σ-Ligands and non-competitive NMDA antagonists inhibit glutamate release during cerebral ischemia

doi:10.1016/0304-3940(90)90139-Z

Neuroscience Letters

Volume 117, Issues 1–2, 4 September 1990, Pages 169-174

https://doi.org/10.1016/0304-3940(90)90139-Z Get rights and content

Abstract

Release of glutamate from brain cells is increased during ischemia and is thought to be involved in ischemic damage. In rat hippocampal slices the release of glutamate during ‘in vitro ischemia’ (anoxia without glucose) is shown to be blocked by two groups of compounds: non-competitive $N- methyl- d -aspartate$ (NMDA) antagonists and sigma ligands. The effects are selective for the ischemic glutamate release, which is independent of extracellular Ca²⁺. High K⁺, Ca²⁺ dependent, induced release of glutamate is not inhibited. NMDA receptor blockade normally does not prevent ischemic transmission damage in the rat hippocampal slice. However, when ischemic glutamate release is attenuated, NMDA receptor antagonists do prevent the damage. This indicates that high levels of glutamate may cause damage via non-NMDA as well as NMDA receptors.

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σ-Ligands and non-competitive NMDA antagonists inhibit glutamate release during cerebral ischemia

Abstract

Neurosci. Lett.

Eur. J. Pharmacol.

Neuroscience

Neurosci. Lett.

Neurosci. Lett.

Neuroscience

Trends Neurosci.

Brain Res.

N-Methyl-d-aspartate receptor antagonists: failure to prevent ischemia-induced selective neuronal damage

Sigma receptors regulate contractions of the guinea pig ileum longitudinal muscle/myenteric plexus preparation elicited by both electrical stimulation and exogenous serotonin

J. Neurosci.

PITC derivatives in amino acid analysis

Nature

Biochemical and behavioral effects of sigma and PCP ligands

Synapse

$N- Methyl- d -aspartate$ receptor antagonists: failure to prevent ischemia-induced selective neuronal damage