Injection of low doses of apomorphine into the nucleus accumbens of rats reduces locomotor activity.
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Animals↗
Biomedical subjects
G Wolterink
Publications and source records attributed to G Wolterink.
Opioid systems in the amygdala can serve as substrate for the behavioral effects of the ACTH-(4-9) analog ORG 2766.
Rats housed individually for 7 days showed a marked decrease in motor activity when tested under intense light conditions in a novel environment as compared to group-housed rats tested under low light conditions. The ACTH analogue ORG 2766 administered into the amygdala decreased the motor activity of group-housed rats tested under low light conditions and increased the motor activity of 7-days isolated rats tested under intense light conditions (ED50: 1-10 pg). Injection of the peptide into the nucleus accumbens was not effective, suggesting that ORG 2766 affects the integration of sensoric stimuli rather than the specific motor output systems. Pretreatment of the rats with the opiate antagonist naltrexone in the amygdala completely blocked the effect of ORG 2766. A similar blockade of the ORG 2766-induced effect could be induced by pretreatment with endorphin antibody suggesting that the "normalizing" activity of ORG 2766 on environmentally induced behavioral changes is mediated by the release of endogenous opioid peptides.
Adrenocorticotropic Hormone↗
Stress-induced hypokinesia is facilitated by ACTH-(7-10).
Subcutaneous treatment with the neuropeptide ACTH-(4-10) induced hypokinesia in rats subjected to a mild stress induced by placing the animals on a non-functional "hot" plate (21 degrees C) for 30 sec, but not in control animals not exposed to this stress-inducing environment. The lowest effective dose of ACTH-(4-10) was 5 micrograms/kg, administered 50 min before testing. The combination of peptide treatment and the mild stress-inducing procedure mimicked the effect of a short intense stress induced by placing the rats on a hot plate (57 degrees C) for 30 sec, suggesting that this stress-induced hypokinesia is mediated by ACTH neuropeptides. Structure-activity relationship studies revealed that the active core for the ACTH-(4-10)-induced hypokinesia is located in the C-terminal tetrapeptide Phe-Arg-Try-Gly (ACTH-(7-10)). Pretreatment with the opioid antagonist naltrexone did not influence the effect of ACTH-(4-10) indicating that activation of opioid systems is not implicated in this behavioral effect of the peptide.
Adrenocorticotropic Hormone↗