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J Neurophysiol 84: 2356-2364, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 84 No. 5 November 2000, pp. 2356-2364
Copyright ©2000 by the American Physiological Society

Cannabinoid and Kappa Opioid Receptors Reduce Potassium K Current via Activation of Gs Proteins in Cultured Hippocampal Neurons

Robert E. Hampson, Jian Mu, and Sam A. Deadwyler

Department of Physiology and Pharmacology, Wake Forest University, Winston Salem, North Carolina 27157

Hampson, Robert E., Jian Mu, and Sam A. Deadwyler. Cannabinoid and Kappa Opioid Receptors Reduce Potassium K Current via Activation of Gs Proteins in Cultured Hippocampal Neurons. J. Neurophysiol. 84: 2356-2364, 2000. The current study showed that potassium K current (IK), which is evoked at depolarizing potentials between -30 and +40 mV in cultured hippocampal neurons, was significantly reduced by exposure to the CB1 cannabinoid receptor agonist WIN 55,212-2 (WIN-2). WIN-2 (20-40 nM) produced an average 45% decrease in IK amplitude across all voltage steps, which was prevented by SR141716A, the CB1 receptor antagonist. The cannabinoid receptor has previously been shown to be Gi/o protein-linked to several cellular processes; however, the decrease in IK was unaffected by modulators of Gi/o proteins and agents that alter levels of protein kinase A. In contrast, CB1 receptor-mediated or direct activation of Gs proteins with cholera toxin (CTX) produced the same decrease in IK amplitude as WIN-2, and the latter was blocked in CTX-treated cells. Gs protein inhibition via GDPbeta S also eliminated the effects of WIN-2 on IK. Consistent with this outcome, activation of protein kinase C (PKC) by arachidonic acid produced similar effects to WIN-2 and CTX. Kappa opioid receptor agonists, which also reduce IK amplitude via Gs proteins, were compared with WIN-2 actions on IK. The kappa receptor agonist U50,488 reduced IK amplitude in the same manner as WIN-2, while the kappa receptor antagonist, nor-binaltorphimine, actually increased IK amplitude and significantly reduced the effect of co-administered WIN-2. The results indicate that CB1 and kappa receptor activation is additive with respect to IK amplitude, suggesting that CB1 and kappa receptors share a common Gs protein signaling pathway involving PKC.




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