Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Fischer-344 rats aged 6, 12, or 24 months were subjected to four-vessel occlusion cerebral ischemia to assess age-dependent ischemic vulnerability of cholinergic and GABAergic neurons based on choline acetyltransferase (EC 2.3.1.6) and glutamic acid decarboxylase (EC 4.1.1.15) activities. Activities of both enzymes were similar (p greater than 0.05) in 6- (n = 5) and 12- (n = 5) month-old rats. Mean +/- SEM choline acetyltransferase activities in the cortex, hippocampus, striatum, and cerebellum of 6-month-old controls were 75 +/- 5, 123 +/- 9, 415 +/- 9, and 50 +/- 4 nmol acetylcholine/hr/mg protein, respectively, and were 20-30% lower (p less than 0.05) in all brain regions except the cerebellum in 24-month-old controls. Choline acetyltransferase activity was unaffected by ischemia in 6- and 12-month-old rats but was reduced by 30-60% in 24-month-old rats. Mean +/- SEM glutamic acid decarboxylase activities in the cortex, hippocampus, striatum, and cerebellum of 6-month-old controls were 98 +/- 8, 86 +/- 7, 144 +/- 13, and 125 +/- 9 nmol gamma-aminobutyric acid/hr/mg protein, respectively, and 25-35% lower in all regions of 24-month-old controls. After 30 minutes of ischemia and 5 days of recovery, glutamic acid decarboxylase activities were reduced (p less than 0.05) in all brain regions and age groups. However, its activity was decreased (p less than 0.05 compared with age-matched controls) by 55% in the cortex and 79% in the hippocampus of 24-month-old rats compared with 30% and 45% in younger rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-dependent vulnerability of brain choline acetyltransferase activity to transient cerebral ischemia in rats. 292 26

The effects of pre-treatment with ENA-713, an acetylcholinesterase (AChE) inhibitor, on changes in pre- and postsynaptic cholinergic indices in gerbil brain following transient ischemia were studied at 4 and 14 days after recirculation. In the ischemic group, hippocampal acetylcholine (ACh) level was significantly reduced (to 23% of sham-operated controls) at 4 days post-ischemia, but this reduction was completely prevented by ENA-713 treatment. Choline acetyltransferase (ChAT) and cholinesterase (ChE) activities were not significantly changed at 4 and 14 days post-ischemia. Although the maximum number (Bmax) of muscarinic ACh receptor (mACh-R) binding in the hippocampus was decreased (to 44%) without any change in affinity at 14 days post-ischemia, this decrease was also inhibited by ENA-713 treatment. In addition, histological experiment indicated that ENA-713 inhibited ischemia-induced pyramidal cell loss in the hippocampal CA1 regions. Thus, these findings suggest that ENA-713 has protective, neurotrophic and therapeutic effects on cerebrovascular type dementia due to cerebral ischemia.
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PMID:Acetylcholinesterase inhibitor ENA-713 protects against ischemia-induced decrease in pre- and postsynaptic cholinergic indices in the gerbil brain following transient ischemia. 818 20

Peripherin is a 57-kDa type III neuronal intermediate filament protein that appears to play a role in neurite elongation during development and axonal regeneration. Its role in the pathogenesis of cognitive deficits caused by cerebral ischemia is unknown. The purpose of this study was to investigate the location and level of peripherin expression in the central nervous system in response to transient global cerebral ischemia, and the resultant effect of peripherin expression on the cholinergic neurons and Choline acetyltransferase (ChAT) activity in this mouse model of ischemia. Transient global cerebral ischemia was induced in C57BL/6 mice by 20-min bilateral common carotid artery occlusion (BCCAO) with microclips. The resulting impairment of spatial learning and memory was investigated by Morris water maze testing. Peripherin expression was evaluated by immunostaining and Western Blot assay of brain sections. Peripherin expression increased in neurons of the cortex, hippocampus, and thalamus after BCCAO. By double immunofluorescence staining, neurons showed a cytoplasmic co-localization of peripherin and MAP-2, but not of peripherin and GFAP. ChAT activity was determined spectrophotometrically using the assay kit. There was significantly decreased ChAT activity in the cerebral cortex, hippocampus and thalamus in mice of the BCCAO group (p<0.05), compared with the sham group. After BCCAO, peripherin overexpression was significantly correlated with reduction in ChAT activity (r=-0.929; p<0.01), spatial learning and memory were impaired, and peripherin expression was induced in neurons but not astrocytes. Thus, peripherin appears to be a participant in learning and memory impairment in mice.
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PMID:The effects of bilateral common carotid artery occlusion on expression of peripherin and choline acetyltransferase activity in C57BL/6 mice. 2316 18