CCKB receptors mediate CCK-8S-induced activation of dorsal hippocampus CA3 pyramidal neurons: An in vivo electrophysiological study in the rat
✍ Scribed by Benjamin Gronier; Guy Debonnel
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 920 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0887-4476
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✦ Synopsis
Abstract
The sulphated octapeptide C‐terminal fragment of cholecystokinin (CCK‐8s) is present in high concentration in the mammalian brain, where it acts via two types of receptor denoted CCK~A~, and CCK~B~. In the dorsal hippocampus, CCK‐8S exerts a potent excitatory effect on pyramidal neurons. The present electrophysiological study was undertaken to determine which CCK receptor type mediates this neuronal activation. Using in vivo extracellular unitary recordings of CA~3~ pyramidal hippocampal neurons, we compared the effect of SNF‐8702, a potent selective CCKB receptor agonist, to that of CCK‐BS, and assessed the effects of selective CCK~A~, and CCK~B~, antagonists. CCK‐8S and SNF‐8702, microiontophoretically applied on the same neurons produced a similar degree and pattern of activation. Both CCK‐8s‐ and SNF‐8702‐induced activations were suppressed by the microiontophoretic application of the CCK~B~ antagonist CI‐988, but not by that of the CCK~A~, antagonist SR 27897. CCK‐8s‐induced activation was not significantly modified by the intravenous administration of the CCK, antagonists devazepide and SR 27897. However, it was reduced by the CCK~B~ antagonist PD 135158, administered intravenously or intracerebroventricularly, and by the intravenous administration of the CCK, antagonist L‐365,260. The intravenous administration of PD 135158 also reduced SNF‐8702‐induced activations. These results indicate that CCK~B~, receptors mediate CC K‐8S‐induced activation of rat CA~3~ pyramidal neurons. © 1995 Wiley‐Liss, Inc.