Inhibition of the tail flick reflex following microinjection of morphine into the amygdala.
Recent evidence indicates that the amygdala plays a critical role in the activation of brain stem antinociceptive systems during stress. In the present experiment, bilateral microinjection of morphine sulfate (10 micrograms) into the amygdala of pentobarbital-anesthetized rats resulted in a time-dependent elevation in latency of the tail flick reflex evoked by radiant heat. The most effective sites within the amygdala were in or immediately adjacent to the basolateral nucleus. The relative amplitude of the tail flick reflex did not differ as a function of repeated testing or morphine treatment. These results suggest that important forebrain inputs which normally activate endogenous antinociceptive systems in behaving animals may be manipulated and studied in detail using the anesthetized rat.
Department of Psychology, University of Wisconsin-Milwaukee 53201.
F J
FJ
Helmstetter
P S
PS
Bellgowan
S A
SA
Tershner
D000679:Amygdala / Q000033:anatomy & histology; D000818:Animals; D008297:Male; D008845:Microinjections; D009020:Morphine / Q000008:administration & dosage / Q000494:pharmacology*; D009619:Nociceptors / Q000187:drug effects; D010147:Pain Measurement / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000187:drug effects*; D012039:Regional Blood Flow / Q000187:drug effects; D012881:Skin Temperature / Q000187:drug effects; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology
D009020:Morphine