Peptides and Psychoneuroendocrinology

Nemeroff, Charles B.; Prange, Arthur J.

doi:10.1001/archpsyc.1978.01770320093009

Cited by 51 publications

(5 citation statements)

References 79 publications

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“…Both steroids accumulate and are metabolized in the brain, including the cortex (Backstrom 1977); the activity of the central nervous system appears to be increased by oestrogen, and decreased by progesterone ). Specific actions have been shown on neurotransmitters and their precursors (Asso 1983), and peptides such as gonadotrophin-releasing factor (Nemeroff 1978) and endorphins (Reid & Yen 1981) have all been implicated in psychological functioning. For example, a deficiency of catecholamines may be involved in the pathogenesis of depression (Schidlkraut 1965) and oestrogens may act as anti-depressant by enhancing central adrenergic activity with an effect on synthesis, degradation, and neuronal uptake (Klaiber et al 1982).…”

Section: Discussionmentioning

confidence: 99%

The effects of norethisterone in postmenopausal women on oestrogen replacement therapy: a model for the premenstrual syndrome

Magos

Brewster

Singh

et al. 1986

BJOG

203

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The influence of norethisterone on mood and behaviour was investigated in prospective placebo-controlled study in 58 postmenopausal hysterectomized women who were being treated with subcutaneous oestradiol and testosterone implants. Norethisterone, 2.5 or 5 mg daily, was given for 7 days and a placebo for two periods of 7 days. Psychological, behavioural and physical variables were assessed using the Menstrual Distress Questionnaire. There were widespread adverse effects which were dose-related. Significant changes in five of the eight symptom complexes studied (pain, concentration, behavioural change, water retention and negative affect) were found with 5 mglday of the progestogen. The symptoms were similar to the typical complaints of the premenstrual syndrome, such that a combination of oestradiol and testosterone implants with cyclical oral norethisterone appears to be a model for this condition. The dose of this progestogen should therefore be the minimum to achieve the desired therapeutic effect.

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Section: Discussionmentioning

confidence: 99%

The effects of norethisterone in postmenopausal women on oestrogen replacement therapy: a model for the premenstrual syndrome

Magos

Brewster

Singh

et al. 1986

BJOG

203

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“…We have suggested, and critically reviewed, a concept of harmony between the endocrine and behavioral action of neuropeptides (32). Guided by this general notion and by the specific suggestion of Klopfer, we proposed to examine the possibility that oxytocin might be a potent inducer of maternal behavior.…”

mentioning

confidence: 99%

Induction of maternal behavior in virgin rats after intracerebroventricular administration of oxytocin

Pedersen

Prange

1979

Proc. Natl. Acad. Sci. U.S.A.

697

357

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Oxytocin produces uterine contractions and milk ejection, functions related to parturition and nurturing. Studies were conducted to determine if this peptide, native to the brain and the posterior pituitary gland, plays a role in the induction of maternal behavior. Intact virgin female rats were given 0.4 ,g of oxytocin, 0.4 1&g of [Arg8Jvasopressin, or saline through lateral ventricular cannulae. Forty-two percent of intact rats receiving oxytocin displayed full maternal behavior towards foster pu s. None of the saline-or vasopressin-treated animals displayed full maternal behavior. Criteria in five behavioral categories had to be fulfilled by an animal within 2 hr of injection for its behavior to be considered fully maternal. When partial maternal responses were considered, oxytocin was significantly more effective than saline and marginally more effective than vasopressin. Five animals responding fully maternally after oxytocin injection were allowed to stay with pups for 10 days. All Rosenblatt (1) demonstrated that male and female rats, including intact virgin females, manifest maternal behavior after contact with foster pups for 5-7 days. Since then, several attempts have been made to shorten the latency for this phenomenon by manipulations of estrogen, progesterone, or prolactin. When these hormones were administered on selected schedules to ovariectomized, nulliparous females over either an 1 -day (2) or 27-day (3) period, latency was reduced to as little as 35 hr.Pharmacologic blockade of prolactin release has no effect on the onset of postpartum maternal behavior (3-5) or estrogen-induced maternal behavior (6). Similarly, induced elevation of prolactin in ovariectomized virgin females does not alter the onset of pup contact-induced maternal behavior (7). Progesterone has been found by most investigators to inhibit the onset of maternal behavior under various experimental conditions (8, 9), though dosage and timing of progesterone administration seem to be important (10).Of the hormones studied singly, estrogen appears most potent in inducing maternal behavior. Hysterectomy in late pregnancy, which probably causes a rapid rise in plasma estrogen (11) as judged by examination of vaginal smears, results in a high incidence of maternal behavior 48-72 hr after pup contactThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact. 6661 initiated 48 hr after surgery (12-14). Ovariectomy simultaneous with hysterectomy prevents this effect. The estrogen dependence of the induction of maternal behavior is further shown by estradiol administration at the time of hysterectomy and ovariectomy in either late gestational or virginal female rats. Animals thus treated show a high rate of maternal response within 24 hr after first presentation of pups 48 hr after surgery (12,15,16).Klopfer is the only investigator who has not focused exclusively on late gestati...

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“…In recent years, several peptides endogenous to brain have been found to produce various effects when administered either systemically or directly into the central nervous system (1,2). Considerable attention has been focused on the endorphins and enkephalins which are endogenous opiate-like peptides that produce antinociception (3)(4)(5), hypothermia (6), and various other behavioral effects (7).…”

mentioning

confidence: 99%

Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine.

Nemeroff¹,

Osbahr²,

Manberg³

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

138

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The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and l-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas l-endorphin was the most potent antinociceptive agent via this route of administration.Both NT and f3-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Metlenkephalin, or [Leujenkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studied [bradykinin, thyrotropin- In recent years, several peptides endogenous to brain have been found to produce various effects when administered either systemically or directly into the central nervous system (1, 2). Considerable attention has been focused on the endorphins and enkephalins which are endogenous opiate-like peptides that produce antinociception (3-5), hypothermia (6), and various other behavioral effects (7). In addition, they bind avidly to brain opiate receptors (8). Neurotensin (NT) and bombesin are potent hypothermic agents after intracerebroventricular administration in rats and mice (9, 10). Furthermore, peptides other than the endorphins and enkephalins have been reported to produce significant analgesia after direct intracerebral injection. These include NT, bradykinin, and substance P (11)(12)(13)(14).The purpose of the present study was to evaluate the antinociceptive properties and the effect on colonic temperature of 11 endogenous neuropeptides and morphine after intracisternal administration in mice. Of particular interest was the evaluation of the dose-response relationship of NT-induced antinociception. MATERIALS AND METHODSAntinociceptive activity was measured in adult male albino Swiss-Webster mice (25-30 g) by the tail-immersion test developed for use in rats by Janssen and coworkers (15) as modified for use in mice by Sewell and Spencer (16). Groups of mice (n > 6 per group) were lightly anesthetized with ether and injected intracisternally with vehicle (0.9% NaCl, pH 7.5) or with one of the following peptides: NT, substance P, thyrotropin-releasing factor (thyroliberin), luteinizing hormone-releasing factor (luliberin), bradykinin, melanocyte-stimulating hormone-release inhibiting factor (melanostatin), somatostatin, 3-endorphin, [Met]enkephalin, [Leu]enkephalin, and bombesin. Morphine sulfate was also tested. Thyroliberin (lot 31-330-AL) was provided by Abbott; NT (lot 14-296-10), f-endorphin (lot 28-111-30), and bombesin (lot 42-206-20) were generously supplied by Jean E. Rivier (The Salk Institute, La Jolla, CA). All the other peptides and morphine were purchased commercially: luliberin...

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Peptides and Psychoneuroendocrinology

Cited by 51 publications

References 79 publications

The effects of norethisterone in postmenopausal women on oestrogen replacement therapy: a model for the premenstrual syndrome

The effects of norethisterone in postmenopausal women on oestrogen replacement therapy: a model for the premenstrual syndrome

Induction of maternal behavior in virgin rats after intracerebroventricular administration of oxytocin

Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine.

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