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

Bilateral occlusion of common carotid arteries in Mongolian gerbils was produced for the periods (up to 15 min) which were shown to be totally reversible. There was an initial increase of cyclic AMP and GABA levels and enhanced activities of adenylate cyclase and glutamate decarboxylase, as well as the reduction of norepinephrine level and decreased activities of monoamine oxidase, GABA-transaminase and Na+-K+-ATPase. Following these changes, decreased concentration of dopamine, serotinin and glutamate were found. The activities of total protein kinase and acetylcholinesterase were found to be reduced after longer periods of short-term ischemia. The data are consistent with the concept of increased non-controled release of putative neurotransmitters in ischemia.
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PMID:Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex. 3 75

Dopamine (DA), serotonin (5-HT), tryptophan (TRP), 5-hydroxyindole acetic acid (5-HIAA), and GABA were assayed spectrofluorometrically in various regions of 16 human post-mortem brains with acute and old cerebral infarction. In both recent and older strokes a total depletion of DA and 5-HT in the necrotic tissue was associated with mild reduction of these compounds in remote non-ischemic areas of the injured, and less of the contralateral cerebral hemispheres. 5-HIAA was significantly reduced in acute ischemic necrosis, while the perifocal edema zone showed considerable accumulation of both 5-HT and 5-HIAA. Marked elevation of the 5-HT precursor TRP and of GABA was present in both the necrotic center and perifocal edema of acute infarcts, which also showed a mild reduction of total proteins. The degradation zone surrounding old infarcts showed a mild decrease of both 5-HT and 5-HIAA with normal TRP levels, indicating normalization of the previously increased 5-HT metabolism and turnover after decrease of acute cerebral edema. These data which confirm previous studies in experimental cerebral ischemia and stroke indicate that disorders in the metabolism of brain monoamines and other putative neurotransmitters contribute to the development of postischemic brain damage and the complicating cerebral edema. They are also in keeping with the concept that unilateral focal ischemia produces bilateral effects on brain monoamines.
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PMID:Changes of some putative neurotransmitters in human cerebral infarction. 3 76

Shifts in the system of GABA transformation in ischemia and specific inhibition of GABA-transaminase under conditions of quantitative measurement of the blood circulation by means of hydrogen clearance permitted to establish a definite association between the increased GABA level in the brain and the tissues of the wall of its arteries, and the development of compensation of disturbed cerebral circulation. Consequently, one of the principal manifestations of an increased amount of endogenous GABA in deficiency of the brain blood supply was GABA capacity to improve the cerebral circulation.
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PMID:[GABA system as a factor facilitating the development of compensation of disordered cerebral hemodynamics]. 62 80

The effects of cellular mediators that contribute to ischemia-induced neuronal degeneration on gamma-aminobutyric acid (GABAA)-receptor function were studied. In vitro, phospholipase A2 (PLA2) inhibited muscimol-induced 36Cl- uptake in cerebral cortical synaptoneurosomes. The major hydrolysis product of PLA2 activity, arachidonic acid, also inhibited GABA-mediated 36Cl- uptake. The unsaturated nature of arachidonic acid makes it (and its metabolites) highly susceptible to peroxidation by oxygen radicals. Incubation of synaptoneurosomes with the superoxide radical-generating system, xanthine and xanthine oxidase, decreased muscimol-induced 36Cl- uptake, suggesting that the peroxidation of arachidonic acid and/or its metabolites interferes with GABAA-receptor function. Another factor involved in ischemia-induced neuronal degeneration is an increase in intracellular Ca2+. Calcium also inhibited GABA-mediated 36Cl- flux, consistent with its ability to activate PLA2. In contrast, Mg2+, which blocks Ca2+ channels, enhanced muscimol-induced 36Cl- uptake, consistent with its neuroprotective effects. Each of these cellular processes is activated during cerebral ischemia and can lead to neuronal degeneration. We used a model of transient forebrain ischemia in gerbils to determine if GABAA-receptor regulation is altered in vivo at a time when CA1 hippocampal cells have degenerated. Four days after a 5 minute bilateral carotid artery occlusion, receptor autoradiography was performed to measure the binding of [35S]t-butylbicyclophosphorothionate (TBPS) to the GABA-gated chloride channel. Significant decreases in TBPS binding were observed only in the dendritic layers (stratum oriens and lacunosem moleculare) of the CA1 hippocampus. The results suggest that ischemia-induced cellular processes that contribute to cell death can decrease GABA-gated chloride channels on dendrites of CA1 pyramidal cells, and that GABAA receptors may also reside on neurons afferent to or intrinsic to the dendritic layers of CA1 hippocampus.
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PMID:Cellular regulation of the benzodiazepine/GABA receptor: arachidonic acid, calcium, and cerebral ischemia. 131 67

After the middle cerebral artery of rats was occluded, changes in the content of 14 free amino acids and the activity of antioxidant enzymes in the ischemic striatum were assessed with respect to the duration of ischemia. Glu and Asp levels were significantly reduced by 60 min of ischemia, GABA was increased by 30 and 60 min and Ala was increased by 5, 15, and 30 min. During ischemia, the levels of striatal Gln, Asn, Ser, Tau, Gly and Pro were found to be normal. In comparison with the sham-operated rats, the changes in the content of Thr, His, Arg and Tyr were inconclusive, since the effect of operative stress could not be ruled out on such occasion. Concomitantly, the Zn-Cu superoxide dismutase and glutathione peroxidase activity were significantly reduced by 30 min of ischemia. It revealed that the reduced capacity to scavenge the oxygen free radicals occurred during the early stage of cerebral ischemia. The above changes of Glu, Gln, GABA and Pro level might be considered as the final outcome of the decrease of glutamate synthesis, the acceleration of its conversion to GABA, and the extracellular leakage of glutamate. According to our data, the oxygen free radicals might be involved in the evolution of primary neuronal damage at the ischemic striatum.
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PMID:[Mechanism of neuronal damage caused by cerebral ischemia]. 133 25

In gerbil brain, levels of hydroxyl radicals (OH.) and neurotransmitters such as glutamate, aspartate, GABA (gamma aminobutyric acid) are low at birth, reach a plateau and decrease with age. On the other hand, when gerbils are exposed to an ischemia reperfusion insult (IRI) the older animals have a higher stroke index and hydroxyl radical as well as glutamate and other neuromediators are concomitantly increased. This discrepancy is probably due to differences in the ability of old individuals to respond to oxidative stress. The still incompletely understood relationship between oxidative damage to proteins and accumulation of amino acids, which have an important role as neurotransmitters at physiologic concentrations, but may become neurotoxic at high concentrations, is discussed.
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PMID:Free radicals and neurotransmitters in gerbil brain. Influence of age and ischemia reperfusion insult. 136 Feb 81

Changes in content of selected neuroactive amino acids [glutamic acid, aspartic acid, glycine, gamma-aminobutyric acid (GABA) and taurine] and acetylcholine (ACh) in the rat hippocampus following transient forebrain ischemia were investigated using male Wistar rats. Rats were allowed to survive for 1 or 5 days following 10 or 20 min of 4-vessel occlusion, and killed by a focused microwave irradiation. A significant reduction in all neuroactive amino acids examined except GABA was noted in the hippocampus on the fifth day. One day after the 4-vessel occlusion for 10 min, no significant effect on the content of neuroactive amino acids in all brain areas was observed. gamma-Aminobutyric acid content in the hippocampus was only significantly reduced on the fifth day after the occlusion for 20 min. Similarly, a significant decrease in ACh content in the hippocampus was observed on the fifth day after the occlusion for 20 min. Considering the data that a significant loss of neuronal cells in the hippocampus (delayed neuronal death) was detected only 5 days after the 4-vessel occlusion, it can be said that the alterations in the hippocampus of neuroactive amino acids such as glutamic acid, aspartic acid, glycine and taurine are more sensitive than those in GABA and ACh against cerebral ischemia. A possible correlation of these changes of neuroactive amino acids in the occurrence of delayed neuronal death in the hippocampus is also suggested.
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PMID:Changes in content of neuroactive amino acids and acetylcholine in the rat hippocampus following transient forebrain ischemia. 136 66

GABAergic inhibitory mechanisms may offer protection to neurons after global ischemia. We tested the effects of gamma-vinyl GABA, a GABA-transaminase inhibitor, via continuous infusion in the third ventricle (Alza pumps) in a gerbil model of repetitive forebrain ischemia. We used two episodes of 3 min duration with a 'reperfusion' interval of 1 h between the insults. Histological analysis was done with silver staining 5 days after the insult. Our results show that there is significant protection of the hippocampus CA1 region and substantia nigra reticulata in treated animals compared to controls. An increase in GABA levels, decrease in glutamate, or mild hypothermia, may be potential mechanisms for this protection. GABAergic agents may prove useful agents in repetitive ischemia.
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PMID:Gamma-vinyl GABA prevents hippocampal and substantia nigra reticulata damage in repetitive transient forebrain ischemia. 142 28

The hypothesis was tested whether perinatal hypoxic ischemia leads to a preferential degeneration of the GABAergic inhibitory neurons in the cerebral cortex which, in turn, could account for the reported higher risk of developing epilepsy later in life. To that end rat pups, aged 12-13 days, were made hypoxic by employing a combination of unilateral ligation of one of the carotid arteries and a 90-min exposure to 8% O2. After recovery periods of 3, 7, 35 and 150 days, the animals were sacrificed by perfusion fixation and the brains embedded in Epon. Transverse semi-thin sections were alternately stained with an antibody against GABA and with Toluidine blue. By using an unbiased morphometric method (the disector) the number of GABA-immunoreactive (GABA-IR) neurons and the total number of nerve cells per unit volume of tissue were estimated in corresponding neocortical areas in the ipsilateral (damaged) and contralateral ('control') hemisphere. For all animals with post-ischemic survival times of 3 and 7 days GABA-IR cells constituted a lower proportion of the total number of nerve cells in the damaged than in the 'control' cortical areas. This finding was consistent with the outcome of an earlier in vitro study. By contrast, in all animals with a survival time of 35 and 150 days, the proportion of GABA-IR neurons was higher on the damaged than on the 'control' side. This switch in the direction of the left/right differences, apparently depending on the length of the post-ischemic survival time, was statistically significant. No lateralization in the proportion of GABA-IR cells was detected in the cerebral cortex of the control rats. These observations, therefore, do not support the hypothesis that perinatal hypoxic ischemia ultimately leads to a preferential loss of GABAergic neurons in the cerebral cortex.
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PMID:Perinatal hypoxic ischemic encephalopathy affects the proportion of GABA-immunoreactive neurons in the cerebral cortex of the rat. 145 Sep 7

Electron microscope analysis of the CA1 Ammon's horn sector was performed in Mongolian gerbils three days after an incident of short-term ischemia of the forebrain. CA1 pyramidal neurons showed advanced disintegration. Some GABA-ergic interneurons revealed ultrastructural alteration of variable degree. The latter finding contradicts the generally helt view on the relative resistance of CA1 sector interneurons to the ischemic injury. Synapses localized in all cortical layers of the CA1 sector exhibited ultrastructural abnormalities involving both pre- and postsynaptic parts. They consisted in marked swelling and accumulation of unbound electron dense material, considered as calcium deposits. Presynaptic parts revealed additionally reduced number of synaptic vesicles and their abnormal distribution. Contrary to the early postischemic period, the most severe synaptic alterations appeared in stratum pyramidale, radiatum and oriens, involving both small dendritic branchings and their spines as well as large shafts of both basal and apical pyramidal dendrites. Synaptic alterations especially features of the postsynaptic damage correspond to those indicating excitotoxic neuronal lesions. Presynaptic alterations may indicate both cessation of neurotransmission function as well as direct ischemic damage. The presence of calcium deposition seems to favour the former possibility.
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PMID:Influence of short-term ischemia on the ultrastructure of hippocampal gyrus in Mongolian gerbil. III. Synapses in late stage of the pathological process. 148 6


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