Cholecystokinin enhances GABAergic inhibitory transmission in basolateral amygdala

• Published in: Neuropeptides (Edinburgh) Vol. 41; no. 6; pp. 453 - 463
• Main Authors: Chung, L, Moore, S.D
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.12.2007; Elsevier
• Subjects: Advanced Basic Science; Amygdala - physiology; Animals; Anxiety; Basolateral amygdala; Biological and medical sciences; Brain - physiology; Cholecystokinin; Cholecystokinin - antagonists & inhibitors; Cholecystokinin - physiology; Endocrinology & Metabolism; Fundamental and applied biological sciences. Psychology; GABA; gamma-Aminobutyric Acid; Inhibitory Postsynaptic Potentials; Interneurons; Patch-Clamp Techniques; Rats; Synaptic Transmission; Vertebrates: endocrinology; Basolateral amygdala; GABA; Interneurons; Cholecystokinin; Amygdala; Central nervous system; Gabaergic transmission; Neurotransmitter; Basal ganglion; Neuropeptide; Encephalon; Interneuron
• ISSN: 0143-4179; 1532-2785
• DOI: 10.1016/j.npep.2007.08.001

Abstract The neuropeptide cholecystokinin (CCK) is anxiogenic in studies of human and animal behavior. As the amygdala formation has been implicated in generation of emotional states such as anxiety, we tested the effect of CCK on spontaneous synaptic events in the basolateral amygdala (BLA) using whole cell patch recordings in rat brain slice preparation. We found that CCK increased the frequency of spontaneous inhibitory postsynaptic potentials (sIPSPs) and currents (sIPSCs). This effect was blocked by the fast sodium channel blocker tetrodotoxin (TTX), indicating that the CCK effect is likely mediated by direct excitation of GABAergic interneurons. The CCKB receptor subtype antagonist, CR2945, blocked the CCK effect, while CCK4, a specific CCKB agonist, increased sIPSC frequency. We hypothesize that these actions may underlie the anxiogenic effects of CCK observed in behavioral studies.