C

and, presumably, synthesis (Nandi, Subramanian, Majumder and Chatterjee,

1974). An interesting experiment was conducted in rats by a research

group in India in 1970. When " 1 mg of histamine was injected into mice,

the increase of histamine in urine was about four times, but returned

almost to normal after administration of ascorbic acid (Subramanian,

Nandi Majumdar and Chatterjee , 1974, p. 639). In humans, integration

with 2000mg/day Vitamin C, histamine levels drop by an average of 40%

(ston, Retrum and Srilakshmi, 1992). One result of the conduct of

teas histamine levels increased appetite. As mentioned above, histamine

plays a role in eating behavior, including suppression of food intake

and stimulates the intake of animals (Sakata and Yoshimatsu, 1995). It

is interesting to note that vitamin C appears to play a positive role in

feeding behavior, because low levels of vitamin C in the brain result in

decreased appetite (, 1982).

As mentioned in the introductory section of this chapter, prostaglandins

affect brain activity and immune activity. Vitamin C plays a role in the

metabolism of prostaglandins, including the breakdown of

dihomo-gamma-linolenic acid (DGLA) in secondary metabolites. DGLA

becomes normal inflammatory metabolite of arachidonic acid (AA)

(Horrobin, 1996). Thus vitamin C plays a role in mediating

anti-inflammatory. Vitamin C and prostaglandin E1 (PGE1) can share a

similar role in regulating collagen synthesis, infection and cholesterol

levels and insulin (Horrobin, 1996). Although histamine plays an

important role in Th2 immune response, it is actually recognized as an

immunosuppressive agent. Two grams of vitamin C increased the migration

of certain immune cells called neutrophils, and this migration is

inversely correlated with histamine levels in the blood. This suggests

that vitamin C may enhance immune function through histamine

detoxification (ston, , and CAI, 1992).

Vitamin C detoxifies histamine for conversion to hydantoin-5-acetic

acid, aspartic acid, and then (Clemetson, 1999). To achieve this, the

vitamin C should be of copper (Cu2 +) as a catalyst to degrade histamine

(Sharma and , 1980). Vitamin C also inhibits the enzyme

phosphodiesterase that degrades cyclic AMP. This results in increased

cAMP levels (Tisdale, 1975). Moreover, vitamin C synergizes with

inducers of cAMP to stimulate cAMP production (Hitomi & Tsukagoshi,

1996). This effect in the field of vitamin C is the second largest

anti-histamine action (in addition to the degradation of histamine),

because cAMP inhibits the release of histamine (Cathcart, 1986). Cyclic

AMP is also a potent inhibitor of allergy IgE stimulated mediator

release, including: histamine, slow reacting substance (SRS-A),

prostaglandin (PG) and an eosinophil chemotactic factor (ECF-A) " (

and , 1980, p. 163). Vitamin C also inhibits GF2a prostaglandin

(PGF2a) synthesis. PGF2a decreased levels of cAMP. Importantly, the

decreased levels of cAMP are associated with histamine release (Mohsenin

& Dubois, 1987).

Abstract:

Histamine is a multifunctional hormone excess has potentially lethal

side effects. Side effects from lethal allergen overstimulation of the

immune system, leading to release of excess histamine, which can reduce

blood pressure to the point of impact (Katzung, 1998). Histamine is

intimately involved in both immune activity and central nervous system.

That affects a number of functions in the CNS, including " excited state,

the functions of brain energy metabolism, locomotor activity,

neuro-endocrine, autonomic and vestibular food, drink, sexual behavior,

and l analgesia (Wada, Inagaki, Yamatodani and Watanabe, 1991, p. 415).

Histamine is formed by amino acid histidine, and is unique among

neurotransmitter amino acid derivatives, as it degrades the

extracellular space (synapse), instead of being received by the release

of the neuron (axons). This is important because the level of vitamin C

in the brain plays an important role in how quickly excess histamine is

removed from the synapse before it has a morbid after effects. Histamine

is an excitatory neurotransmitter, and seems to cause anxiety in some

people (Hasenöhrl, Weth, and Huston, 1999).

H1 and H2 receptors are the most important of the four types of

histamine receptors. The H1 receptor is coupled to the inositol

triphosphate (IP3) / diacylglycerol (DAG) route, and the H2 receptor is

coupled through cAMP. Although histamine sends a signal through both

excitatory receptors, activation of a street can lead to depression. H1

receptor, this is probably due to activation of calcineurin, a protein

involved in long-term depression (LTD) of neurotransmission (Winder et

al., 1998). The depression created by the H2 receptor activation is

probably due to the inhibition of neuronal firing down (s,

Yamatodani, and Timmerman, 2000). Another theory is that the H2 receptor

activation causes inhibition of the serotonergic system (Lakoski &

Aghajanian, 1983), which is the purpose of activation of many

antidepressants. A third theory is that histamine indirectly causes the

depression of the inhibition of the release of other neurotransmitters

(Brown, s, & Haas, 2001).

There is evidence that some individuals are much more sensitive to

histamine than in others (Katzung, 1998). In addition to anxiety,

histamine has also been linked to Attention Deficit Disorder (ADD) (pass

through, Bacciottini, Mannion, and Blandina, 2000) and alcoholism

(Lintunen, et. Al, 2002). , The major inhibitory neurotransmitter in the

brain, gamma-amino butyric acid (GABA), inhibits histamine release

(s and Yamatodani Timmerman, 2000), suggesting that control of

histamine levels in the brain is important . Many of the anti-anxiety

drugs affect the GABAergic system.

Histamine can activate the hypothalamic-pituitary-adrenal (HPA), the

main neuroregulatory system in the body. Normally the neurotransmitters

dopamine, serotonin, norepinephrine, control and release of a key

hormone of the HPA axis, corticotropin-releasing factor (CRF) (Tuomisto

& Mannisto, 1985). Given that histamine inhibits the release of

neurotransmitters mentioned above, can unbalance the HPA axis through

overstimulation. Chronic stimulation of the HPA axis can lead to

depression (Hurwitz & Morgenstern, 2001). Histamine release another key

HPA axis adrenocorticotropic hormone (ACTH) (Knigge and Warberg, 1991),

which is directly downstream of the IRC.

We assume that the DAG path generally plays a positive role in mental

health, while the IP3 path can play a negative role (Wachtel, 1990).

Interestingly, histamine has strong potential to stimulate the

activities of IP3 and DAG stimulation, a weak activity (Sarri, croutons,

and Claro, 1995). Of calcium ions (Ca2 +) is released after activation

of the IP3 path. Studies have shown that the release of Ca2 + is greater

in major depression (Kusumi, Koyama and Yamashita, 1991). Calcineurin

protein is downstream of the release of Ca2 +. As mentioned above,

calcineurin is a neurotransmitter involved in depression. Histamine and

calcineurin are involved in mental illnesses and allergic reactions

(Abbas, Lichtman, and Pober, 2000) and therefore the activation of

histamine in calcineurin may play a key role in both these morbid

results.

Further evidence of the potential morbidity of the track is that the

activation of IP3 receptors H1 can inhibit learning and memory (Knoche

et al., 2003), causes hyperactivity (Chiavegatti, hake, and Bernardi,

1998), l " ; case of assault (Yanai et al., 1998). An H2-receptor

mutation may lead to schizophrenia (Brown, s, & Haas, 2001). Some

antihistamines can reduce anxiety by the H1 receptor antagonism (Lader

and o, 1998), while H2 antagonists may have antidepressant effects

(Cantu and Korek, 1991). Both H1 and H2 antagonists may cause a variety

of physical and mental side effects.

Had increased levels of histamine in the increased use of vitamin C

(Nandi, Subramanian, Majumder and Chatterjee, 1974), suggests that

vitamin C regulates the levels of histamine through its antihistamine

effect. Vitamin C is a very effective detoxifying histamine (Clemetson,

1999). " After two weeks of 2,000 mg of vitamin C per day, the level of

histamine in the blood decreased by about 40% below the reference value "

(ston, Retrum and Srilakshmi, 1992, p. 989). Vitamin C increases the

cAMP level (Tisdale, 1975), a key molecule in improving mental health

through cAMP. Perhaps equally important, cAMP inhibits the release of

histamine (Cathcart, 1986). In contrast, low levels of cAMP can increase

the release of histamine (Mohsenin & Dubois, 1987).

Chapter 4: Results and conclusions

Introduction:

In Chapters 1 and 2, this paper has established a theoretical framework

that vitamin C reduces histamine mediated by mental illness. In Chapter

4, the data will be presented that illustrates the many positive effects

on the body of vitamin C, including positive effects on mental illness.

It is known that vitamin C is an essential nutrient for brain function

(Marcos and Marcos, 1989). Positive role of vitamin C in terms of mental

health, as evidenced by its potential to reduce anxiety when used at

high doses (Balch & Balch, 1997). It also has a mild antidepressant

effect (Brody, 2002). Conversely, lack of vitamin C consistently

produces abnormal behavior and fatigue, in addition to the typical skin

lesions seen in scurvy (Petrie and Ban, 1985; Kallner, 1987). When

vitamin C levels are low, the central nervous system and the attempt by

the brain to maintain normal tissue depleting other tissues of vitamin C

(Rose 1988). This finding raises the question of how high or low levels

of vitamin C can affect mental health, if the central nervous system and

brain continually strive to maintain homeostasis of the vitamin.

Understanding this theoretical question lies in the conclusions and

implications section of Chapter 5.

ANALYSIS: N / A

Rating:

Vitamin C induces the formation of myelin, the enzyme activity of the

membrane, the synthesis of hormones, acetylcholine and norepinephrine

release, and also affects neurotransmitter binding, the distribution of

neurotransmitter receptors, and the density of neurotransmitters (Rebec

and Pierce, 1994). At physiological pH (7. 4), " Ascorbic acid causes an

increase in the concentration-dependent, the affinity of

5-hydroxytryptamine (5-HT) for 5-HT3 receptor binding sites (3 sites

serotonin receptors ) (Katsuki, 1996, p. 299). Vitamin C also modulates

dopamine levels. High brain levels of dopamine are associated with

psychosis. This can be achieved with the chronic use of amphetamine

stimulants. Traditional antipsychotics lower levels of dopamine, and are

called neuroleptics. Vitamin C has an experimental syndrome like action,

inhibition by amphetamine-induced locomotion, probably by inhibiting the

neurotransmitter dopamine stimulates (rebecks and Pierce, 1994). When

the neurotransmitter glutamate is injected into the brain potentially

neurotoxic in animals, there is a dramatic increase in the extracellular

release of vitamin C (Katsuki, 1996).

There are a number of ways in which vitamin C improves mental health.

Vitamin C increases the secretion of the hormone oxytocin, which

increases the excitement and Welfare (Brody, 2002). " Ascorbic favors the

formation of myelin " (Rice, 2000, p. 214), which is essential for proper

nerve function. Supplementation of vitamin C inhibits stress-induced

cortisol release, and reduces stress-related mortality (Brody Preut,

Schommer, and Schurmeyer, 2002). The intake of vitamin C to 4 g / day

significantly reduced cortisol levels and increased levels of the

steroid hormone androgen dihydroepiandosterone (DHEA) (Komindr,

Nichoalds, and Kitabchi, 1987).

Vitamin C has been shown to protect the brain from drugs neurotoxicity

(Shankaran, Yamamoto, and Gudelsky, 2001). Elderly with high levels of

vitamin C are better memory performance (Perrig, Perrig, and Stahelin,

1997). Another study found that pensioners who have served with vitamin

C had a lower rate of cognitive decline (Paleologos, Cumming, & Lazarus,

1998). Supplementation of vitamin C 3 g / day has been reduced and

subjective anxiety responses to psychological stress (Brody, Preut,

Schommer, and Schurmeyer, 2002). Vitamin C can reduce anxiety in animal

behavior (Brody, 2002).

Neuronal oxidative damage has proved to be inhibited by vitamin C

(Hediger, 2002). Vitamin C also protects against neuronal death by

glutamate buffer generated reactive oxygen species, known as ROS (Rice

2000). The catecholamine catecholamine neurotransmitters epinephrine,

norepinephrine and dopamine are easily oxidized, oxidized and may be

neurotoxic. Vitamin C prevents metal ion-induced oxidation of

catecholamines and also detoxifies the degradation products of

catecholamines (Gruenwald, 1993). Vitamin C inhibits glutamate-induced

rapid firing neurons (Kiyatkin and rebec, 1998), which provide a

protective effect against glutamate-mediated neurotoxicity.

Vitamin C stimulates dopamine inhibits adenylate cyclase, even at low

concentrations (not alter the basal activity of adenylate cyclase)

( & Zemp, 1977). Adenylate cyclase produces cAMP. However, vitamin

C does not inhibit noradrenaline stimulates adenylate cyclase (Tolbert,

, Middaugh, and Zemp, 1979). The aforementioned difference in

adenylate cyclase interactions have important theoretical implications.

Given that high levels of dopamine can cause psychosis, vitamin C

inhibition of dopamine stimulated adenylate cyclase may be the primary

mechanism of its action on the type of neuroleptic drugs. By inhibiting

dopamine stimulates adenylate cyclase, vitamin C may be useful in the

treatment of dopamine-related disorders such as tardive dyskinesia,

schizophrenia and Huntington's disease (Tolbert, , Middaugh, and

Zemp, 1979 ). Vitamin C reduces many symptoms of neurological disease

Huntington's disease (rebec, Barton, Marseille, and , 2003).

There are a multitude of environmental contaminants that can reduce

levels of vitamin C. Snuff, alcohol, steroids, analgesics, oral

contraceptives, antidepressants, anticoagulants and may reduce the

tissue and blood levels of vitamin C (Balch & Balch, 1997). The lack of

vitamin C can cause susceptibility to carbon monoxide, lead and mercury

poisioning (Vayda, 1994), because vitamin C plays an active role in the

detoxification of these chemicals. The three chemicals listed above have

shown brain toxins. The lack of vitamin C can lead to anemia, soft

tires, capillary weakness, tooth decay, bleeding of skin, loss of

appetite and weakness (Hoffer and , 1978). Not only is excess

glucose leads to many chronic diseases, which also inhibits cellular

uptake and accumulation of vitamin C in immune system cells in

neutrophils (Washkar, Rotra, and Levine, 1991).

Abstract:

There are many reasons to complete (megadoses) with vitamin C, in

addition to improving and / or maintain mental health. White blood cell

levels in the blood of vitamin C is only raised in line with the

recruitment of six grams or more per day (Janson, 2000). Vitamin C helps

the cellular and humoral immune response (Janson, 2000). Epidemiological

studies have shown that elevated plasma levels of vitamin C correlated

with a reduction in the mortality rate of approximately 33% (Boeing &

Rausch, 1996). Vitamin C appears to facilitate social interactions, and

that depletion of vitamin C in rats inhibits social behavior (rebec &

Wang, 2001).

Vitamin C attenuates the subjective responses to psychological stress

and also " reduces stress-induced release of cortisol stress indicators

and others, including mortality after stressors (Brody Preut, Schommer,

and Schurmeyer, 2002 , p. 320). Vitamin C can also improve mental health

in a more indirect. And " know that allergies and asthma are physically

and mentally irritating to people. People who doubled their intake of

vitamin C 100-200 mg / day had 30% less bronchitis and / or dyspnea

(Feinstein, 1996). Vitamin C also partially blocks the synthesis of

inflammatory prostaglandins and leukotrienes (Feinstein, 1996).

There are a number of different foods and vitamin C and vitamin

interactions with pharmaceutical antihistamines that are worthy of note.

Folic acid supplements may increase histamine-related allergic symptoms

(Pfeiffer, 1987). Therefore, people with allergies, and a vitamin B

complex can decide not to include folic acid. High copper content can be

destructive of vitamin C and can also produce a pellagra-like mental

illness (Pfeiffer, 1987). Once again, people who take dietary

supplements, for example, a multimineral supplement may be helpful to

avoid integration with copper, unles

Tags: Attenuation

<http://lymedisease.medical-topics.com/tag/attenuation/> , Histamine

<http://lymedisease.medical-topics.com/tag/histamine/> , Illness

<http://lymedisease.medical-topics.com/tag/illness/> , Mental

<http://lymedisease.medical-topics.com/tag/mental/> , part

<http://lymedisease.medical-topics.com/tag/part/> , Role

<http://lymedisease.medical-topics.com/tag/role/> , Vitamin

<http://lymedisease.medical-topics.com/tag/vitamin/>

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warning: I briefly looked through the text and there are some obvious errors;

maybe some of them are typing errors or translation problems (some parts look

like they were automatically translated from another language, without and

editing ...).