scholarly journals No evidence for prolactin’s involvement in the post-ejaculatory refractory period

2020 ◽  
Author(s):  
Susana Valente ◽  
Tiago Marques ◽  
Susana Q. Lima

AbstractIn many species, ejaculation is followed by a state of decreased sexual motivation, the post-ejaculatory refractory period. Several lines of evidence have suggested prolactin, a pituitary hormone released around the time of ejaculation in humans and other animals, to be a decisive player in the establishment of the refractory period. However, data supporting this hypothesis is controversial. We took advantage of two different strains of house mouse, a wild derived and a classical laboratory strain, that differ substantially in their sexual behavior, to investigate prolactin’s involvement in sexual motivation and the refractory period. First, we show that there is prolactin release during sexual behavior in male mice. Second, using a pharmacological approach, we show that acute manipulations of prolactin levels, either mimicking the natural release during sexual behavior or inhibiting its occurrence, do not affect sexual motivation or shorten the refractory period, respectively. Therefore, we show compelling evidence refuting the idea that prolactin released during copulation is involved in the establishment of the refractory period, a long-standing hypothesis in the field of behavioral endocrinology.

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Susana Valente ◽  
Tiago Marques ◽  
Susana Q. Lima

AbstractIn many species, ejaculation is followed by a state of decreased sexual activity, the post-ejaculatory refractory period. Several lines of evidence have suggested prolactin, a pituitary hormone released around the time of ejaculation in humans and other animals, to be a decisive player in the establishment of the refractory period. However, data supporting this hypothesis is controversial. We took advantage of two different strains of house mouse, a wild derived and a classical laboratory strain that differ substantially in their sexual performance, to investigate prolactin’s involvement in sexual activity and the refractory period. First, we show that there is prolactin release during sexual behavior in male mice. Second, using a pharmacological approach, we show that acute manipulations of prolactin levels, either mimicking the natural release during sexual behavior or inhibiting its occurrence, do not affect sexual activity or shorten the refractory period, respectively. Therefore, we show compelling evidence refuting the idea that prolactin released during copulation is involved in the establishment of the refractory period, a long-standing hypothesis in the field of behavioral endocrinology.


2004 ◽  
Vol 171 (4S) ◽  
pp. 429-429
Author(s):  
Masayoshi Nomura ◽  
Naohiro Fujimoto ◽  
Donald W. Pfaff ◽  
Sonoko Ogawa ◽  
Tetsuro Matsumoto

2014 ◽  
Vol 18 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Zhi Jun Zang ◽  
Su Yun Ji ◽  
Wang Dong ◽  
Ya Nan Zhang ◽  
Er Hong Zhang ◽  
...  

2018 ◽  
Vol 81 ◽  
pp. 34-40 ◽  
Author(s):  
Renata K. Carvalho ◽  
Maingredy R. Souza ◽  
Monaliza L. Santos ◽  
Francisco S. Guimarães ◽  
Roger Luís H. Pobbe ◽  
...  

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Kimberly J Jennings ◽  
Luis de Lecea

Abstract Gonadal hormones contribute to the sexual differentiation of brain and behavior throughout the lifespan, from initial neural patterning to “activation” of adult circuits. Sexual behavior is an ideal system in which to investigate the mechanisms underlying hormonal activation of neural circuits. Sexual behavior is a hormonally regulated, innate social behavior found across species. Although both sexes seek out and engage in sexual behavior, the specific actions involved in mating are sexually dimorphic. Thus, the neural circuits mediating sexual motivation and behavior in males and females are overlapping yet distinct. Furthermore, sexual behavior is strongly dependent on circulating gonadal hormones in both sexes. There has been significant recent progress on elucidating how gonadal hormones modulate physiological properties within sexual behavior circuits with consequences for behavior. Therefore, in this mini-review we review the neural circuits of male and female sexual motivation and behavior, from initial sensory detection of pheromones to the extended amygdala and on to medial hypothalamic nuclei and reward systems. We also discuss how gonadal hormones impact the physiology and functioning of each node within these circuits. By better understanding the myriad of ways in which gonadal hormones impact sexual behavior circuits, we can gain a richer and more complete appreciation for the neural substrates of complex behavior.


Chemosphere ◽  
2018 ◽  
Vol 195 ◽  
pp. 312-324 ◽  
Author(s):  
Thales Chagas Quintão ◽  
Letícia Martins Rabelo ◽  
T.G.S. Alvarez ◽  
A.T. Guimarães ◽  
A.S.L. Rodrigues ◽  
...  

2014 ◽  
Vol 34 (17) ◽  
pp. 5747-5753 ◽  
Author(s):  
M. A. Farmer ◽  
A. Leja ◽  
E. Foxen-Craft ◽  
L. Chan ◽  
L. C. MacIntyre ◽  
...  
Keyword(s):  

1997 ◽  
Vol 153 (1) ◽  
pp. R5-R10 ◽  
Author(s):  
N Masumoto ◽  
Y Ikebuchi ◽  
T Matsuoka ◽  
K Tasaka ◽  
A Miyake ◽  
...  

Abstract The synaptic membrane protein synaptosomal-associated protein (SNAP-25) has recently been implicated as one of the key proteins involved in exocytotic membrane fusion in neurons. However, the role of SNAP-25 in pituitary hormone release is not known. In this study, we determined that SNAP-25 is involved in regulated exocytosis in the clonal pituitary cell line GH4C1. SNAP-25 messenger RNA and protein were detected in GH4C1 cells by RT-PCR and immunoblot analysis, respectively. Immunofluorescence analysis indicated that SNAP-25 protein was localized in the plasma membrane. Next, to determine the function of SNAP-25 in GH4C1 cells, specific inhibitors of SNAP-25, botulinum neurotoxin (BoNT) /A or /E, and antisense SNAP-25 oligonucleotide were used. Neither BoNT/A nor BoNT/E affected thyrotropin-releasing hormone (TRH)-induced cytosolic Ca2+ increase, but both inhibited TRH-induced exocytosis. Moreover, they dose-dependently inhibited TRH-induced prolactin release. The introduction of antisense oligonucleotide into the cells also inhibited TRH-induced prolactin release. These results suggest that SNAP-25 is involved in regulated exocytosis in GH4C1 cells.


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