Cholecystokinin facilitates neuronal excitability in the entorhinal cortex via activation of TRPC-like channels

• Published in: Journal of neurophysiology Vol. 106; no. 3; pp. 1515 - 1524
• Main Authors: Wang, Shouping, Zhang, An-Ping, Kurada, Lalitha, Matsui, Toshimitsu, Lei, Saobo
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.09.2011
• Subjects: Animals; Antibodies - toxicity; Cholecystokinin - antagonists & inhibitors; Cholecystokinin - deficiency; Cholecystokinin - physiology; Entorhinal Cortex - physiology; Mice; Mice, Knockout; Neurons - immunology; Neurons - physiology; Pyramidal Cells - immunology; Pyramidal Cells - physiology; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin B - deficiency; Receptor, Cholecystokinin B - genetics; TRPC Cation Channels - immunology; TRPC Cation Channels - physiology

Cholecystokinin (CCK) is one of the most abundant neuropeptides in the brain, where it interacts with two G protein-coupled receptors (CCK-1 and CCK-2). Activation of both CCK receptors increases the activity of PLC, resulting in increases in intracellular calcium ion (Ca 2+ ) release and activation...