Pharmacological studies on the monoaminergic influence on the synthesis and expression of neuropeptide Y and corticotropin releasing factor in rat brain amygdala

Our earlier findings concerning the 6-OHDA lesion suggested dopaminergic re gulation of neuropeptide Y (NPY) and corticotropin releasing factor (CRF) s ynthesis and expression in amygdala neurons, On the other hand, some other studies indicated that not only dopamine, but also other monoamines may mod ulate peptidergic neurons. Therefore the present study examined the effect of pharmacological deprivation of monoaminergic influences on NPY and CRF n eurons in rat brain amygdala by means of in situ hybridization and immunohi stochemical methods, It was found that NPY mRNA expression in the amygdala decreased after 24h blockade of dopaminergic D1 and D2 receptors, by halope ridol or SCH23390. At the same time the NPY-peptide expression measured imm unohistochemically was not significantly changed. A prolonged, 14-day, bloc kade of dopaminergic receptors by haloperidol induced an opposite effect, a n increase in NPY mRNA expression. Impairment of the serotonergic transmiss ion by blockade of 5-HT synthesis using p-chlorophenylalanine, as well as a ttenuation of the noradrenergic transmission by NA depletion from terminals by DSP4, did not significantly change NPY mRNA expression or the mean numb er of NPV-immunoreactive neurons in the amygdala. Only a decrease in the st aining intensity observed as a decreased number of darkly stained neurons w as found after both compounds. Neither the dopamine receptor blockade nor t he impairment of serotonergic or noradrenergic transmission changed CRF mRN A or the peptide expression in the amygdala. The obtained results indicate that in rat brain amygdala, of all the monoam ines, dopamine seems to be the most important modulator of NPY biosynthesis and expression. The effect of blockade of dopaminergic receptors is biphas ic, first it induces a decrease and then - after prolonged treatment an inc rease in NPY mRNA, Serotonergic and noradrenergic systems in the amygdala s eem to be connected with regulation of NPY release rather than the biosynth esis. (C) 2001 Harcourt Publishers Ltd.