Restraint stress stimulation of prolactin and ACTH secretion: Role of brain histamine

Seltzer, Alicia; Donoso, Alfredo O.; Podesta, EJ

doi:10.1016/0031-9384(86)90012-0

Cited by 42 publications

(20 citation statements)

References 27 publications

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“…However, discrepant results have been reported; Mazurkiewicz-Kwilecki [18] observed increase in the hypothalamic HA level associated with increase in the plasma CS level follow ing air blast stress and Takeda et al [31 ] obtained similar results on double rotation stress of rats. However, Seltzer et al [27] and Kobayashi and Kopin [ 12] suggested the lack of histaminergic participation in the hypophysiocorticoadrenal response to acute restraint stress, a finding that is consistent with our results. There are also some reports stating that increase in HDC activ ity is associated with [ 19] or without an increase in the HA con tent [37] or rather decreased [ 16,32] in response to stress.…”

Section: Discussionsupporting

confidence: 83%

See 1 more Smart Citation

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Itowi¹,

Yamatodani²,

Cacabelos

et al. 1989

Neuroendocrinology

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The effects of cerebral histamine depletion induced by α-fluoromethylhistidine (FMH) on corticotropin (ACTH) and corticosterone secretions were examined. Neither acute nor chronic FMH treatment altered the corticoadrenal responses to three types of stress: transposition, immobilization and water immersion. And exposure to stress did not affect the hypothalamic content of histamine. However, chronic intracerebral treatment with FMH had a significant effect on the circadian rhythm of the plasma corticosterone (CS) level in rats. Namely, it caused a marked attenuation of the amplitude of the peaks of the CS level resulting in an almost arrythmic state. The maximum differences between FMH treated and untreated groups were seen at 8.00 and 20.00 h, the times when the illumination condition changed (light onset 8.00 h). This treatment with FMH also had a similar effect on the plasma ACTH concentration; namely the plasma ACTH level in the saline-treated group was lower than that of the FMH-treated group at light onset and higher than the latter at dark onset, but was similar to the latter at other sampling points. These results indicate the histaminergic modulation of the circadian rhythm of hormonal secretion of the adrenal cortex and show that this phenomenon is mediated through the central nervous system by an influence on the rhythm of hypophyseal ACTH secretion possibly through alteration in the concentration of corticotropin-releasing factor.

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Section: Discussionsupporting

confidence: 83%

“…Control plasma values of ACTH and CS obtained in these assays were consistent with those reported by Mazurkiewicz-Kwilecki [18], Mazurkiewicz-Kwilecki and Bielkiewicz [19], Seltzer et al [27] and Szafarczyk et al [30].…”

Section: Methodssupporting

confidence: 80%

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Itowi¹,

Yamatodani²,

Cacabelos

et al. 1989

Neuroendocrinology

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“…It has earlier been shown that depletion o f brain HA by a-FM H decreased the basal plasma corticosterone level in young and old male rats [19], and that a-FM H had a significant effect on the circadian rhythm o f ACTH and corticosterone secretion in female rats [20]. However, it has also been reported that a-FM H did not inlluence the stress-stimulated plasma corticosterone level in female rats [20] or plasma ACTH bioactivity in male rats [21]. The discrepancies between these studies are difficult to explain since almost the same time schedule and the same doses of a-FM H were used.…”

Section: Discussionmentioning

confidence: 75%

Involvement of Histamine in the Mediation of the Stress-Induced Release of Alpha-Melanocyte-Stimulating Hormone in Male Rats

et al. 1991

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The involvement of histaminergic neurons in the neuroendocrine regulation of the release of the pro-opiomelanocortin-derived peptides adrenocorticotropin (ACTH; anterior pituitary lobe) and α-melanocyte-stimulating hormone (α-MSH; intermediate pituitary lobe) was studied in conscious male rats. Pretreatment with the histamine (HA) synthesis inhibitor (S)-α-fluoromethylhistidine (100 µmol/kg i.p. at -6 h or 400 µmol/kg i.p. at –20 and –6 h) had no effect on basal ACTH release but decreased basal α-MSH release. The two doses of (S)-α-fluoromethylhistidine inhibited by 35 and 50% the ACTH response to 5 min of restraint stress and almost prevented the stress-induced α-MSH release. (S)-α-fiuoromethylhistidine (100 µmol/kg) inhibited the ACTH and α-MSH response to ether stress by 50 and 70%, respectively. Intracerebroventricular administration of the HA metabolism inhibitor SKF 91488 (400 or 800 nmol at-15 min) stimulated basal secretion of ACTH and α-MSH dose-dependently and augmented slightly the restraint- and ether-stress-induced release of ACTH and α-MSH. Intracerebroventricular infusion of the H₁ receptor antagonist mepyramine (0.37 µmol) or the H₂ receptor antagonists cimetidine (0.40 µmol) or ranitidine (0.40 µmol) inhibited or prevented the α-MSH response to intracerebroventricular administration of HA (0.27 µmol), restraint or ether stress. Pretreatment with the dopamine receptor agonist bromocriptine or the β-adrenergic receptor antagonist propranolol inhibited the α-MSH response to HA or stress. The results indicate that hypothalamic histaminergic neurons participate in the neuroendocrine regulation of the pro-opiomelanocortin-derived peptides from the anterior (ACTH) and intermediate (α-MSH) pituitary lobe of male rats. The effect of HA and stress is caused via activation of H₁ and H₂ receptors, and may – concerning the effect on α-MSH secretion – be mediated by tuberohypophysial dopaminergic neurons and peripheral circulating epinephrine.

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“…Histamine (HA), which acts as a hypothalamic neuro transmitter [1,2], stimulates prolactin (PRL) secretion when administered intracerebroventricularly [3,4], In ad dition, histaminergic neurons seem to be involved in the stress-induced release of PRL, as indicated by the finding that the PRL response to restraint or ether stress is inhib ited by blockade of central HA synthesis or blockade of HA receptors [5][6][7], HA does not stimulate the release of PRL by a direct action on the lactotrophs [4,8], and it is therefore likely that the effect of HA is exerted via release of hypothalamic factors which subsequently affect PRL secretion directly.…”

mentioning

confidence: 99%

Involvement of Vasopressin in Histamine- and Stress-Induced Prolactin Release: Permissive, Mediating or Potentiating Role?

Kjær

Knigge²,

Vilhardt³

et al. 1993

Neuroendocrinology

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Arginine vasopressin (AVP) appears to be involved in the histamine (HA)-and stress-induced prolactin (PRL) release. The present investigation was performed in male rats to clarify whether the role of AVP in HA- and restraint stress-induced secretion of PRL is mediating (i.e., the effect of HA or stress is transmitted via AVP) or permissive (i.e., the presence of AVP is required to obtain a stimulatory effect of HA or stress on PRL secretion). Furthermore, we studied whether AVP possessed a potentiating effect on the HA- or stress-induced PRL release. PRL secretion was stimulated 14- to 17-fold by intra-cerebroventricular infusion of HA (270 nmol) or by 5 min of restraint stress. These effects were inhibited about 80% by immunoneutralization of endogenous AVP with a specific AVP antiserum (abAVP). When specific AVP V₁- or V₂-receptor agonists, which were not bound by the AVP antiserum, were administered intravenously together with the AVP antiserum, the PRL response to HA or restraint stress was partly ( > 50%) reestablished. This effect was observed at low (1.2 or 0.1 nmol) as well as high (3.8 or 0.4 nmol) doses of agonists and when these were administered alone or in combination. In non-immunoneutralized animals, separate administration of agonists at low or high doses as well as combined administration of agonists at low doses had no or only a minor effect on PRL secretion, while combined administration of Viand V2-agonist in high doses stimulated PRL secretion 6-fold. Taken together, these observations indicate that AVP has a permissive role. Since the response to HA or restraint stress was only partly reestablished by AVP agonists, it appears that AVP plays a mediating role as well. When AVP was administered in a dose (240 pmol) which had no PRL-releasing effect in itself, the PRL-stimulating effect of a submaximal HA dose or restraint stress was not altered. This excludes a potentiating effect of AVP. We suggest that AVP (probably of hypothalamic origin) has a permissive and probably also a mediating effect on the PRL response to HA or restraint stress.

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Restraint stress stimulation of prolactin and ACTH secretion: Role of brain histamine

Cited by 42 publications

References 27 publications

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Involvement of Histamine in the Mediation of the Stress-Induced Release of Alpha-Melanocyte-Stimulating Hormone in Male Rats

Involvement of Vasopressin in Histamine- and Stress-Induced Prolactin Release: Permissive, Mediating or Potentiating Role?

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