An enkephalinergic mechanism involved in amygdaloid suppression of affective defence behavior elicited from the midbrain periaqueductal gray in the cat.
A series of recent studies in our laboratory have provided evidence that opioid peptides powerfully suppress feline affective defense behavior at the level of the midbrain periaqueductal gray (PAG). In the present study, we tested the hypothesis that the central (CE) nucleus of the amygdala constitutes a significant inhibitory input to the PAG which utilizes enkephalins as its neurotransmitter or neuromodulator. Cannula-electrodes were implanted into the PAG for the elicitation of affective defense behavior as well as for infusion of opioid antagonists. Monopolar stimulating electrodes were also implanted into the central, lateral and medial amygdaloid nuclei from which suppression or facilitation of affective defense behavior could be obtained. Initially, 4 trials of concurrent, subseizure stimulation of the CE or lateral amygdala at very low (100 microA, 60 Hz) currents and PAG resulted in an immediate suppression of this response which displayed a time dependent decline after 30 min. In the next stage of the experiment, naloxone (2.7, 18.9 and 27.5 nM) was microinjected through the cannula-electrode into the PAG affective defense site and the experimental procedures noted above were repeated. Naloxone treatment (at 27.5 and 18.9 nM) blocked the suppressive effects of CE and lateral amygdaloid stimulation in a dose and time dependent manner. Further analysis revealed that this effect is likely mediated via the mu receptor since the suppressive effects of amygdaloid stimulation were blocked by the selective mu antagonist, beta-Funaltrexamine (0.05 and 0.2 nM) but not by the selective delta-antagonist, ICI 174,864 (0.7 nM).(ABSTRACT TRUNCATED AT 250 WORDS)
Shaikh
M B
MB
Department of Neurosciences, New Jersey Medical School, Newark 07103.
Lu
C L
CL
Siegel
A
A
D000339:Affect / Q000502:physiology*; D000374:Aggression / Q000502:physiology*; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D004743:Enkephalin, Leucine / Q000031:analogs & derivatives / Q000494:pharmacology; D004745:Enkephalins / Q000502:physiology*; D005260:Female; D005456:Fluorescent Dyes; D006710:Homocysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010487:Periaqueductal Gray / Q000033:anatomy & histology / Q000502:physiology*; D011957:Receptors, Opioid / Q000502:physiology; D017465:Receptors, Opioid, delta; D017450:Receptors, Opioid, mu; D013239:Stereotyped Behavior / Q000502:physiology; D013266:Stilbamidines
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D004745:Enkephalins; D005456:Fluorescent Dyes; D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D017465:Receptors, Opioid, delta; D017450:Receptors, Opioid, mu; D013266:Stilbamidines; D006710:Homocysteine; C007956:homocysteic acid; D009270:Naloxone; D004743:Enkephalin, Leucine; D009271:Naltrexone; C024524:beta-funaltrexamine; C040643:N,N-diallyl-tyrosyl-alpha-aminoisobutyric acid-phenylalanyl-leucine