Article date: 1992/9/1
PubMed ID: 1327423
Journal name: Brain research bulletin (ISSN: 0361-9230)
Preconditioning the brain with sublethal ischemia induces tolerance to subsequent ischemic insult. Using [3H]quinuclidinyl benzilate (QNB), [3H]MK 801, [3H]cyclohexyladenosine, [3H]muscimol, and [3H]PN200-110, we investigated the alterations in neurotransmitter receptor and calcium channel binding in the gerbil hippocampus following ischemia with or without preconditioning. Two-minute forebrain ischemia, which produced no neuronal damage, resulted in no alterations in binding except for a slight reduction in [3H]QNB binding in the CA1 subfield. Three-minute ischemia destroyed the majority of CA1 pyramidal cells and caused, in CA1, reductions in binding of all ligands used. Preconditioning with 2-min ischemia followed by 4 days of reperfusion protected against CA1 neuronal damage and prevented the reductions in binding although [3H]QNB and [3H]PN200-110 binding transiently decreased in the early reperfusion period, suggesting down-regulation. Thus, preconditioning protects against damage to the neurotransmission system as well as histopathological neuronal death.
Author List: Kato H, Araki T, Kogure K
Publication Types: Journal Article
Substances mentioned in the article: Receptors, Neurotransmitter; Muscimol; N(6)-cyclohexyladenosine; Quinuclidinyl Benzilate; Dizocilpine Maleate; Adenosine; Isradipine;
Mesh terms: Adenosine/analogs & derivatives; Animals; Autoradiography; Brain Ischemia/metabolism; Conditioning (Psychology)/physiology; Dizocilpine Maleate/metabolism; Down-Regulation; Gerbillinae; Hippocampus/anatomy & histology; Isradipine/metabolism; Male; Muscimol/metabolism; Quinuclidinyl Benzilate/metabolism; Receptors, Neurotransmitter/metabolism;