Abstract

To further examine the role of central catecholamine neurons on aggressive behavior, we observed the effects of 6-hydroxydopamine (6-OHDA) bilaterally injected into the lateral hypothalamus in rat on the latencies for attacking and killing a natural prey, frog. For the group, intrahypothalamic 6-OHDA, but not vehicle control, resulted in a reduction in the probabilities that an individual rat would attack or kill a frog, in the latencies for attack or kill, and in the intensity in the execution of the act of killing itself. The impaired behavior persisted up to 45 days and fluctuated from day to day. On some days treated animals would kill most frogs; on others none. While the latencies in treated animals for attack and kill were often increased on some days, these latencies would be close to control on others. Motor activity and feeding and drinking behavior remained depressed throughout. The injection significantly reduced the concentrations of norepinephrine in the forebrain and hypothalamus and dopamine in the caudate nucleus. Norepinephrine in the brain stem was not changed. We conclude that interruption of central catecholamine pathways passing through or terminating in the lateral hypothalamus impairs predatory aggression by interfering with the ability of a rat to initiate sustained killing (motivational deficit) and/or in recognizing the frog as prey (perceptual defect) and not in the ability to execute and perform the motor act of killing.

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