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Changes of Neuropeptide Y Messenger RNA and Peptide by Drugs Influencing Endogenous Norepinephrine Content in Cerebrocortex of the Rat

Authors

  • Chiang-Shan Niu,

    1. Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, and
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    • The present address of C.-S. Niu is Department of Pharmacology, Tzu-Chi Junior College of Nursing, Hualien City, Taiwan 97001, R.O.C.

  • Tzen Kwan Chang,

    1. Department of Neurology, China Medical College, Taichung City, Taiwan, Republic of China
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  • Juei-Tang Cheng

    Corresponding author
    1. Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, and
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Address correspondence and reprint requests to Prof. J.-T. Cheng at Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan 70101, R.O.C.

Abstract

Abstract: Cotransmission of classic transmitters at the synapse has been mentioned for both the CNS and the PNS. Neuropeptide Y (NPY) is a cotransmitter in noradrenergic neurotransmission. In an attempt to understand the heteroregulation of norepinephrine (NE) and NPY biosynthesis, the present study was performed using radioimmunoassay of NPY and northern blotting of cDNA probes for characterization of NPY mRNA. Values of NPY-like immunoreactivity (NPY-ir) were elevated in the cerebrocortex from rats that received treatment with fusaric acid, an inhibitor of dopamine-β-hydroxylase, with a parallel decrease in NE. Similar results were also observed in rats treated with DSP-4, an alkylator of vesicles in noradrenergic nerve terminals. Moreover, cerebrocortical NPY-ir was reduced in rats receiving treatment with pargyline, an inhibitor of monoamine oxidase, with an elevation of catecholamine in parallel. Activity of NPY mRNA was modified by these drugs in a similar way. However, values of NPY-ir and NE in the cerebrocortex were not influenced by treatment with sodium nitroprusside or guanethidine at a dose producing hypotensive effect. Mediation of hypotensive reflex can thus be ruled out. The data obtained suggest that in vivo decrease of NE by drugs increases biosynthesis of NPY in the cerebrocortex of rats.

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