Selective neuron loss after cerebral ischemia in the rat: possible role of transmitter glutamate.
Male Wistar rats were subjected to 20 min of cerebral ischemia by means of 4-vessel occlusion. The topography of regional, selective neuron loss in this model corresponded to areas with pronounced glutamate high affinity uptake (presynaptic receptors), suggesting that transmitter glutamate is involved in the mechanism of neuron damage. One group of animals was injected with the glutamate antagonist, glutamic acid diethyl ester (GDEE) before ischemia. The regional neuron loss was rated using a semiquantitative scale. No statistically significant difference was found between the groups. The results do not exclude a possible role of transmitter glutamate in the pathogenesis of ischemic brain damage. More specific and potent glutamate antagonists are needed in order to clarify such a mechanism.
D000818:Animals; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology; D002544:Cerebral Infarction / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003342:Corpus Striatum / Q000473:pathology; D003712:Dendrites / Q000648:ultrastructure; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000008:administration & dosage / Q000378:metabolism*; D006624:Hippocampus / Q000473:pathology; D008297:Male; D009410:Nerve Degeneration / Q000187:drug effects; D009474:Neurons / Q000648:ultrastructure; D011689:Purkinje Cells / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D013787:Thalamic Nuclei / Q000473:pathology
D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; C011829:glutamic acid diethyl ester