CCKB receptor activation reduces glutamate-induced depolarization in slices of rat cerebral cortex.
Recent studies on cell cultures have indicated that the neuropeptide cholecystokinin (CCK) can prevent glutamate-induced cytotoxicity. In a preparation of rat cortical tissue placed into a two-compartment bath, the cortical tissue could be depolarized, relative to the corpus callosum, by superfusions of KCl or glutamate (1.25-10 mM). Caerulein (1-100 nM), a CCK receptor agonist, caused a rightward shift of the glutamate dose-response curve. The effect of caerulein was abolished by adding L365,260 (1 microM), a selective CCKB receptor antagonist. These findings suggest that CCK may be a physiological antagonist of glutamate-mediated neurotransmission in the rat brain.
Harro
J
J
Department of Medical Pharmacology, Uppsala University, Sweden.
Westerling
P
P
Oreland
L
L
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000502:physiology; D002108:Ceruletide / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011949:Receptors, Cholecystokinin / Q000378:metabolism*
D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D011949:Receptors, Cholecystokinin; D018698:Glutamic Acid; D002108:Ceruletide