The role of taurine in neuronal protection following transient global forebrain ischemia.

Osmoregulation and post ischemic glutamate surge suppression (PIGSS) are important mechanisms in the neuroprotective properties of taurine. We studied the role of taurine in PIGSS following transient global forebrain ischemia (TGFI). A group of gerbils received a high dose of continuous intracerebral taurine during the peri-ischemic period. Beta-alanine was given similarly to a negative control group. The control group consisted of animals undergoing only TGFI. On the fourth day following commencement of drug administration, TGFI was induced. Concurrently, half the animals from each group receiving an agent had intracerebral microdialysis. All animals underwent histological assessment at day 7. The microdialysis and histological data was analyzed. Our results showed that taurine treatment did not cause PIGSS. The histological difference between the three groups was statistically insignificant. We conclude that intracerebral taurine in the dosage administered during peri-ischemic period, does not result in PIGSS or histologically evident neuroprotection.

Increased "peripheral-type" benzodiazepine receptor sites and mRNA in thalamus of thiamine-deficient rats.

"Peripheral-type" benzodiazepine receptors (PTBRs) are highly expressed on the outer mitochondrial membrane of several types of glial cells. In order to further elucidate the nature of the early glial cell changes in thiamine deficiency, PTBR sites and PTBR mRNA were measured in thalamus, a brain structure which is particularly vulnerable to thiamine deficiency, of thiamine-deficient rats at presymptomatic and symptomatic stages of deficiency. PTBR sites were measured using an in vitro binding technique and the selective radio ligand [3H]-PK11195. PTBR gene expression was measured by RT-PCR using oligonucleotide primers based upon the published sequence of the cloned rat PTBR. Microglial and astrocytic changes in thalamus due to thiamine deficiency were assessed using immunohistochemistry and antibodies to specific microglial (ED-1) and astrocytic (GFAP) proteins respectively. Significant increases of [3H]-PK11195 binding sites and concomitantly increased PTBR mRNA were observed in thalamus at the symptomatic stage of thiamine deficiency, coincident with severe neuronal cell loss and increased GFAP-immunolabelling (indicative of reactive gliosis). Positron Emission Tomography using 11C-PK11195 could provide a novel approach to the diagnosis and assessment of the extent of thalamic damage due to thiamine deficiency in humans with Wernicke's Encephalopathy.