Opposite effects of centrally administered neuropeptide Y (NPY) on locomotor activity of spontaneously hypertensive (SH) and normal rats

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Abstract
Centrally administered neuropeptide Y has been shown to produce sedation manifested by a suppression of locomotor activity and a synchronizing effect on the EEG pattern in normal rats. It has been suggested that this sedative effect of NPY is largely due to a facilitation of the .alpha.-adrenergic transmission line. In the spontaneusly hypertensive (SH) rat, the NPY-induced up-regulation of .alpha.2-adrenoceptors observed in normal rats is absent, and NPY produces a desynchronization of the EEG. In the present study, we have therefore examined the effects of NPY on locomotor activity of SH rats and of inbred controls of the Wistar-Kyoto (WKy) strain, in both morning and evening sessions. In morning sessions, NPY (0.2-5.0 nmol intracerebroventricularly, i.c.v.) increased locomotor activity of SH rats in a dose-related manner. WKy rats were largely inactive per se, and no effects of NPY could be detected. In evening sessions, when spontaneous activity is high, NPY (1.0 nmol i.c.v.) still increased the activity of the SH rats. In WKy rats, an activity suppression similar to that previously reported for normal Sprague-Dawley rats was seen. The present results indicate that the sedative action of NPY in different rats strains correlates with the ability of the peptide to up-regulate .alpha.2-adrenergic receptors.