Guest guest Posted April 23, 2005 Report Share Posted April 23, 2005 According to my very superficial knowledge, the interrelationships of neurotransmitter level fluxes and neural activity vary thruout the brain, so that while GABA signalling will reduce the firing of your average neuron, it can in fact excite the neurons of certain loci. This abstract seems to deal exlusively with the respiratory drive center in the medula, so it would have been useful back when I had an occasional interest in how much wine I could safely drink after snorting one of my housemates Percosets. But I'm not sure what else to say? Do you find that these multi-pharma and/or multi-signaling interactions apply to analgesia? I am aware that there has been some work on combining opiates with drugs that are mainly just NMDA antagonists - I dont know how it turned out. > Dr. Hodologica, you are being paged. > > Abstract: [paragraph breaks added] > Addiction. 1999 Jul;94(7):961-72. > > Comment in: > Addiction. 1999 Jul;94(7):973-4. > > Mechanisms of fatal opioid overdose. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 23, 2005 Report Share Posted April 23, 2005 A point of biology , which you may already know, is that even the exact same receptor can be coupled to different (even opposite) downstream responses in different cells. Not only may an X1 receptor tend to exert different actions than an X2 receptor that binds the same signal molecule X - it can also be the case that X1 activation in/on cell type A has very different results from X1 activation in/on cell type B. Even if A and B are both types of neurons. Quote Link to comment Share on other sites More sharing options...
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