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Testosterone plays a key role in the expression of male sex behavior by influencing cellular activity and synapses within the magnocellular medial preoptic nucleus (MPN mag), a sub-nucleus of the medial preoptic area (MPOA) in the Syrian hamster. Although the mechanisms underlying hormonally-induced synaptic plasticity in this region remain elusive, the data suggests that an increase in synaptic density may mediate testosterone's effects on copulation. As brain derived neurotrophic factor (BDNF) plays an integral role in regulating synaptic plasticity and gonadal steroids regulate the levels of BDNF, we hypothesize that BDNF may mediate the effects of gonadal hormones on copulatory behavior. To test this hypothesis, we infused BDNF or controls into the MPN mag of long-term castrates. Our results indicate that BDNF, but not the controls, restored copulatory behavior in castrated male Syrian hamsters. Furthermore, the rise of BDNF expression in the MPOA preceded the rise of synaptophysin following testosterone replacement in castrated males. These data are consistent with our hypothesis, implicating a role for BDNF in mediating testosterone's action on copulation and suggest that the delay in testosterone's restoration of copulation is, in part, due to the delay in the increase of BDNF and synaptophysin.
Pubmed ID: 29750970 RIS Download
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This polyclonal targets IgG (H+L)
View all literature mentionsThis polyclonal targets Brain Derived Neurotrophic Factor
View all literature mentionsThis polyclonal targets Goat anti-Mouse IgG H&L (HRP) secondary antibody
View all literature mentionsThis monoclonal targets beta Actin
View all literature mentionsThis polyclonal targets Synaptophysin antibody produced in rabbit
View all literature mentionsThis monoclonal targets BDNF antibody [EPR1292]
View all literature mentionsThis unknown targets
View all literature mentionsThis unknown targets Sheep IgG (H+L)
View all literature mentionsThis polyclonal targets IgG (H+L)
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