Literature DB >> 2739753

Effects of withdrawal from chronic exposure to cigarette smoke on hypothalamic and preoptic catecholamine nerve terminal systems and on the secretion of pituitary hormones in the male rat.

K Andersson1, K Fuxe, P Eneroth, A Jansson, A Härfstrand.   

Abstract

A 48 h but not a 72 h or 7 day withdrawal from chronic exposure to cigarette smoke was associated with increased noradrenaline levels (quantitative histofluorimetry) in the subependymal layer (SEL) of the median eminence, the anterior periventricular hypothalamic region (PV I) and the parvocellular part of the hypothalamic nucleus (PA FP) and an increased noradrenaline utilization (tyrosine hydroxylase inhibition by alpha MT) in the SEL and the PV I. Following a 48 h or 72 h but not a 7 day withdrawal from chronic exposure to cigarette smoke an increased catecholamine utilization was found in the medial palisade zone (MPZ) of the median eminence. Reduced serum prolactin, FSH and corticosterone levels were found following a 48 h withdrawal from chronic exposure to cigarette smoke. Following a 72 h withdrawal from chronic exposure to cigarette smoke a reduced concentration of serum prolactin was noted. Chronic exposure to cigarette smoke reduced serum TSH levels and lead to a tolerance development with regard to noradrenaline levels and utilization within the preoptic region with the exception of the periventricular preoptic region. The finding of special interest in the present study is the demonstration of a highly significant lowering of corticosterone serum levels despite maintained blood levels of ACTH as seen 48 h following withdrawal. It is suggested that this type of endocrine change may lead to changes in fear-motivated behaviour and contribute to behavioural withdrawal reactions. The maintained reductions of serum prolactin levels found after 48 h and 72 h of withdrawal from cigarette smoke exposure (cf. Andersson et al. 1985a) is discussed in terms of an increased catecholamine utilization in the medial palisade zone of the median eminance. This activation is suggested to be caused by the development of a prolactin receptor supersensitivity within the medium eminence. The present evidence indicates withdrawal effects mainly in the noradrenaline nerve terminals of the subependymal layer of the median eminence, the anterior periventricular hypothalamic region and the parvocellular part of the paraventricular hypothalamic nucleus which inter alia are involved in regulation of ACTH secretion (cf. Andersson et al. 1985a).

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Year:  1989        PMID: 2739753     DOI: 10.1007/bf00736052

Source DB:  PubMed          Journal:  Naunyn Schmiedebergs Arch Pharmacol        ISSN: 0028-1298            Impact factor:   3.000


  21 in total

1.  Microfluorimetric quantitation of catecholamine fluorescence in rat median eminence. I. Aspects on the distribution of dopamine and noradrenaline nerve terminals.

Authors:  A Löfström; G Jonsson; K Fuxe
Journal:  J Histochem Cytochem       Date:  1976-02       Impact factor: 2.479

2.  Phosphorylation and activation of tyrosine hydroxylase mediate the acetylcholine-induced increase in catecholamine biosynthesis in adrenal chromaffin cells.

Authors:  J W Haycock; J A Meligeni; W F Bennett; J C Waymire
Journal:  J Biol Chem       Date:  1982-11-10       Impact factor: 5.157

3.  Inhalation bioassay chemistry--Walton Horizontal Smoking Machine for inhalation exposure of rodents to cigarette smoke.

Authors:  M R Guerin; J R Stokely; C E Higgins; J H Moneyhun; R W Holmberg
Journal:  J Natl Cancer Inst       Date:  1979-08       Impact factor: 13.506

4.  Differential effects of mecamylamine on the nicotine induced changes in amine levels and turnover in hypothalamic dopamine and noradrenaline nerve terminal systems and in the secretion of adenohypophyseal hormones in the castrated female rat. Evidence for involvement of cholinergic nicotine-like receptors.

Authors:  K Anderson; K Fuxe; P Eneroth; L F Agnati
Journal:  Acta Physiol Scand       Date:  1984-04

5.  Mecamylamine pretreatment counteracts cigarette smoke induced changes in hypothalamic catecholamine neuron systems and in anterior pituitary function.

Authors:  K Andersson
Journal:  Acta Physiol Scand       Date:  1985-11

6.  Rat prolactin and hypothalamic catecholamine nerve terminal systems. Evidence for rapid and discrete increases in dopamine and noradrenaline turnover in the hypophysectomized male rat.

Authors:  K Andersson; K Fuxe; P Eneroth; F Nyberg; P Roos
Journal:  Eur J Pharmacol       Date:  1981-12-03       Impact factor: 4.432

7.  Involvement of cholinergic nicotine-like receptors as modulators of amine turnover in various types of hypothalamic dopamine and noradrenaline nerve terminal systems and of prolactin, LH, FSH and TSH secretion in the castrated male rat.

Authors:  K Andersson; K Fuxe; P Eneroth; L F Agnati
Journal:  Acta Physiol Scand       Date:  1982-09

8.  Phosphorylation of adrenal medulla cell proteins in conjunction with stimulation of catecholamine secretion.

Authors:  C M Amy; N Kirshner
Journal:  J Neurochem       Date:  1981-03       Impact factor: 5.372

9.  Effects of acrylonitrile on rat liver cytochrome P-450, benzo(a)pyrene metabolism and serum hormone levels.

Authors:  O G Nilsen; R Toftgard; P Eneroth
Journal:  Toxicol Lett       Date:  1980-10       Impact factor: 4.372

10.  Dopamine in hypophysial portal plasma of the rat during the estrous cycle and throughout pregnancy.

Authors:  N Ben-Jonathan; C Oliver; H J Weiner; R S Mical; J C Porter
Journal:  Endocrinology       Date:  1977-02       Impact factor: 4.736

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