Studies on the effects of opioid, noradrenergic and serotonergic antagonists on the antinociceptive effects of electroconvulsive shock.
Electroconvulsive shock (ECS) evoked a short-latencied elevation in the hot plate and tail flick response latencies. Naloxone administered before or immediately after ECS produced a dose-dependent antagonism of the antinociceptive effect measured at 7 min but not at 2 min after ECS. Intrathecally administered propranolol, methysergide or naloxone had no effect when administered either before or after ECS. In contrast, phentolamine given intrathecally produced a significant antagonism of the reflex latencies otherwise elevated after ECS. These effects appear mediated by an alpha 2-receptor as they were more readily antagonized by yohimbine than prazosin. These observations suggest the presence of two systems, one supraspinal and opioid in character and the other adrenergic with spinal receptors. The differential effects of injecting naloxone before and after ECS suggests that the opioid system is activated between 2 and 5 min after the ECS, while the adrenergic system, as examined by the effects of intrathecal alpha- and alpha 2-antagonists, appears to be activated immediately after the application of the ECS.
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D000698:Analgesia; D000818:Animals; D002490:Central Nervous System / Q000503:physiopathology*; D004597:Electroshock; D004723:Endorphins / Q000502:physiology; D008297:Male; D018377:Neurotransmitter Agents / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012021:Reflex, Abnormal / Q000503:physiopathology; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission
D004723:Endorphins; D018377:Neurotransmitter Agents; D012701:Serotonin; D009638:Norepinephrine