Glutamate transport in ALS

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See, I'm posting an abstract. Woohoo. Too bad I can't read it. But

for reasons I'd rather not go into, I have to look at ALS now.

Can anyone tell me what this says?

Ann Neurol. 1995 Jul;38(1):73-84. Related Articles, Links

Selective loss of glial glutamate transporter GLT-1 in amyotrophic

lateral sclerosis.

Rothstein JD, Van Kammen M, Levey AI, LJ, Kuncl RW.

Department of Neurology, s Hopkins University, Baltimore, MD,

USA.

The pathogenesis of sporadic amyotrophic lateral sclerosis (ALS) is

unknown, but defects in synaptosomal high-affinity glutamate

transport have been observed. In experimental models, chronic loss

of glutamate transport can produce a loss of motor neurons and,

therefore, could contribute to the disease. With the recent cloning

of three glutamate transporters, i.e., EAAC1, GLT-1, and GLAST, it

has become possible to determine if the loss of glutamate transport

in ALS is subtype specific. We developed C-terminal,

antioligopeptide antibodies that were specific for each glutamate

transporter. EAAC1 is selective for neurons, while GLT-1 and GLAST

are selective for astroglia. Tissue from various brain regions of

ALS patients and controls were examined by immunoblot or

immunocytochemical methods for each transporter subtype. All tissue

was matched for age and postmortem delay. GLT-1 immunoreactive

protein was severely decreased in ALS, both in motor cortex (71%

decrease compared with control) and in spinal cord. In approximately

a quarter of the ALS motor cortex specimens, the loss of GLT-1

protein (90% decrease from control) was dramatic. By contrast, there

was only a modest loss (20% decrease from control) of immunoreactive

protein EAAC1 in ALS motor cortex, and there was no appreciable

change in GLAST. The minor loss of EAAC1 could be secondary to loss

of cortical motor neurons. As a comparison, glial fibrillary acidic

protein, which is selectively localized to astroglia, was not

changed in ALS motor cortex. Because there is no loss of astroglia

in ALS, the dramatic abnormalities in GLT-1 could reflect a primary

defect in GLT-1 protein, a secondary loss due to down regulation, or

other toxic processes.

PMID: 7611729 [PubMed - indexed for MEDLINE]