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Brain Res. 1989 Oct 2;498(2):333-8.

Neuropeptide Y-induced effects on hypothalamic corticotropin-releasing factor content and release are dependent on noradrenergic/adrenergic neurotransmission.

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Department of Medicine, University of Toronto, Ont., Canada.


Neuropeptide Y (NPY) administration increases both hypothalamic corticotropin-releasing factor-like immunoreactivity (CRF-ir) and plasma adrenocorticotropin (ACTH). The dependence of these effects on noradrenaline and adrenaline was investigated by selectively depleting these neurotransmitters with 6-hydroxydopamine (6-OHDA) prior to administration of NPY. This combined treatment decreased hypothalamic CRF-ir (P less than 0.025), an effect isolated to the median eminence (P less than 0.025), whereas plasma ACTH increased greatly compared to 6-OHDA treatment alone (P less than 0.0005). In order to further investigate the potential mechanism of this NPY effect, the alpha 2-adrenergic agonist clonidine was administered to normal rats. This treatment increased plasma ACTH (P less than 0.005) and decreased hypothalamic CRF-ir (P less than 0.025), an effect localized to the median eminence (P less than 0.01). The results from both of these treatments are consistent with increased release of hypothalamic CRF. These data imply that the NPY-induced effects are dependent on normal noradrenergic/adrenergic neurotransmission. Depletion of these neurotransmitters allowed NPY to profoundly stimulate CRF release with no evidence for alteration in synthesis, a result common to alpha 2 stimulation.

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