Citation

Han Y, Shaikh MB, Siegel A. Alcohol Alcohol. 1997; 32(6): 657-670.

Affiliation

Department of Neurosciences, University of Medicine & Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA.

Copyright

(Copyright © 1997, Oxford University Press)

DOI

unavailable

PMID

9463720

Abstract

The present study tested the hypothesis that the suppressive effects of ethanol upon predatory attack behaviour in the cat involve a pathway from the medial amygdala to the lateral hypothalamus, and that these suppressive effects are mediated by gamma-aminobutyric acid (GABAA) receptors located in the lateral hypothalamus. Cannula electrodes were implanted into the lateral hypothalamus for elicitation of predatory attack behaviour and for microinjections of the GABAA receptor antagonist, bicuculline. Monopolar stimulating electrodes were implanted into the medial amygdala from which subseizure levels of electrical stimulation suppressed predatory attack behaviour. In the first phase of the study, we compared response latencies for predatory attack behaviour following single stimulation of the lateral hypothalamus alone with those following paired trials of dual stimulation of the medial amygdala plus lateral hypothalamus. Dual stimulation significantly suppressed predatory attack. In the second phase of the study, peripheral ethanol administration (in doses of 0.01, 0.5 and 1.0 g/kg, i.p.) enhanced the suppressive effects of medial amygdaloid stimulation in a dose- and time-dependent manner in which peak effects were obtained 60 min post-injection. In the third phase of the study, bicuculline (0.15 nmol) was microinjected into the lateral hypothalamus both prior to and following paired trials of dual stimulation. Drug infusion blocked the suppressive effects of medial amygdaloid stimulation upon predatory attack behaviour elicited from the lateral hypothalamus, indicating the importance of GABAA receptors in mediating this suppression. In the fourth phase of the study, bicuculline, microinjected into the lateral hypothalamus at the time when ethanol's effects were maximal (i.e. 60-80 min post-ethanol administration), totally blocked the suppressive effects of medial amygdaloid stimulation as well as the enhancing effects of ethanol upon medial amygdaloid suppression of this form of aggressive behaviour. In the last phase of the study, bicuculline (0.15 nmol) infusion into the lateral hypothalamus significantly reduced the suppressive effects of ethanol (1.0 g/kg, i.p.) upon predatory attack behaviour elicited from the lateral hypothalamus. These results support the hypothesis that ethanol's suppressive effects upon predatory attack behaviour in the cat are mediated, at least in part, by GABAA receptors in the lateral hypothalamus. The present and recent findings in our laboratory support the view that GABAA receptors in the lateral hypothalamus are activated, in turn, by a GABAergic pathway which arises from the medial hypothalamus whose neurons receive inputs from the medial amygdala.

Language: en