Morphine-Induced Excitation of Pyramidal Neurons is Inhibited by Cholecystokinin in the CAl Region of the Rat Hippocampal

Opiolds increase the excitability of CAl pyramidal neurons in the hippocampus through the inhibition of y-aminobutyric acid re-lease from intemeurons. This can be observed extracellularly as an increase in population spike amplitude. The sulfated form of the neuropeptide cholecystokinin (CCK-8S) has been shown in a variety of in vivo models to inhibit the response to oploids. We have utilized the well-characterized hippocampal response to opioids to examine the potential interactions between morphine and the neuropeptide cholecystokinin (CCK) in vitro. Morphine (1-500 zM; ECso 22.1 M, 95 % confidence interval = 6.5-75.9 zM) alone caused concentration-dependent increases in CAl population spike amplitudes that were reversible upon washout or application of the opiold antagonist naloxone (10 sM). In contrast to the morphine effect, CCK-8S (0.001-1 zM