Abstract
Studies were conducted with the putative δ-opioid receptor antagonist ICI 154,129 (ICI) and the putative δ-receptor antagonist β-funaltrexamine (β-FNA) to investigate their ability to block the acute opioid-like effects of a single electroconvulsive shock (ECS). ICI, but not β-FNA, attenuated the increase in hot-plate escape latencies seen following ECS. From these data, we conclude that ECS activates endogenous opioids which act upon δ rather than μ receptors to result in an increase in hot-plate escape latencies.
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