Effects of apomorphine, clonidine or 5-methoxy-NN-dimethyltryptamine on approach and escape components of lateral hypothalamic and mesencephalic central gray stimulation in two inbred strains of mice.
Pharmacology, biochemistry, and behavior – January 01, 1983
Source: PubMed
Summary
Apomorphine significantly increased approach latency for lateral hypothalamic stimulation and escape latency for central gray stimulation in BALB/c mice, who were more reactive than DBA/2 mice. Clonidine only reduced approach latency in BALB/c mice, while 5-methoxy-NN-dimethyltryptamine (5-m-DMT) extended escape latency for both types of stimulation in DBA/2 mice. These findings indicate different neurochemical pathways regulating escape reactions, with dopamine linked to aversive responses and serotonin influencing both types of escape behaviors. This highlights the complexity of neuronal involvement in these reactions.
Abstract
The effects of intraperitoneal injections of increasing doses of apomorphine, clonidine or 5-methoxy-NN-dimethyltryptamine (5-m-DMT) on approach and escape reactions induced by lateral hypothalamic (LH) or mesencephalic central gray (CG) stimulation were compared in BALB/c and DBA/2 mice. Apomorphine increased both the approach latency for LH stimulation and the escape latency for CG stimulation; the BALB/c strain was more reactive than DBA/2 animals. Clonidine reduced the approach latency for LH stimulation only in the BALB/c strain. 5-m-DMT increased escape latency both for LH and CG stimulation only in the DBA/2 strain. These results suggest that the neurochemical regulation of escape reactions respectively generated by LH or CG activation is partially different: dopamine seems to be involved only in CG aversion, whereas serotonin (5-HT) modulates both LH and CG escape reactions. Moreover, our results demonstrate a noradrenergic influence on the appetitive component of LH stimulation. Finally, they confirm that approach and escape reactions, particularly when induced from lateral hypothalamus, depend on distinct neuronal populations.