Gonadal Steroid Action on the Brain: Neurochemistry and Neuropharmacology

McEwen, Bruce S.; Parsons, Bruce

doi:10.1146/annurev.pa.22.040182.003011

Cited by 189 publications

(65 citation statements)

References 151 publications

(98 reference statements)

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“…The coexistence of this interaction and direct pituitary effects of EB should also be considered. The mechanisms underlying these effects may require classical steroid receptor activation or may be mediated by actions on neuronal membranes [22], Further investigations are re quired to establish ovarian hormonal influences on opiate peptide synthesis, release, degradation and receptor me chanisms and the consequences for monoaminergic neuro transmission.…”

Section: Discussionmentioning

confidence: 99%

“…Tissue samples were expelled into 50 g! of ice-cold 0.1 M HCIO-i, briefly centrifuged, and sonicated for approximately 3 s. Aliquots of 3 or 5 gl were then removed for protein analysis [22]. Indoleamines were measured using an LC304CA liquid chromato graph with electrochemical detection (Bioanalytic Systems).…”

Section: Experiments 2: Effects O F Morphine and Naloxone On Lh And Prmentioning

confidence: 99%

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Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Johnson¹,

Crowley

1984

Neuroendocrinology

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Previous findings indicate that estradiol benzoate (EB) acutely activates serotonergic projections in the medial preoptic area that are stimulatory to prolactin (PRL) secretion. Because opioid agonists also stimulate both PRL release and serotonin (5-HT) turnover, the present experiments tested whether endogenous opioid neurons may mediate estrogen feedback effects. In experiment 1, ovariectomized rats received either 50 µg EB or oil vehicle, and either saline or a long-acting opiate receptor blocker, nalmetrene (10 mg/kg), simultaneously, 3 h prior to decapitation. The pargyline method was used to determine 5-HT turnover; hence members of each treatment group received either saline or pargyline (75 mg/kg i.p.) 30 min prior to decapitation. Plasma PRL and luteineizing hormone (LH) concentrations were determined by radioimmunoassays, and 5-HT concentrations from microdissected, individual brain nuclei were measured by liquid chromatography with electrochemical detection. Nalmetrene blocked both the acute elevation of PRL and the increase in 5-HT turnover in the medial preoptic nucleus and ventromedial nucleus induced by EB. Nalmetrene alone also enhanced LH release and 5-HT turnover in the bed nucleus of the stria terminalis, and these effects were prevented by EB. A second study tested whether the opioid agonist, morphine, mimics estrogen effects on PRL and preoptic 5-HT turnover. Animals received saline, morphine (10 mg/kg i.p.) and/or naloxone (5 mg/kg i.p.) 30 min prior to decapitation. Simultaneously, half in each group received pargyline as above. Morphine stimulated both PRL release and medial preoptic 5-HT turnover, and naloxone prevented both effects. In addition, morphine enhanced 5-HT turnover in the central amygdala, and naloxone increased 5-HT turnover in the bed nucleus of the stria terminalis, and these changes appeared to be related to opioid-induced alterations in LH.

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Section: Discussionmentioning

confidence: 99%

Section: Experiments 2: Effects O F Morphine and Naloxone On Lh And Prmentioning

confidence: 99%

Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Johnson¹,

Crowley

1984

Neuroendocrinology

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“…The ovarian hormones could exert their effects on mood directly or indirectly by their effect on neurotransmitter, neuroendocrine, or circadian systems (McEwen and Parsons 1982;Albers 1981;Albers et al 1981;Thomas and Armstrong 1989; Parry 1995a,b). Although each of these systems has been implicated in the pathogenesis of depressive illness, the circadian basis of these disorders has received the least attention.…”

Section: Women Have Twice the Incidence Of Major Depression Compared mentioning

confidence: 99%

Chronobiological Basis of Female-Specific Mood Disorders

Parry

Newton

2001

Neuropsychopharmacology

112

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Women have twice the incidence of major depression compared with men. They are prone to develop episodes of depression during times of reproductive hormonal change at puberty, with use of oral contraceptives, during the premenstrual phase of the menstrual cycle, postpartum and during the perimenopause (see review: Parry 1995a). WirzJustice (1995) In women, hormonal changes associated with the reproductive cycle may provoke affective changes in predisposed individuals. Examples include depression associated with oral contraceptives (Parry and Rush 1979), the luteal phase of the menstrual cycle (Hamilton et al. 1984;Endo et al. 1978;Halbreich and Endicott 1985), the postpartum period (Parry and Hamilton 1990), and menopause (Winokur 1973). Sex differences in the rates of depression begin to appear after puberty (Weissman et al. 1984;Angold et al. 1998), a time of major change in the neuroendocrine reproductive axis. From this time onward, women have a greater lifetime risk for major depression than men. Women predominate with respect to unipolar depression (Weissman et al. 1984), the depressive subtype of bipolar illness (Angst 1978), and cyclical forms of affective illness such as rapid cycling manic-depressive illness (Wehr 1984) and seasonal affective disorder (Rosenthal et al. 1984). Furthermore, the risk for major depression in both men and women appears to be increasing in recent generations (Weissman et al. 1984;Klerman and Weissman 1989).The fluctuation of ovarian steroids during specific phases of the reproductive cycle may bear some relationship to the particular vulnerability of women for mood disorders. The ovarian hormones could exert their effects on mood directly or indirectly by their effect on neurotransmitter, neuroendocrine, or circadian systems (McEwen and Parsons 1982;Albers 1981;Albers et al. 1981;Thomas and Armstrong 1989; Parry 1995a,b). Although each of these systems has been implicated in the pathogenesis of depressive illness, the circadian basis of these disorders has received the least attention. We have designed our studies with their particular chronobiological focus because the predisposition of women for major depression has not been investigated systematically with respect to the interaction of Chronobiology, Women and Depression S103 the unique cyclic reproductive neuroendocrine axis in women and circadian physiology. Although chronobiological disturbances have been described in depression (Kripke et al. 1978;Wehr and Goodwin 1980), the characterization of chronobiological disturbances in reproductive-related mood disorders in women remains to be elucidated. Below we review the circadian rhythm abnormalities that we have observed in premenstrual dysphoric disorder, pregnancy and postpartum depression and menopause. As reproductive hormones modulate the synchrony or coherence between different components of the circadian system (Thomas and Armstrong 1989), we hypothesize that these changing hormones during the premenstrual, postpartum and menopausal periods may destabilize circ...

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“…Our findings indicate that either GABA is not involved in the negative feedback effects of steroids, o r any steroid-induced changes have already occurred a t a n earlier time-point; this is currently being investigated. An alternative possibility may be that steroids can alter GABA release independently of synthesis, perhaps inducing changes directly a t the membrane level (46,47).…”

Section: Ospmentioning

confidence: 99%

Ovarian Steroid Regulation of Glutamic Acid Decarboxylase Gene Expression in Individual Hypothalamic Nuclei

Leigh

Carter

Horton

et al. 1990

J Neuroendocrinology

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The possibility that steroids exert their effects on luteinizing hormone (LH) and prolactin release and female sexual behaviour via altering 7-arninobutyric acid (GABA) synthesis within the hypothalamus was investigated. Ovariectomized rats were treated with e$ther oil, 5 pg oestradiol benzoate (OB) or 5 pg OB plus 0.5 mg progesterone (P) 48 h later; autopsy was carried out 54 h after the OB injection. At this time, both steroid treatments stimulated prolactin release and lordotic activity. OB alone exerted a negative feedback effect on LH release while OB plus P stimulated an LH surge.The brains of the rats in these three treatment groups were microdissected and glutamic acid decarboxylase messenger ribonucleic acid (GAD mRNA) was estimated in specific hypothalamic areas obtained from individual brains; these areas included the preoptic area (POA), ventromedial nucleus (VMN), anterior medial portion of the zona incerta (ZI) and the arcuatehedian eminence area (ARC/ME). GAD mRNA concentrations were assessed by the slot-blotting technique and expressed as a ratio of GAD mRNA: b-actin mRNA.Both steroid treatments significantly reduced GAD mRNA in the ARCIME and ZI and OB plus P also reduced the concentration in the POA, while OB alone had no effect in this area. Neither treatment affected GAD mRNA in the VMN. These results indicate that when steroids stimulate LH and prolactin release and female sexual behaviour, they reduce GABA activity probably by reducing GABA synthesis in the POA, ZI and ARCIME. This suggests that GABA normally has an inhibitory influence on these parameters. G4BA synthesis does not however, appear to be involved in the negative feedback effects of steroids on LH release as measured 54 h after OB treatment.;,-,iminobutyric acid (GABA) is widely distributed in the hypothalmius with its highest concentrations in the preoptic area (POA) aiid ventromedial nucleus (VMN) (1 -3). GABA-containing neurons possess steroid receptors (4, 5 ) and it has becn suggested that sri:roids might exert some of their CNS effects via GABAergic s! stems (6-9). These effects include the control of luteinizing hormone (LH) and prolactin release and sexual behaviour. Rep x t s in the literature indicate that GABA can influence sexual bchaviour in females (10, 11) and has a dual effect on the release of I €1 and prolactin (12, 13). The results show that GABA is inhibitory to LH release in the POA and anterior medial portion o!' the zona incerta (ZI) (14-17). The site of it's stimulatory effect is not really known, although some data indicate that it may be in the medial basdl hypothalamus (12,18,19). Within the hypothalaIlIus GABA stimulates prolactin release, but it is inhibitory at the level of the pituitary (12)(13)(14)20). There are many reports investigating the inter-relationship of the gonadal steroids and GABA, in particular noting the effect of oestrogen and progesterone (P) on GABA activity in specific brain areas. Since GABA is present in both neuronal and glial tissue (1, 21) changes in its concentra...

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Gonadal Steroid Action on the Brain: Neurochemistry and Neuropharmacology

Cited by 189 publications

References 151 publications

Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Effects of Opiate Antagonists on Serotonin Turnover and on Luteinizing Hormone and Prolactin Secretion in Estrogen- or Morphine-Treated Rats

Chronobiological Basis of Female-Specific Mood Disorders

Ovarian Steroid Regulation of Glutamic Acid Decarboxylase Gene Expression in Individual Hypothalamic Nuclei

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