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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The role of glutamate in producing tissue damage during cerebral anoxia was investigated in brain slices using antagonists to the NMDA and AMPA receptor types. 2. Tissue function was assessed by field recordings of the synaptically evoked potentials elicited by stimulating the main afferent input to the olfactory cortex, the lateral olfactory tract. Anoxia was produced by bathing the slice in glucose-free solution equilibrated with 95% N2/5% CO2. 3. The amount of recovery of the evoked potential was inversely dependent on the period of anoxia and temperature: at 24 degrees C, 15 min of anoxia followed by reoxygenation produced a 14.6 +/- 4.1% recovery whereas there was no recovery at 35 degrees C. 4. Dizocilpine and ketamine had no effect on synaptic transmission in oxygenated media but following anoxia they produced an increased recovery of the responses: from 14.6 +/- 4.1% to 48.3 +/- 7.8% for dizocilpine (10 microM) and 21.6 +/- 7.7% to 87.2 +/- 7.1% for ketamine (200 microM); the tissue endurance to anoxia was increased by around 5 min. 5. Blockade of the AMPA receptors did not influence recovery in spite of the depressed synaptic transmission. A similar synaptic attenuation produced by lignocaine provided some increase in post-anoxic recovery. 6. The NMDA receptor antagonist, AP5, antagonized NMDA at 50 microM by 3.7 fold and at 200 microM by 15 fold but only 200 microM increased post-anoxic recovery. This suggests that a substantial degree of NMDA antagonist is required before anoxic tissue damage due to NMDA receptor activation can be nullified. The antagonist to the glycine binding site, 7-chlorokynurenic acid also increased recovery. 7. These in vitro experiments confirm the idea that NMDA receptor activation makes a substantial contribution to cerebral tissue damage and that this can be reduced by a substantial blockade of these receptors.
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PMID:NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia. 791 73

Anoxia rapidly elicits hyper-excitability and cell death in mammal brain but this is not so in anoxia-tolerant turtle brain where spontaneous electrical activity is suppressed by anoxia (i.e. spike arrest; SA). In anoxic turtle brain extracellular GABA concentrations increase dramatically and impact GABAergic synaptic transmission in a way that results in SA. Here we briefly review what is known about the regulation of glutamatergic signalling during anoxia and investigate the possibility that in anoxic turtle cortical neurons GABA(A/B) receptors play an important role in neuroprotection. Both AMPA and NMDA receptor currents decrease by about 50% in anoxic turtle cerebrocortex and therefore exhibit channel arrest, whereas GABA-A receptor currents increase twofold and increase whole-cell conductance. The increased post synaptic GABA-A receptor current is contrary to the channel arrest hypothesis but it does serve an important function. The reversal potential of the GABA-A receptor (E(GABA)) is only slightly depolarized relative to the resting membrane potential of the neuron and not sufficient to elicit an action potential. Therefore, when GABA-A receptors are activated, membrane potential moves to E(GABA) and prevents further depolarization by glutamatergic inputs during anoxia by a process termed shunting inhibition. Furthermore we discuss the presynaptic role of GABA-B receptors and show that increased endogenous GABA release during anoxia mediates SA by activating both GABA-A and B receptors and that this represents a natural oxygen-sensitive adaptive mechanism to protect brain from anoxic injury.
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PMID:Oxygen sensitive synaptic neurotransmission in anoxia-tolerant turtle cerebrocortex. 2308 Jan 45