Effect of hypothalamic surgery on prolactin release induced by 5-hydroxytryptophan (5-HTP) in rats.

Ohgo, Shozo; Kato, Yuzuru; Chihara, Kazuo; Imura, Hiroo; Maeda, Kiyoshi

doi:10.1507/endocrj1954.23.485

Cited by 30 publications

(8 citation statements)

References 15 publications

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“…Dennison et al [5] have reported similar increases in prolactin induced by chlorpromazine or metaclopromide in pituitary stalksectioned, estrogen-treated female monkeys. Our data are also consistent with the reports by Iwasaki et al [8] and Ohgo et al [13], who observed similar increases in prolactin in medial basal hypothalamic-lesioned rats following treat ment with the dopaminergic antagonists sulpiride and chlorpromazine.…”

Section: Discussionsupporting

confidence: 93%

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Stimulation of Prolactin Secretion by Neuroleptics in Rats with Medial Basal Hypothalamic Lesions

Cheung¹,

Neill²,

Weiner³

1981

Neuroendocrinology

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The ability of dopamine receptor antagonists to stimulate prolactin release in rats with medial basal hypothalamic lesions was investigated. Starting levels of prolactin were elevated to approximately 400 ng/ml in animals in which the tuberoinfundibular dopaminergic neurons were completely destroyed by the lesion. In lesioned animals, chlorpromazine administration at doses of 0.1 and 5 mg/kg induced a further 2- to 3-fold significant increase in plasma prolactin levels. The incubation of anterior pituitaries from lesioned animals with 10^–6M chlorpromazine had no effect on prolactin secretion, thereby eliminating the possibility that chlorpromazine itself stimulates prolactin release from the anterior pituitary. A similar increase in plasma prolactin in lesioned rats was also observed with the potent dopamine antagonist d-butaclamol (1 mg/kg). The effect was stereospecific since the inactive isomer l-butaclamol did not produce any change in the circulating levels of prolactin. Pimozide, another dopaminergic antagonist, was ineffective in inducing a further increase in prolactin in lesioned rats when 0.63 mg/kg was used. However, at a 10-fold lower concentration (0.063 mg/kg), pimozide stimulated a significant increase in prolactin in lesioned rats. The involvement of an α-adrenergic mechanism was ruled out by the inability of phentolamine (2.5 mg/kg) to increase prolactin secretion. These data suggest that dopaminergic antagonists can further increase prolactin levels in medial basal hypothalamic-lesioned rats possibly by blocking the inhibitory action of dopamine from nonhypothalamic sources, or by releasing a substance which possesses prolactin-releasing activity.

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Section: Discussionsupporting

confidence: 93%

“…This substance would be under inhibi tory dopaminergic control. The existence of a prolactin-re leasing factor in plasma has been demonstrated in lactating rats [3], 5-hydroxytryptophan-treated rats [13] and hyper prolactinemic women [6].…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Prolactin Secretion by Neuroleptics in Rats with Medial Basal Hypothalamic Lesions

Cheung¹,

Neill²,

Weiner³

1981

Neuroendocrinology

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“…Lu and Meites [21] have reported that MES can block the prolactin releasing effect of serotonin in rats; this inhibition occurs in rats pretreated with fluoxetine, a drug that prevents serotonin reuptake [3], Moreover, prolactin release in response to suckling, a stimulus probably induced by serotonin [17,23], is blocked by MES pretreatment [II]. Some of the excitatory effects of serotonin on prolactin release are thought to occur within the MBH because an increase in prolactin secretion has been observed after 5-hydroxytryptophan administration in rats with an isolated MBH, but not in rats with MBH lesions [26]. Conversely, MacLeod [22] and Kridich el at.…”

Section: Discussionmentioning

confidence: 99%

Evidence that Serotonin Is Involved in Prolactin Release by Electrical Stimulation of the Medial Basal Hypothalamus in the Rhesus Monkey

1980

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The possibility that serotonin plays a role in prolactin secretion after electrical stimulation of the rhesus medial basal hypothalamus (MBH) was investigated. Prolactin responses to electrical stimulation and intravenous injection of 0.5 and 1.0 µg of thyrotropin-releasing hormone (TRH) were evaluated before and after administration of methysergide (MES), a serotonin receptor blocker (2 mg orally every 12 h for 48 h), and bromocriptine (CB-154), a dopamine agonist (2.5 mg orally every 12 h for 48 h). Both electrical stimulation and TRH caused prompt increases in serum prolactin. Prestimulation (basal) prolactin levels in both drug-treated groups were not significantly lower than basal levels in control groups. Pretreatment with MES significantly attenuated the electrically induced release of prolactin but had no effect on the TRH-induced release; CB-154 blocked prolactin release induced by both types of stimulation. The study reported here has provided evidence of a possible role for hypothalamic serotonin in releasing pituitary prolactin.

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“…Diluted rat plasma obtained 40 min after the injection of 5HT was capable of binding of 37% of 1 2 5~-~~~ addedin vitro Discussion. It is well known that 5HT stimulates the secretion of PRL by acting through the central nervous system (21)(22)(23). We have previously reported that hypothalamic VIP is involved, at least in part, in the secretion of PRL induced by 5HT in the rat, since 5HT stimulated VIP release from the hypothalamus (16,17)and immunoneutralization of endogenous VIP with anti-VIP serum blunted PRL release induced by 5HT in the rat (18)(19)(20).…”

Section: Nrsmentioning

confidence: 93%

“…The PSRS was specific for C-terminal residues of porcine PHI, showing no cross reactivity with porcine PHI(1-15), VIP, secretin, glucagon, TRH, human growth hormone releasing factor (GRF) and rat GRF (20). The extract of rat hypothalamus showed a parallel displacement of 1 2 5~-~~~( 1 -2 7 ) binding to the antiserum with porcine synthetic PHI(1-27) and PHI (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27). Analysis of variance and Student's ttest were used for statistical evaluat ion.…”

mentioning

confidence: 99%

Involvement of Peptide Histidine Isoleucine (PHI) In Prolactin Secretion Induced by Serotonin in Rats

Tojo

Kato

Inoue

et al. 1985

Experimental Biology and Medicine

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The possible role of hypothalamic peptide histidine isoleucine (PHI) in prolactin (PRL) secretion induced by serotoninergic mechanisms was investigated in male rats using a passive immunization technique. Intracerebroventricular injection of serotonin (5HT, 10 yg/rat) raised plasma PRL levels both in urethane-anesthetized rats and in conscious rats pretreated with normal rabbit serum (0.5 ml/ rat, iv, 30 min before). Plasma PRL responses to 5HT were blunted in these animals when they were pretreated with rabbit antiserum specific for PHI (0.5 mllrat, iv, 30 min before)(meankSE peak plasma PRL: anesthetized rats 271.3k38.3 n g / m l z 150.0+12.6 ng/ml, p<0.01, conscious rats 54.3'6.8 ng/ml 30.7'4.1 ng/ml, p<0.025). These results suggest that hypothalamic PHI is involved, at least in part, in PRL secretion induced by central serotoninergic stimulation in the rat.

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Effect of hypothalamic surgery on prolactin release induced by 5-hydroxytryptophan (5-HTP) in rats.

Cited by 30 publications

References 15 publications

Stimulation of Prolactin Secretion by Neuroleptics in Rats with Medial Basal Hypothalamic Lesions

Stimulation of Prolactin Secretion by Neuroleptics in Rats with Medial Basal Hypothalamic Lesions

Evidence that Serotonin Is Involved in Prolactin Release by Electrical Stimulation of the Medial Basal Hypothalamus in the Rhesus Monkey

Involvement of Peptide Histidine Isoleucine (PHI) In Prolactin Secretion Induced by Serotonin in Rats

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