CCKB receptor activation protects CA1 neurons from ischemia-induced dysfunction in stroke-prone spontaneously hypertensive rats hippocampal slices.
We examined the effect of cholecystokinin octapeptide sulfated type (CCK-8S) on dysfunction of CA1 pyramidal neurons induced by in vitro ischemic insult in hippocampal slices of stroke-prone spontaneously hypertensive rats (SHRSP). CCK-8S shortened the time required for partial recovery from block of a population spike produced by ischemia. Furthermore, CCK-8S reduced ischemic insult-induced accumulation of K+ in extracellular space. Suppression of the K+ conductance by the CCKB receptor activation is suggested to contribute to neuroprotection by CCK-8S.
Yasui
M
M
Division of Pharmacology, Shionogi & Co., Ltd., Osaka, Japan.
Kawasaki
K
K
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology; D002545:Brain Ischemia / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000235:genetics / Q000503:physiopathology*; D020109:Devazepide; D004594:Electrophysiology; D006624:Hippocampus / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors / Q000502:physiology*; D012844:Sincalide / Q000494:pharmacology
D001570:Benzodiazepinones; D011949:Receptors, Cholecystokinin; D020109:Devazepide; D012844:Sincalide; D011188:Potassium