Neuropeptide Y increases the inhibitory effects of clonidine on potassium evoked3H-noradrenaline but not3H-5-hydroxytryptamine release from synaptosomes of the hypothalamus and the frontoparietal cortex of the male Sprague-Dawley rat

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Abstract
The release of3H-noradrenaline (3H-NA) and of3H-5-hydroxytryptamine (3H-5-HT) evoked by high-K+ (15 mM) was studied in synaptosomes isolated from the hypothalamus and the frontoparietal cortex of the male Sprague-Dawley rat using a superfusion apparatus. Based on concentration-response curves obtained by analyzing the full-time course of the inhibitory effects of clonidine on3H-NA and on3H-5-HT release neuropeptide Y (NPY) (1 nM) was shown to significantly increase the ability of clonidine to inhibit3H-NA release in synaptosomes isolated from the hypothalamus and from the frontoparietal cortex. NPY (1 nM) alone had no effect on K+-evoked3H-NA release from these regions. In contrast, NPY (1 nM) did not modulate the inhibitory effects of clonidine on3H-5-HT release in the above mentioned regions. These results indicate that NPY can increase the sensitivity of the α2-autoreceptors belonging to hypothalamic NA and/or to adrenaline nerve terminals and to cortical NA nerve terminals, while the α2-heteroreceptors inhibiting3H-HT release in the same brain regions appear not to be regulated by high affinity NPY receptors. Thus, α2-autoreceptors and α2-heteroreceptors appear to be differentially controlled by high affinity NPY receptors at least with regard to regulation of3H-NA and3H-5-HT release, respectively.

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