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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using experimental cerebral ischemia induced in rats with 4-vessel occlusion, the effects of 2-hour ischemia (ligation group) and 30-minute ischemia followed by 72-hour reperfusion (reperfusion group) on cholinergic system (ChS) was investigated with acetylcholine receptor (AChR), choline acetyltransferase (CAT) and acetylcholine esterase (AChE) as indicators of ChS in seven sections of the brain. The activity of CAT was reduced just after ischemia and tended to decrease further after reperfusion. CAT is known as the specific enzyme of cholinergic neuron (ChN), so the reduction of activity of CAT probably means that the ischemic change of ChN was irreversible after 30-minute occlusion. The activity of AChE was also reduced just after ischemia but tended to recover after reperfusion. AChE is not specific in ChN, so the activity of this enzyme may also reflect activity of postsynaptic neuron. The recovery tendency of AChE, therefore, may have the meaning that the ischemic change of the postsynaptic neuron was reversible. The number of AChR was found to have the tendency to increase after ischemia in more sections of reperfusion group compared with ligation group, which is supposed to show that compensatory reactive increase of the receptor may be retained after reperfusion.
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PMID:[The effects of ischemia and postischemic reperfusion on the brain cholinergic system of the rat]. 273 67

Nonsynaptic mitochondria isolated from rat brain hippocampus were compared with those obtained by means of the same preparative procedure from cerebral cortex and striatum. Protein recovery, marker enzyme activities (lactate dehydrogenase, citrate synthase, and acid phosphatase), state 4 respiration, and response to hypoosmotic shock showed no difference among the three cerebral regions, suggesting homogeneous behavior during the subfractionation procedure. Cholinergic markers--choline acetyltransferase, acetylcholinesterase activities, and high-affinity choline uptake--evaluated on synaptosomes showed the classic regional pattern with an enrichment in the striatum (striatum much greater than hippocampus). The coupling state of the mitochondrial fractions was maintained (respiratory control ratios ranging from 3.62 to 5.08 with glutamate + malate as oxidizable substrates), showing a metabolic competence sufficient to perform metabolic studies. Regional differences were found in state 3, uncoupled state of respiration, and cytochrome oxidase activity. Hippocampus showed the lower values (hippocampus less than striatum less than cortex). A possible role of this lower capacity of mitochondrial energy metabolism in determining the sensitivity of hippocampal neurons to ischemia or epileptic seizures is suggested.
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PMID:Oxidative metabolism of nonsynaptic mitochondria isolated from rat brain hippocampus: a comparative regional study. 283 1

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

We studied the effect of early postnatal hypoxia-ischemia on cholinergic neurons in the developing rat forebrain using immunohistochemistry for choline acetyltransferase (ChAT). In 7-day-old rat pups, hypoxia-ischemia was induced in one cerebral hemisphere by combining unilateral carotid ligation with exposure to 8% oxygen for 2.5 h. This procedure caused brain injury in the hemisphere ipsilateral to ligation, most prominent in the corpus striatum, hippocampus and overlying cortex. In animals sacrificed 2-3 weeks after the insult, at approximately 3 weeks of age, the density of cholinergic cell bodies was slightly higher in the lesioned rostral caudate-putamen than the opposite side (+12%, P less than 0.05). In the more caudal portion of caudate-putamen, this effect was greater. In contrast, the size of the cholinergic perikarya in the injured striatum was significantly reduced. Cholinergic neurons in the septum (Ch1, Ch2), globus pallidus and nucleus basalis (Ch4) were relatively unaffected. Considered together with previously reported neurochemical data, these observations suggest that the immature cholinergic neurons are less vulnerable to death from hypoxia-ischemia than other components of the striatum. However, differentiation of surviving cholinergic perikarya and possibly their axonodendritic processes may be disrupted by the early insult.
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PMID:Effects of postnatal hypoxia-ischemia on cholinergic neurons in the developing rat forebrain: choline acetyltransferase immunocytochemistry. 330 39

Activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in the ventral spinal cord, ventral spinal roots and in the central and peripheral stumps of the sciatic nerve transected under conditions of partial ischemia (produced by aortic ligation just below the renal arteries) were compared to those obtained under intact blood supply in time intervals 5, 10, or 15 days after surgery. The significant increase of ChAT activity in the central part of the sciatic nerve following 15 days of partial ischemia correlated with less significant elevation of ChAT in the ventral spinal cord. The changes of AChE activity were not significant during partial ischemia. ChAT in the peripheral stump of the sciatic nerve following 5 days of partial ischemia was preserved by 40% and AChE by 20% more than under normal blood supply. On the contrary, in the next 5 days interval losses of enzymes activity in the degenerating nerve were greater. ChAT was almost totally inactivated whereas 50% of AChE activity was preserved until the end of period examined.
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PMID:Effect of partial ischemia and axotomy on activities of cholinergic enzymes in lower motor neurons of the dog. 373 73

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75

Activity of cholinacetyltransferase (ChAT. EC 2.3.1.6) and acetylcholinesterase (AChE, EC 3.1.1.7) was monitored during occlusion of arteria cerebri media dx. (MCA) in five areas of the brain cortex, in nucleus caudatus and in the thalamus of the ipsilateral and contralateral hemisphere. After 1 hour of MCA occlusion ChAT and AChE activity was reduced in the ischemised region of the hemisphere, i. e. in gyrus ectosylvius anterior and gyrus sylvius anterior, whereas after 4 hours of occlusion the differences were not significant. In nc. caudatus and thalamus the activity of enzymes during ischemia did not change much.
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PMID:Cholinergic enzyme activity during partial brain ischemia in the dog. 685 92

The vulnerability of striatal and hippocampal neurons to ischemia was studied by measuring the activity of neurotransmitter-related enzymes after transient forebrain ischemia in rats. Activities of glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) were measured 6 h to 8 days after 20, 30 or 40 min of forebrain ischemia, as markers for GABAergic and cholinergic neurons respectively. Transient forebrain ischemia resulted in depression of striatal GAD activity while striatal CAT and hippocampal GAD activities were unaffected. Striatal GAD activity progressively decreased during the first 24 h postischemia and remained depressed 5--8 days later, suggesting irreversible damage to this population of neurons. The stability of striatal CAT and hippocampal GAD activity indicates that these cells were resistant to the present ischemic conditions.
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PMID:The response of GABAergic and cholinergic neurons to transient cerebral ischemia. 710 39

The effects of transient cerebral ischemia by the four-vessel occlusion model on balance beam performance and regional activity of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) and muscarinic binding (MusBnd) were evaluated over a six-month postischemia period in 6- and 24-month-old rats. Cerebral ischemia resulted in an early reduction in balance beam performance in young and old rats that partially recovered. GAD in young and old animals and ChAT in old animals and MusBnd in young and old animals were also significantly altered by ischemia. There was partial recovery of each neurochemical marker noted. In some cases the recovery was partially accounted for by the absence of any age-associated changes in the ischemic group. The results of the present study suggest an age-dependent vulnerability to ischemic injury occurs and that aged brain's gamma-aminobutyric and cholinergic systems are capable of measurable recovery.
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PMID:Temporal profile of neurochemical recovery following injury by transient cerebral ischemia. 767 Oct 23

Effects of pentobarbital on the release of acetylcholine (ACh), the area of CA1 pyramidal cell soma and the immunoreactivity of choline acetyltransferase (ChAT) in the hippocampus following ischemia were investigated. Five minute ischemia significantly decreased the KCl-, atropine-induced and basal release of ACh and the area of CA1 pyramidal cell soma in the hippocampus. Moreover, ChAT immunoreactivity, a marker of pre-synaptic terminal survival in the cholinergic neurons, was lowered 14 days after ischemia-recirculation. Although treatment with pentobarbital (50 mg/kg) 30 min before ischemia provided complete protection against hippocampal CA1 pyramidal cell death, pentobarbital failed to improve the decrements of ACh release and the low ChAT immunoreactivity over the test period. Our study thus showed discrepancies between pre-synaptic neurochemical estimation and post-synaptic morphological observation of the effect of pentobarbital on ischemic damage.
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PMID:Pentobarbital protects against CA1 pyramidal cell death but not dysfunction of hippocampal cholinergic neurons following transient ischemia. 775 62


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