Central gray modulation of affective defense is differentially sensitive to naloxone.

Specific areas of feline central gray (CG) modulate affective aggression elicited by hypothalamic stimulation and produce analgesia, possibly mediated by enkephalins. Despite correlations between opiates and aggressive behavior suggested previously, their relationship has not been clearly demonstrated. The goal of this study was to examine the possible role of endogenous opiate mechanisms in CG modulation of affective aggression. Electrodes were placed in the ventromedial hypothalamus (VM) which, when stimulated, elicited affective attack. Control latency to VM-elicited hiss was established. CG cannula-electrodes were then implanted. Response modulation was determined by dual stimulation of CG and VM electrodes, alternated with VM stimulation alone. Naloxone was introduced through the CG electrodes and VM-elicited hiss latency was again determined, followed by paired trials of dual and single stimulation. Six ventral facilitatory and eight dorsal inhibitory sites were identified. Naloxone had no effect on CG facilitation but completely blocked CG inhibition of VM-elicited hissing. In support of these findings, it was observed that D-A1A2-MET5-enkephalin injected directly into CG-inhibitory sites suppressed VM-elicited hissing. These results demonstrate that opiate mechanisms are operative in the inhibitory modulation of intra-specific aggression.

An adrenergic mechanism for visual neuroregulation.

Studies of the diffuse electroretinogram (ERG) and evoked reponses in the optic lobe in the baby chick have shown that epinephrine produces changes in both. Epinephrine produces enhancement of the a-wave and depression of the b- and d-waves in both intact and isolated eyes. In the optic lobe it produces enhancement of both components of the evoked response. The presence of epinephrine in the vertebrate retina and the optic lobe of chicks suggests that these changes may reflect the involvement of epinephrine in synaptic transmission.