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 regulation of neuropeptide Y (NPY) and corticotropin releasing factor (CRF) synthesis and expression in amygdala neurons. On the other hand, some other studies indicated that not only dopamine, but also other monoamines may modulate peptidergic neurons. Therefore the present study examined the effect of pharmacological deprivation of monoaminergic influences on NPY and CRF neurons in rat brain amygdala by means of in situ hybridization and immunohistochemical methods. It was found that NPY mRNA expression in the amygdala decreased after 24h blockade of dopaminergic D1 and D2 receptors, by haloperidol or SCH23390. At the same time the NPY-peptide expression measured immunohistochemically was not significantly changed. A prolonged, 14-day, blockade of dopaminergic receptors by haloperidol induced an opposite effect, an increase in NPY mRNA expression. Impairment of the serotonergic transmission by blockade of 5-HT synthesis using p-chlorophenylalanine, as well as attenuation of the noradrenergic transmission by NA depletion from terminals by DSP4, did not significantly change NPY mRNA expression or the mean number of NPY-immunoreactive neurons in the amygdala. Only a decrease in the staining intensity observed as a decreased number of darkly stained neurons was found after both compounds. Neither the dopamine receptor blockade nor the impairment of serotonergic or noradrenergic transmission changed CRF mRNA or the peptide expression in the amygdala. The obtained results indicate that in rat brain amygdala, of all the monoamines, dopamine seems to be the most important modulator of NPY biosynthesis and expression. The effect of blockade of dopaminergic receptors is biphasic: first it induces a decrease and then - after prolonged treatment an increase in NPY mRNA. Serotonergic and noradrenergic systems in the amygdala seem to be connected with regulation of NPY release rather than the biosynthesis.
Smiałowska
M
M
Department of Neurobiology, Institute of Pharmacology, Kraków, Poland. nfsmialo@cyf-kr.edu.pl
Bajkowska
M
M
Heilig
M
M
Obuchowicz
E
E
Turchan
J
J
Maj
M
M
Przewłocki
R
R
D000679:Amygdala / Q000737:chemistry / Q000502:physiology*; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000032:analysis / Q000235:genetics*; D018492:Dopamine Antagonists / Q000494:pharmacology*; D010134:Fenclonine / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D006220:Haloperidol / Q000494:pharmacology*; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D009478:Neuropeptide Y / Q000032:analysis / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012702:Serotonin Antagonists / Q000494:pharmacology
D001552:Benzazepines; D018492:Dopamine Antagonists; D009478:Neuropeptide Y; D012333:RNA, Messenger; D012702:Serotonin Antagonists; D003346:Corticotropin-Releasing Hormone; D006220:Haloperidol; D010134:Fenclonine