scholarly journals Corticotropin-Releasing Factor Receptor Binding in the Amygdala Changes Across Puberty in a Sex-Specific Manner

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5701-5705 ◽  
Author(s):  
Jill M. Weathington ◽  
Bradley M. Cooke
Keyword(s):  
Sex Differences ◽  
Receptor Binding ◽  
Specific Binding ◽  
Stress Sensitivity ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Medial Amygdala ◽  
Adult Males ◽  
Adult Rats ◽  
Hypothalamic Pituitary Adrenal

Abstract Corticotropin-releasing factor receptors type 1 (CRF1) and type 2 (CRF2) have complementary roles in controlling the hypothalamic-pituitary-adrenal (HPA) axis. Because CRF receptors are expressed in sex steroid-sensitive areas of the forebrain, they may contribute to sex-specific patterns of stress sensitivity and susceptibility to stress-related mood disorders, which are more frequent in women. To determine whether CRF receptors vary as a function of age and/or sex, we measured receptor binding in the amygdala of male and female, prepubertal and adult rats. Both receptor subtypes demonstrated age- and sex-specific binding patterns. In the basolateral amygdala and posteroventral medial amygdala, CRF1 binding decreased in males and increased in females after puberty, there, CRF2 binding increased in males and was unchanged in females. In the posterodorsal medial amygdala, CRF1 binding was unchanged across puberty, whereas CRF2 binding increased across puberty far more in males than in females. Binding was lowest overall in the central amygdala; there, CRF1 was unchanged while CRF2 binding increased across puberty only in males. Thus, in all four examined areas across prepuberty to adulthood, CRF2 binding increased far more in males than in females and resulted in significantly more binding in adult males than in adult females. These sex-specific developmental patterns are consistent with sex differences in hypothalamic-pituitary-adrenal responsiveness and may thus contribute to sex differences in mood disorder susceptibility.

scholarly journals Antiinflammatory Treatment Ameliorates HPA Stress Axis Dysfunction in a Mouse Model of Stress Sensitivity

Endocrinology ◽  
2012 ◽  
Vol 153 (10) ◽  
pp. 4830-4837 ◽  
Author(s):  
Alexis R. Gerber ◽  
Tracy L. Bale
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Stress Sensitivity ◽  
Corticotropin Releasing Factor ◽  
Acidic Protein ◽  
Stress Axis ◽  
Nsaid Treatment ◽  
Neuropsychiatric Disease ◽  
Hypothalamic Pituitary Adrenal ◽  
Stress Pathway ◽  
Pathway Dysregulation

Abstract Dysregulated stress responsivity is a hallmark of neuropsychiatric disease. The regulation of stress activation and recovery involves tight coordination between neuronal and glial networks. At a certain threshold of sensitivity, stress exposure can evoke a neuroimmune response. Astrocytes are potential mediators of these effects because they are able to respond to neuroimmune effector molecules and regulate neuronal activity. Mice deficient in corticotropin-releasing factor receptor-2 display increased stress sensitivity and are therefore a useful model in which to examine the intersection of neuroimmune activation and stress pathway dysregulation. We hypothesized that a component of elevated stress reactivity may involve an engagement of neuroimmune effectors, including astrocytes. Therefore, we hypothesized that this phenotype may be rescued by concomitant nonsteroidal antiinflammatory drug (NSAID) treatment. To examine this, mice exposed to chronic stress were treated with NSAID in their drinking water, and changes in hypothalamic-pituitary-adrenal stress axis function were examined. As a correlate of altered astrocyte function, levels of glial fibrillary acidic protein were measured. Supportive of our hypothesis, NSAID treatment rescued the hypothalamic-pituitary-adrenal stress axis dysfunction in stress-sensitive corticotropin-releasing factor receptor-2−/− mice and also reversed the stress-induced increase in glial fibrillary acidic protein in stress-regulating brain regions including the paraventricular nucleus of the hypothalamus, ventral hippocampus, and prefrontal cortex. These findings support the local involvement of astrocytes in the exacerbation of stress pathway dysregulation. The specificity of these effects in a stress-sensitive genotype highlights the importance of utilizing a model of stress dysregulation in the examination of factors that may translate to neuropsychiatric disease.

Corticotropin-releasing factor receptor 1 mediates acute and delayed stress-induced visceral hyperalgesia in maternally separated Long-Evans rats

2005 ◽  
Vol 289 (4) ◽  
pp. G704-G712 ◽  
Author(s):  
Ines Schwetz ◽  
James A. McRoberts ◽  
Santosh V. Coutinho ◽  
Sylvie Bradesi ◽  
Greg Gale ◽  
...  
Keyword(s):  
Visceral Pain ◽  
Colonic Motility ◽  
Stress Sensitivity ◽  
Corticotropin Releasing Factor ◽  
Visceral Hypersensitivity ◽  
Visceral Hyperalgesia ◽  
Adult Rats ◽  
Stress Responsiveness ◽  
Rearing Conditions ◽  
Long Evans

In rodents, maternal pup interactions play an important role in programming the stress responsiveness of the adult organism. The aims of this study were 1) to determine the effect of different neonatal rearing conditions on acute and delayed stress-induced visceral sensitivity as well as on other measures of stress sensitivity of the adult animal; and 2) to determine the role of corticotropin-releasing factor receptor (CRF-R) subtype 1 (CRF1R) in mediating visceral hypersensitivity. Three groups of male Long-Evans rat pups were used: separation from their dam for 180 min daily from postnatal days 2–14 (MS180), daily separation (handling) for 15 min (H), or no handling. The visceromotor responses (VMR) to colorectal distension, stress-induced colonic motility, and anxiety-like behavior were assessed in the adult rats. The VMR was assessed at baseline, immediately after a 1-h water avoidance (WA) stress, and 24 h poststress. Astressin B, a nonselective CRF-R antagonist, or CP-154,526, a selective CRF1R antagonist, was administered before the stressor and/or before the 24-h measurement. MS rats developed acute and delayed stress-induced visceral hyperalgesia. In contrast, H rats showed hypoalgesia immediately after WA and no change in VMR on day 2. MS rats with visceral hyperalgesia also exhibited enhanced stress-induced colonic motility and increased anxiety-like behavior. In MS rats, both CRF-R antagonists abolished acute and delayed increases in VMR. Rearing conditions have a significant effect on adult stress responsiveness including immediate and delayed visceral pain responses to an acute stressor. Both acute and delayed stress-induced visceral hypersensitivity in MS rats are mediated by the CRF/CRF1R system.

scholarly journals Sex differences in the behavioral and synaptic consequences of a single exposure to cannabinoid at puberty and adulthood

2018 ◽  
Author(s):  
Milene Borsoi ◽  
Antonia Manduca ◽  
Anissa Bara ◽  
Olivier Lassalle ◽  
Anne-Laure Pelissier-Alicot ◽  
...  
Keyword(s):  
Sex Differences ◽  
Social Behavior ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Adult Males ◽  
Adult Rats ◽  
Term Potentiation ◽  
Cannabis Consumption

AbstractHeavy cannabis consumption among adolescents is associated with significant and lasting neurobiological, psychological and health consequences that depend on the age of first use. Chronic exposure to cannabinoid (CB) agonists during adolescence alters social behavior and prefrontal cortex (PFC) activity in adult rats. However, sex differences on social behavior as well as PFC synaptic plasticity after acute CB activation remain poorly explored. Here, we determined the consequences of a single CB activation differently affects PFC in males and females by assessing social behavior and PFC neuronal and synaptic functions in rats during pubertal or adulthood periods, 24h after a single in-vivo cannabinoid exposure (SCE). During puberty, SCE reduced play behavior in females but not males. In contrast, SCE impaired sociability in both sexes at adulthood. General exploration and memory recognition remained normal at both ages and both sexes. At the synaptic level, SCE ablated endocannabinoid-mediated long-term depression (eCB-LTD) in the PFC of females of both ages and heightened excitability of PFC pyramidal neurons at adulthood, while males were spared. In contrast, SCE was associated to impaired long-term potentiation in adult males. Together, the data indicate behavioral and synaptic sex differences in response to a single in-vivo exposure to cannabinoid at puberty and adulthood.

Androgen-dependent sex differences in the hypothalamic serotoninergic system

1996 ◽  
Vol 134 (2) ◽  
pp. 232-235 ◽  
Author(s):  
Nina A Borisova ◽  
Evgeniya V Proshlyakova ◽  
Anna Ya Sapronova ◽  
Michael V Ugrumov
Keyword(s):  
Sex Differences ◽  
Serotoninergic System ◽  
Adult Males ◽  
Adult Rats ◽  
New Information ◽  
Specific Uptake ◽  
5 Ht Uptake ◽  
Academy Of Sciences ◽  
Neonatal Castration

Borisova NA, Proshlyakova EV, Sapronova AY, Ugrumov MV. Androgen-dependent sex differences in the hypothalamic serotoninergic system. Eur J Endocrinol 1996;134:232–5. ISSN 0804–4643 This study has attempted to fulfil our knowledge on the sex differences in the hypothalamic serotoninergic (5-HT) system in adult rats, and also to evaluate the role of neonatal androgens in the appearance of this sexual dimorphism. Such integrative characteristics of the 5-HT system as 5-HT content and specific uptake were estimated and compared in the anterior and middle hypothalami in intact adult females and males, as well as in neonatally castrated adult males. According to our data, the 5-HT content and [3H]5-HT specific uptake both in the anterior and middle hypothalami of intact females exceeded significantly those in intact males. Neonatal castration of males resulted in an increase of the 5-HT content and [3H]5-HT uptake in both hypothalamic regions up to their levels in intact females. Thus, the present study provides new information on the sex differences in the hypothalamic 5-HT system, which are apparently related to the neonatal masculinization of the hypothalamus. Michael V Ugrumov, Institute of Developmental Biology, Russian Academy of Sciences, Vavilov str., Moscow 117808, Russia

scholarly journals Sex Difference in Self-Reported Sexual Functioning Among Frail Older Adults

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 313-313
Author(s):  
Brianne Olivieri-Mui ◽  
Sandra Shi ◽  
Ellen McCarthy ◽  
Dae Kim
Keyword(s):  
Older Adults ◽  
Logistic Regression ◽  
Sex Differences ◽  
Sexual Function ◽  
Older Adult ◽  
Sexual Functioning ◽  
Social Life ◽  
Well Being ◽  
Adult Males ◽  
Males And Females

Abstract Frailty may differentially impact how older adult males and females perceive sexual functioning, an important part of well-being. We assessed the level of frailty (robust, pre-frail, frail) for anyone with data on 11 sexual functioning questions asked in wave 2 of the National Social Life, Health, and Aging Project, 2010-2011 (n=2060). Questions covered five domains: overall sexual function (OSF), sexual function anxiety (SFA), changes in sexual function (CSF), erectile/vaginal dysfunction (EVD), and masturbation. Logistic regression identified sex differences in frailty and reporting worse sexual functioning. Linear regression predicted the number of domains reported as worse. Among males (n=1057), pre-frailty meant higher odds of reporting SFA (OR 1.8 95%CI 1.2-6.6), CSF (OR 1.7 95%CI 1.1-2.7), and EVD (OR 1.5 95%CI 1.0-2.2). Among females (n=1003), there was no difference in reporting by frailty. Females were more likely to report worse OSF (Robust: OR 7.4, 95%CI 4.8-11.4; Pre-frail: OR 6.2, 95%CI 3.9-9.9; Frail: OR 3.4 95%CI 1.7-6.6), but less likely to report SFA (Robust OR .3, 95%CI .2-.5; Pre-frail OR .2, 95%CI .1-.3; Frail OR .2 95%CI .1-.3). Pre-frail and frail females reported fewer domains as worse (Pre-frail coefficient -0.21 SE 0.09, Frail -0.43 SE 0.14). As frailty worsened, males reported more domains as worse (Pre-frail 0.24 SE 0.07, Frail 0.29 SE 0.08). Self-reported sexual functioning differs by sex at all levels of frailty, and reporting by males, but not females, changes with frailty. Providers should be aware that sexual functioning is of importance to both sexes despite varying degrees of frailty.

Effect of SR-49059, a vasopressin V1a antagonist, on human vascular smooth muscle cells

1995 ◽  
Vol 268 (1) ◽  
pp. H404-H410 ◽  
Author(s):  
C. Serradeil-Le Gal ◽  
J. M. Herbert ◽  
C. Delisee ◽  
P. Schaeffer ◽  
D. Raufaste ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Specific Binding ◽  
Muscle Cells ◽  
Maximal Response ◽  
Receptor Subtypes ◽  
Functional Studies ◽  
Antagonist Binding

The effects of SR-49059, a new nonpeptide and selective arginine vasopressin (AVP) V1a antagonist, were investigated in binding and functional studies on cultured human aortic vascular smooth muscle cells (VSMC). Characterization of human vascular V1a receptors, using a specific V1a radioiodinated ligand, showed that [125I]-linear AVP antagonist binding to human VSMC membranes was time dependent, reversible, and saturable. A single population of high-affinity binding sites (apparent equilibrium dissociation constant = 15 +/- 6 pM; maximum binding density = 36 +/- 5 fmol/mg protein, i.e., approximately 3,000 sites/cell) with the expected V1a profile was identified. Exposure of these cells to AVP dose-dependently produced cytosolic free [Ca2+] increase [AVP concentration required to obtain a half-maximal response (EC50) = 23 +/- 9 nM] and proliferation (EC50 = 3.2 +/- 0.5 nM). SR-49059 strongly and stereospecifically inhibited [125I]-linear AVP antagonist binding to VSMC V1a receptors [inhibition constant (Ki) = 1.4 +/- 0.3 nM], AVP-evoked Ca2+ increase [concentration of inhibitor required to obtain 50% inhibition of specific binding (IC50) = 0.41 +/- 0.06 nM], and the mitogenic effects induced by 100 nM AVP (IC50 = 0.83 +/- 0.04 nM). OPC-21268, another nonpeptide V1a antagonist, was more than two orders of magnitude less potent than SR-49059 in these models. However, the consistent affinity (Ki = 138 +/- 21 nM) and activity found with OPC-21268 on human VSMC in comparison with the inactivity already observed for other human V1a receptors (liver, platelets, adrenals, and uterus) strongly suggested the existence of human AVP V1a-receptor subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

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