scholarly journals Silencing and stimulating the medial amygdala impairs ejaculation but not sexual incentive motivation in male rats

2021 ◽  
Author(s):  
Patty T. Huijgens ◽  
Roy Heijkoop ◽  
Eelke M.S. Snoeren
Keyword(s):  
Viral Vectors ◽  
Behavioral Control ◽  
Sensory Information ◽  
Incentive Motivation ◽  
Male Rats ◽  
Sexually Dimorphic ◽  
Medial Amygdala ◽  
Neuronal Populations ◽  
Ejaculation Latency

The medial amygdala (MeA) is a sexually dimorphic brain region that integrates sensory information and hormonal signaling, and is involved in the regulation of social behaviors. Lesion studies have shown a role for the MeA in copulation, most prominently in the promotion of ejaculation. The role of the MeA in sexual motivation, but also in temporal patterning of copulation, has not been extensively studied in rats. Here, we investigated the effect of chemogenetic inhibition and stimulation of the MeA on sexual incentive motivation and copulation in sexually experienced male rats. AAV5-CaMKIIa viral vectors coding for Gi, Gq, or no DREADDs (sham) were bilaterally infused into the MeA. Rats were assessed in the sexual incentive motivation test and copulation test upon systemic CNO or vehicle administration. We report that MeA stimulation and inhibition did not affect sexual incentive motivation. Moreover, both stimulation and inhibition of the MeA decreased the number of ejaculations in a 30 minute copulation test and increased ejaculation latency and the number of mounts and intromissions preceding ejaculation, while leaving the temporal pattern of copulation intact. These results indicate that the MeA may be involved in the processing of sensory feedback required to reach ejaculation threshold. The convergence of the behavioral effects of stimulating as well as inhibiting the MeA may reflect opposing behavioral control of specific neuronal populations within the MeA.

γ-Aminobutyric acid regulation of neurohypophysial hormone secretion in male and female rats

1989 ◽  
Vol 121 (2) ◽  
pp. 343-349 ◽  
Author(s):  
E. Saridaki ◽  
D. A. Carter ◽  
S. L. Lightman
Keyword(s):  
Hormone Secretion ◽  
Model Systems ◽  
Female Rats ◽  
Aminobutyric Acid ◽  
Male Rats ◽  
Sexually Dimorphic ◽  
Male And Female ◽  
Endogenous Gaba ◽  
Male And Female Rats

ABSTRACT The role of γ-aminobutyric acid (GABA) in the control of oxytocin and arginine vasopressin (AVP) release from the posterior pituitary was investigated using the GABA agonist muscimol and the GABA antagonists bicuculline and picrotoxin. Two perifusion model systems were studied using (a) intact isolated posterior pituitaries (IPP) and (b) neurosecretosomes from both male and female rats. In experiments on tissue from male rats, the stimulated release of oxytocin and AVP in both models was inhibited by muscimol, an effect which was reversed in the presence of bicuculline. Bicuculline alone increased the release of oxytocin only. Although similar responses to muscimol or bicuculline were seen in neurosecretosomes from female animals, neither agent affected oxytocin and AVP release from the intact IPP. Picrotoxin had a similar effect to bicuculline on oxytocin in isolated posterior pituitaries from male as well as female rats, although at the neurosecretosome level a paradoxical inhibition was observed. These results provide evidence for an endogenous GABA receptor mechanism at the level of the neurosecretory terminals in both male and female rats. The sexually dimorphic IPP response suggests a second more complex mechanism involving either pituicytenerve terminal interactions and/or a secondary role of other neurotransmitters in the GABA regulation of neurohypophysial hormones. Journal of Endocrinology (1989) 121, 343–349

scholarly journals The maternal hormone in the male brain: sexually dimorphic distribution of prolactin signalling in the mouse brain

2018 ◽  
Author(s):  
Hugo Salais-López ◽  
Carmen Agustín-Pavón ◽  
Enrique Lanuza ◽  
Fernando Martínez-García
Keyword(s):  
Mouse Brain ◽  
Prolactin Receptor ◽  
Sexually Dimorphic ◽  
Medial Amygdala ◽  
Signal Transducer ◽  
Prolactin Release ◽  
Hypothalamic Nuclei ◽  
Central Actions ◽  
Males And Females

ABSTRACTResearch of the central actions of prolactin is virtually restricted to females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supplemented males.Prolactin-supplemented males displayed a widespread pattern of pSTAT5 immunoreactivity, restricted to brain centres showing expression of the prolactin receptor. Immunoreactivity for pSTAT5 was present in several nuclei of the preoptic, anterior and tuberal hypothalamus, as well as in the septofimbrial nucleus or posterodorsal medial amygdala of the telencephalon. Conversely, non-supplemented control males were virtually devoid of pSTAT5-immunoreactivity, suggesting that central prolactin actions in males are limited to situations concurrent with substantial hypophyseal prolactin release (e.g. stress or mating). Furthermore, comparison of prolactin-supplemented males and females revealed a significant, female-biased sexual dimorphism, supporting the view that prolactin has a preeminent role in female physiology and behaviour. Finally, in males, castration significantly reduced pSTAT5 immunoreactivity in some structures, including the paraventricular and ventromedial hypothalamic nuclei and the septofimbrial region, thus indicating a region-specific regulatory role of testosterone over central prolactin signalling.

scholarly journals New Insights into the Role of Androgens in Wolffian Duct Stabilization in Male and Female Rodents

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2472-2480 ◽  
Author(s):  
Michelle Welsh ◽  
Richard M. Sharpe ◽  
Marion Walker ◽  
Lee B. Smith ◽  
Philippa T. K. Saunders
Keyword(s):  
Epithelial Cell ◽  
Female Rats ◽  
Male Rats ◽  
Wolffian Duct ◽  
Sexually Dimorphic ◽  
Male And Female ◽  
Cell Height ◽  
Androgen Action ◽  
Butyl Phthalate

Androgen-mediated wolffian duct (WD) development is programmed between embryonic d 15.5 (e15.5) and 17.5 in male rats, and WD differentiation has been shown to be more susceptible to reduced androgen action than is its initial stabilization. We investigated regulation of these events by comparing fetal WD development at e15.5–postnatal d0 in male and female androgen receptor knockout mice, and in rats treated from e14.5 with flutamide (100 mg/kg/d) plus di-n(butyl) phthalate (500 mg/kg/d) to block both androgen action and production, testosterone propionate (20 mg/kg/d) to masculinize females, or vehicle control. In normal females, WD regression occurred by e15.5 in mice and e18.5 in rats, associated with a lack of epithelial cell proliferation and increased apoptosis, disintegration of the basement membrane, and reduced epithelial cell height. Exposure to testosterone masculinized female rats including stabilization and partial differentiation of WDs. Genetic or chemical ablation of androgen action in males prevented masculinization and induced WD regression via similar processes to those in normal females, except this occurred 2–3 d later than in females. These findings provide the first evidence that androgens may not be the only factor involved in determining WD fate. Other factors may promote survival of the WD in males or actively promote WD regression in females, suggesting sexually dimorphic differences in the preprogrammed setup of the WD.

scholarly journals Arginine vasopressin in the medial amygdala causes greater post-stress recruitment of hypothalamic vasopressin neurons

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Wen Han Tong ◽  
Samira Abdulai-Saiku ◽  
Ajai Vyas
Keyword(s):  
Negative Feedback ◽  
Arginine Vasopressin ◽  
Stress Hormones ◽  
Gonadal Hormones ◽  
Stress Axis ◽  
Sexually Dimorphic ◽  
Medial Amygdala ◽  
Neuronal Populations ◽  
Vasopressin Neurons ◽  
Neuronal Groups

AbstractArginine vasopressin (AVP) is expressed in both hypothalamic and extra-hypothalamic neurons. The expression and role of AVP exhibit remarkable divergence between these two neuronal populations. Polysynaptic pathways enable these neuronal groups to regulate each other. AVP neurons in the paraventricular nucleus of the hypothalamus increase the production of adrenal stress hormones by stimulating the hypothalamic–pituitary–adrenal axis. Outside the hypothalamus, the medial amygdala also contains robust amounts of AVP. Contrary to the hypothalamic counterpart, the expression of extra-hypothalamic medial amygdala AVP is sexually dimorphic, in that it is preferentially transcribed in males in response to the continual presence of testosterone. Male gonadal hormones typically generate a negative feedback on the neuroendocrine stress axis. Here, we investigated whether testosterone-responsive medial amygdala AVP neurons provide negative feedback to hypothalamic AVP, thereby providing a feedback loop to suppress stress endocrine response during periods of high testosterone secretion. Contrary to our expectation, we found that AVP overexpression within the posterodorsal medial amygdala increased the recruitment of hypothalamic AVP neurons during stress, without affecting the total number of AVP neurons or the number of recently activated neurons following stress. These observations suggest that the effects of testosterone on extra-hypothalamic AVP facilitate stress responsiveness through permissive influence on the recruitment of hypothalamic AVP neurons.

scholarly journals The use of viral gene transfer in studies of brainstem noradrenergic and serotonergic neurons

2009 ◽  
Vol 364 (1529) ◽  
pp. 2565-2576 ◽  
Author(s):  
S. Kasparov ◽  
A. G. Teschemacher
Keyword(s):  
Viral Vectors ◽  
Pyramidal Neurons ◽  
Viral Gene ◽  
Volume Transmission ◽  
Neuronal Populations ◽  
Central Neurons ◽  
Wide Range ◽  
Cortical Pyramidal Neurons ◽  
The Brain

In contrast to some other neuronal populations, for example hippocampal or cortical pyramidal neurons, mechanisms of synaptic integration and transmitter release in central neurons that contain noradrenaline (NA) and serotonin (5HT) are not well understood. These cells, crucial for a wide range of autonomic and behavioural processes, have long un-myelinated axons with hundreds of varicosities where transmitters are synthesized and released. Both seem to signal mostly in ‘volume transmission’ mode. Very little is known about the rules that apply to this type of transmission in the brain and the factors that regulate the release of NA and 5HT. We discuss some of our published studies and more recent experiments in which viral vectors were used to investigate the physiology of these neuronal populations. We also focus on currently unresolved issues concerning the mechanism of volume transmission by NA and 5HT in the brain. We suggest that clarifying the role of astroglia in this process could be essential for our understanding of central noradrenergic and 5HT signalling.

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