المؤلفون: Potvin W; Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada., Mulay S, Varma DR

المصدر: British journal of pharmacology [Br J Pharmacol] 1991 Oct; Vol. 104 (2), pp. 379-84.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Atrial Natriuretic Factor/*antagonists & inhibitors , Mifepristone/*pharmacology , Progesterone/*pharmacology , Receptors, Progesterone/*antagonists & inhibitors , Tocolytic Agents/*antagonists & inhibitors, Animals ; Drug Synergism ; Estrus/physiology ; Female ; In Vitro Techniques ; Ovary/physiology ; Pregnancy ; Progesterone/blood ; Rats ; Rats, Inbred Strains

مستخلص: 1. The influence of progesterone on the activity of atrial natriuretic factor (ANF) on rat myometrial motor activity was determined in vitro. 2. ANF inhibited the tension development by myometrium from cycling or oestrogen-treated rats in a dose-dependent manner; maximal inhibition was 100%. 3. Injections of progesterone into rats inhibited the tocolytic activity of ANF in a dose and time-dependent manner. The tocolytic effects of ANF were completely abolished by 3 daily injections of 1 mg kg-1 progesterone. 4. Pregnancy-related increase in plasma progesterone was accompanied by a corresponding decrease in the tocolytic effects of ANF; myometria from gestational day 10 to 21 were completely refractory and those from earlier gestational age and immediate postpartum were responsive to ANF to varying degrees. 5. Treatment of pregnant rats with the progesterone antagonist, RU486, caused abortions and vaginal bleeding, decreased plasma progesterone concentrations and restored the tocolytic activity of ANF. Tocolytic activity of ANF on virgin rat myometria was potentiated by RU486. 6. Progesterone also inhibited the effects of ANF on myometria from ovariectomized rats. 7. Tocolytic activity of isoprenaline was not modified by progesterone, pregnancy, RU486 or ovariectomy. 8. It is concluded that progesterone antagonizes myometrial effects of ANF by an oestrogen-independent mechanism and the pregnancy-induced refractoriness to the tocolytic effects of ANF is caused by progesterone.

المؤلفون: Limmroth V; Stroke and Neurovascular Regulation, Massachusetts General Hospital, Charlestown 02129, USA., Lee WS, Moskowitz MA

المصدر: British journal of pharmacology [Br J Pharmacol] 1996 Jan; Vol. 117 (1), pp. 99-104.

نوع المنشور: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Brain Edema/*drug therapy , Meninges/*drug effects , Progesterone/*pharmacology , Receptors, GABA-A/*drug effects, Animals ; Bicuculline/pharmacology ; Brain Edema/etiology ; Capillary Permeability/drug effects ; Dose-Response Relationship, Drug ; Female ; GABA Antagonists/pharmacology ; Isomerism ; Male ; Meninges/metabolism ; Pregnanolone/pharmacology ; Progesterone/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Serum Albumin, Bovine ; Substance P/pharmacology

مستخلص: 1. The effects of progesterone, its A-ring-reduced metabolites, allopregnanolone, tetrahydroxydeoxycorticosterone and the synthetic neuroactive steroid alphaxalone were evaluated in a rat model of plasma extravasation within the meninges following unilateral electrical stimulation (ES) of the trigeminal ganglion (0.6 mA, 5 ms, 5 min) or substance P administration (1 nmol kg-1, i.v.). 2. When administered 55 min prior to electrical stimulation, progesterone (> or = 500 micrograms, s.c.) dose-dependently decreased plasma extravasation within the meninges (ED50: 650 micrograms) but not within conjunctiva and tongue. Promegestone (R5020), a non-metabolized progesterone agonist (1000 micrograms, i.p.) was ineffective. The administration of progestrone (> or = 500 micrograms s.c.) 55 min prior to substance P partially suppressed plasma extravasation within the meninges (ED50: 550 micrograms). 3. The GABAA-antagonist, bicuculline (ED50: 8.2 micrograms kg-1, i.p.) but not the GABAB-antagonist, phaclofen (100 micrograms kg-1, i.p.) attenuated the effects of progesterone after electrical stimulation and substance P administration. 4. The metabolites of progesterone, allopregnanolone (3 alpha-hydroxy-5 alpha- pregnan-20-one (THP); ED50: 0.58 micrograms kg-1, i.p.), tetrahydroxydeoxycorticosterone (3 alpha,21- dihydroxy-5 alpha-pregnan-20-one (THDOC); ED50: 1.2 micrograms kg-1, i.p.) as well as the synthetic steroid alphaxalone (3 alpha-hydroxy-5 alpha-pregnane-11,20-dione; ED50: 1.8 micrograms kg-1, i.p.) suppressed plasma extravasation dose-dependently following ES, whereas the epimer of allopregnanolone, 3 beta-hydroxy-5 alpha-pregnan-20-one (100 micrograms kg-1, i.p.), did not. Extravasation caused by SP administration was partially suppressed by allopregnanolone (> or = 1 microgram kg-1, i.p.) (ED50: 2.1 micrograms kg-1). 5. The effect of progesterone (1000 micrograms, s.c.) and allopregnanolone (100 micrograms kg-1, i.p.) on neurogenic plasma extravasation was reversed by bicuculline (10 micrograms kg-1, i.p.) or by a congener, bicuculline-methiodide (10 micrograms kg-1, i.p.) which does not cross the blood brain barrier. 6. Progesterone (1000 micrograms, s.c.) had no effect on mean arterial blood pressure or heart rate when measured for 60 min after administration. 7. These results indicate that neurosteroid modulation of a GABAA-receptor located outside the blood brain barrier suppresses neurogenic and substance P-induced plasma extravasation within the meninges. The findings are consistent with previously reported data showing that valproic acid and muscimol inhibit meningeal oedema by bicuculline-sensitive mechanisms. Drugs which activate GABAA-receptors and its modulatory sites might be clinically effective in the treatment of migraine and cluster headache.

المؤلفون: Fry JP; Department of Neuroscience, Physiology and Pharmacology, University College London (UCL), London, UK., Li KY, Devall AJ, Cockcroft S, Honour JW, Lovick TA

المصدر: British journal of pharmacology [Br J Pharmacol] 2014 Dec; Vol. 171 (24), pp. 5870-80. Date of Electronic Publication: 2014 Nov 24.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)/*antagonists & inhibitors , Brain/*drug effects , Fluoxetine/*pharmacology , Pregnanolone/*metabolism , Selective Serotonin Reuptake Inhibitors/*pharmacology, 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)/metabolism ; 5-alpha-Dihydroprogesterone/metabolism ; Aldehyde Reductase/drug effects ; Aldehyde Reductase/metabolism ; Aldo-Keto Reductases ; Animals ; Brain/metabolism ; Female ; HEK293 Cells ; Humans ; Male ; Pregnanolone/biosynthesis ; Progesterone/metabolism ; Rats

مستخلص: Background and Purpose: Fluoxetine, a selective serotonin reuptake inhibitor, elevates brain concentrations of the neuroactive progesterone metabolite allopregnanolone, an effect suggested to underlie its use in the treatment of premenstrual dysphoria. One report showed fluoxetine to activate the aldo-keto reductase (AKR) component of 3α-hydroxysteroid dehydrogenase (3α-HSD), which catalyses production of allopregnanolone from 5α-dihydroprogesterone. However, this action was not observed by others. The present study sought to clarify the site of action for fluoxetine in elevating brain allopregnanolone.
Experimental Approach: Adult male rats and female rats in dioestrus were treated with fluoxetine and their brains assayed for allopregnanolone and its precursors, progesterone and 5α-dihydroprogesterone. Subcellular fractions of rat brain were also used to investigate the actions of fluoxetine on 3α-HSD activity in both the reductive direction, producing allopregnanolone from 5α-dihydroprogesterone, and the reverse oxidative direction. Fluoxetine was also tested on these recombinant enzyme activities expressed in HEK cells.
Key Results: Short-term treatment with fluoxetine increased brain allopregnanolone concentrations in female, but not male, rats. Enzyme assays on native rat brain fractions and on activities expressed in HEK cells showed fluoxetine did not affect the AKR producing allopregnanolone from 5α-dihydroprogesterone but did inhibit the microsomal dehydrogenase oxidizing allopregnanolone to 5α-dihydroprogesterone.
Conclusions and Implications: Fluoxetine elevated allopregnanolone in female rat brain by inhibiting its oxidation to 5α-dihydroprogesterone by a microsomal dehydrogenase. This is a novel site of action for fluoxetine, with implications for the development of new agents and/or dosing regimens to raise brain allopregnanolone.
(© 2014 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of The British Pharmacological Society.)

المؤلفون: Senior J, Whalley ET

المصدر: British journal of pharmacology [Br J Pharmacol] 1974 Mar; Vol. 50 (3), pp. 467-8.

نوع المنشور: Journal Article

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol

مواضيع طبية MeSH: Animals, Laboratory* , Blood* , Estrogens* , Progesterone* , Research*, Biology ; Endocrine System ; Hormones ; Physiology ; Progestins

المؤلفون: Allen KE, Jordan VC

المصدر: British journal of pharmacology [Br J Pharmacol] 1980 Jan; Vol. 68 (1), pp. 156P-157P.

نوع المنشور: Journal Article

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Estrogen Antagonists/*pharmacology , Nafoxidine/*pharmacology , Naphthalenes/*pharmacology , Pyrrolidines/*pharmacology , Receptors, Progesterone/*biosynthesis, Animals ; Female ; In Vitro Techniques ; Nafoxidine/analogs & derivatives ; Rats ; Receptors, Progesterone/drug effects

المؤلفون: Majeed Y; Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds, UK., Amer MS, Agarwal AK, McKeown L, Porter KE, O'Regan DJ, Naylor J, Fishwick CW, Muraki K, Beech DJ

المصدر: British journal of pharmacology [Br J Pharmacol] 2011 Apr; Vol. 162 (7), pp. 1509-20.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Gonadal Steroid Hormones/*pharmacology , TRPC Cation Channels/*antagonists & inhibitors, Calcium/metabolism ; Cells, Cultured ; Dihydrotestosterone/pharmacology ; Estradiol/pharmacology ; HEK293 Cells ; Humans ; Lysophospholipids/pharmacology ; Myocytes, Smooth Muscle/metabolism ; Patch-Clamp Techniques ; Phospholipids/metabolism ; Pregnenolone/pharmacology ; Progesterone/pharmacology ; Sphingosine/analogs & derivatives ; Sphingosine/pharmacology ; Stereoisomerism ; Structure-Activity Relationship ; TRPC Cation Channels/chemistry ; TRPC Cation Channels/genetics ; TRPC Cation Channels/metabolism

مستخلص: Background and Purpose: Transient receptor potential canonical 5 (TRPC5) channels are widely expressed, including in the CNS, where they potentiate fear responses. They also contribute to other non-selective cation channels that are stimulated by G-protein-coupled receptor agonists and lipid and redox factors. Steroids are known to modulate fear and anxiety states, and we therefore investigated whether TRPC5 exhibited sensitivity to steroids.
Experimental Approach: Human TRPC5 channels were conditionally expressed in HEK293 cells and studied using intracellular Ca2+ measurement, whole-cell voltage-clamp and excised patch techniques. For comparison, control experiments were performed with cells lacking TRPC5 channels or expressing another TRP channel, TRPM2. Native TRPC channel activity was recorded from vascular smooth muscle cells.
Key Results: Extracellular application of pregnenolone sulphate, pregnanolone sulphate, pregnanolone, progesterone or dihydrotestosterone inhibited TRPC5 activity within 1-2min. Dehydroepiandrosterone sulphate or 17β-oestradiol had weak inhibitory effects. Pregnenolone, and allopregnanolone, a progesterone metabolite and stereo-isomer of pregnanolone, all had no effects. Progesterone was the most potent of the steroids, especially against TRPC5 channel activity evoked by sphingosine-1-phosphate. In outside-out patch recordings, bath-applied progesterone and dihydrotestosterone had strong and reversible effects, suggesting relatively direct mechanisms of action. Progesterone inhibited native TRPC5-containing channel activity, evoked by oxidized phospholipid.
Conclusions and Implications: Our data suggest that TRPC5 channels are susceptible to relatively direct and rapid stereo-selective steroid modulation, leading to channel inhibition. The study adds to growing appreciation of TRP channels as non-genomic steroid sensors.
(© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.)

المؤلفون: Turkmen S; Department of Obstetrics & Gynaecology, Sundsvall County Hospital, Sweden. sahruh.turkmen@lvn.se, Backstrom T, Wahlstrom G, Andreen L, Johansson IM

المصدر: British journal of pharmacology [Br J Pharmacol] 2011 Jan; Vol. 162 (2), pp. 311-27.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Review

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Drug Tolerance*, Gonadal Steroid Hormones/*metabolism , Pregnanolone/*metabolism , Pregnanolone/*pharmacology , Receptors, GABA-A/*metabolism, Animals ; Female ; Gonadal Steroid Hormones/pharmacology ; Humans ; Pregnancy ; Progesterone/metabolism ; RNA, Messenger/metabolism ; Rats ; Receptors, GABA-A/genetics ; Stress, Psychological ; Substance Withdrawal Syndrome ; Time Factors ; gamma-Aminobutyric Acid/metabolism ; gamma-Aminobutyric Acid/pharmacology

مستخلص: Many studies have suggested a relationship between stress, sex steroids, and negative mental and mood changes in humans. The progesterone metabolite allopregnanolone is a potent endogenous ligand of the γ-amino butyric acid -A (GABA-A) receptor, and the most discussed neuroactive steroid. Variations in the levels of neuroactive steroids that influence the activity of the GABA-A receptor cause a vulnerability to mental and emotional pathology. There are physiological conditions in which allopregnanolone production increases acutely (e.g. stress) or chronically (e.g. menstrual cycle, pregnancy), thus exposing the GABA-A receptor to high and continuous allopregnanolone concentrations. In such conditions, tolerance to allopregnanolone may develop. We have shown that both acute and chronic tolerances can develop to the effects of allopregnanolone. Following the development of acute allopregnanolone tolerance, there is a decrease in the abundance of the GABA-A receptor α4 subunit and the expression of the α4 subunit mRNA in the ventral-posteriomedial nucleus of the thalamus. Little is known about the mechanism behind allopregnanolone tolerance and its effects on assembly of the GABA-A receptor composition. The exact mechanism of the allopregnanolone tolerance phenomena remains unclear. The purpose of this review is to summarize certain aspects of current knowledge concerning allopregnanolone tolerance and changes in the GABA-A receptors.
(© 2010 The Authors. British Journal of Pharmacology © 2010 The British Pharmacological Society.)

المؤلفون: Roy JW; Department of Physiology and Biophysics, Dalhousie University, Halifax, Canada. jwroy@dal.ca, Cowley EA, Blay J, Linsdell P

المصدر: British journal of pharmacology [Br J Pharmacol] 2010 Feb 01; Vol. 159 (3), pp. 650-8. Date of Electronic Publication: 2009 Dec 24.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Potassium Channels, Calcium-Activated*/antagonists & inhibitors , Potassium Channels, Calcium-Activated*/metabolism , Potassium Channels, Calcium-Activated*/physiology, Breast Neoplasms/*drug therapy , Breast Neoplasms/*metabolism , Estradiol/*pharmacology , Tamoxifen/*pharmacology, Calcium/metabolism ; Calcium/pharmacology ; Calcium/therapeutic use ; Cell Line, Tumor ; Cells/metabolism ; Cells/pathology ; Cellular Structures/metabolism ; Cellular Structures/pathology ; Estradiol/metabolism ; Estradiol/therapeutic use ; Estrogen Receptor alpha/metabolism ; Estrogens/metabolism ; Estrogens/pharmacology ; Estrogens/therapeutic use ; Female ; Gene Expression/drug effects ; Humans ; Ion Transport/drug effects ; Pyrazoles ; RNA, Messenger/metabolism ; RNA, Messenger/pharmacology ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/metabolism ; Tamoxifen/metabolism ; Tamoxifen/therapeutic use

مستخلص: Background and Purpose: K(+) channels play a role in the proliferation of cancer cells. We have investigated the effects of specific K(+) channel inhibitors on basal and oestrogen-stimulated proliferation of breast cancer cells.
Experimental Approach: Using the mammary adenocarcinoma cell line MCF-7 we assayed cell proliferation by radiolabelled thymidine incorporation in the absence or presence of various K(+) channel inhibitors with or without 17beta-oestradiol.
Key Results: Inhibitors of K(v)10.1 and K(Ca)3.1 K(+) channels suppressed basal proliferation of MCF-7 cells, but not oestrogen-stimulated proliferation. TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration. At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation. The enhancement of cell proliferation caused by TRAM-34 was blocked by the oestrogen receptor antagonists ICI182,780 and tamoxifen. TRAM-34 also increased progesterone receptor mRNA expression, decreased oestrogen receptor-alpha mRNA expression and reduced the binding of radiolabelled oestrogen to MCF-7 oestrogen receptor, in each case mimicking the effects of 17beta-oestradiol.
Conclusions and Implications: Our results demonstrate that K(+) channels K(v)10.1 and K(Ca)3.1 play a role in basal, but not oestrogen-stimulated MCF-7 cell proliferation. TRAM-34, as well as inhibiting K(Ca)3.1, directly interacts with the oestrogen receptor and mimics the effects of 17beta-oestradiol on MCF-7 cell proliferation and gene modulation. Our finding that TRAM-34 is able to activate the oestrogen receptor suggests a novel action of this supposedly specific K(+) channel inhibitor and raises concerns of interpretation in its use.

المؤلفون: Edwardson JA, Macgregor LA

المصدر: British journal of pharmacology [Br J Pharmacol] 1969 Feb; Vol. 35 (2), pp. P367-9.

نوع المنشور: Journal Article

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Embryo Implantation/*drug effects , Ergot Alkaloids/*pharmacology , Progesterone/*pharmacology, Animals ; Chlorpromazine/pharmacology ; Female ; Pregnancy ; Progesterone/administration & dosage ; Prolactin/pharmacology ; Rats ; Reserpine/pharmacology ; Uterus/drug effects

المؤلفون: Bergeron R; Neuroscience Laboratory, Department of Psychiatry, Harvard Medical School, 940 Belmont Street, Brockton, MA, 0230 USA., de Montigny C, Debonnel G

المصدر: British journal of pharmacology [Br J Pharmacol] 1999 Aug; Vol. 127 (8), pp. 1769-76.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Print ISSN: 0007-1188 (Print) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE

مواضيع طبية MeSH: Adjuvants, Immunologic/*pharmacology , Analgesics, Opioid/*pharmacology , Anticonvulsants/*pharmacology , Dehydroepiandrosterone/*pharmacology , Guanidines/*pharmacology , Pentazocine/*pharmacology , Receptors, sigma/*drug effects, Action Potentials/drug effects ; Action Potentials/physiology ; Animals ; Female ; Hippocampus/drug effects ; Hippocampus/physiology ; Ovariectomy ; Postpartum Period/drug effects ; Postpartum Period/physiology ; Pregnancy ; Progesterone/blood ; Progesterone/pharmacology ; Pyramidal Cells/drug effects ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, N-Methyl-D-Aspartate/physiology ; Receptors, sigma/physiology

مستخلص: 1. Sigma (sigma) receptors have recently been cloned, though their endogenous ligand(s) remain unidentified. However, some neuroactive steroids, such as progesterone, have a high affinity for these receptors. Some sigma ligands, such as DTG, (+)-pentazocine and DHEA, act as sigma 'agonists' by potentiating the neuronal response to NMDA. Others, such as haloperidol, NE-100 and progesterone, act as sigma 'antagonists' by reversing the potentiations induced by sigma 'agonists'. 2. We compared the effects of sigma 'agonists' in four series of female rats: in controls, at day 18 of pregnancy, at day 5 post-partum, and in ovariectomized rats following a 3-week treatment with a high dose of progesterone. 3. In pregnant rats and following a 3-week treatment with progesterone, 10 fold higher doses of DTG, (+)-pentazocine and DHEA were required to elicit a selective potentiation of the NMDA response comparable to that obtained in control females. Conversely, at day 5 post-partum and following the 3-week treatment with a progesterone and after a 5-day washout, the potentiation of the NMDA response induced by the sigma 'agonist' DTG was greater than in control females. 4. The present data suggest that endogenous progesterone acts as an 'antagonist' at sigma receptors. The resulting changes in the function of sigma receptors during pregnancy and post-partum may be implicated in emotional phenomena occurring during these periods.