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Husain, B. F. A.

Publications and source records attributed to Husain, B. F. A..

2 recordsLinked to original sources

Cyclical control of female rejection behavior by progesterone receptor expressing neurons of the anterior ventromedial hypothalamus

Internal state-dependent behavioral responses, such as the switch between rejection and acceptance of sexual advances depending on a females reproductive capacity, are fundamental to maintain social interactions and wellbeing. Here we characterize a dedicated circuit for the cyclical control of rejection behavior in the mouse, located in the anterior ventrolateral ventromedial hypothalamus (aVMHvl). In vivo recordings reveal that progesterone receptor expressing neurons of the aVMHvl (aVMHvlPr+) are active during rejection but silent when females accept the male. Moreover, we show that aVMHvlPr+ neurons receive reduced excitatory to inhibitory synaptic input balance during the receptive phase of the reproductive cycle. Finally, optogenetic activation of aVMHvlPr+ neurons in receptive females is sufficient to increase rejection behavior, disrupting the probability of copulation, without affecting other male-directed interactions. This population of aVMHvlPr+ neurons is thus a key neural substrate controlling female sexual behavior, providing an additional barrier to mating when fertilization is not possible.

neuroscience↗

Genetic loss of norepinephrine does not alter adult hippocampal neurogenesis in dopamine β-hydroxylase deficient mice

Norepinephrine (NE), and specific adrenoceptors, have been reported to influence distinct aspects of adult hippocampal neurogenesis, including latent stem cell activation, progenitor proliferation, and differentiation. These findings are predominantly based on the use of pharmacological approaches in both in vitro and in vivo systems. Here, we sought to assess the consequences of genetic ablation of NE on adult hippocampal neurogenesis, by examining dopamine {beta} hydroxylase knockout (Dbh-/-) mice, which lack NE from birth. We find that Dbh-/- mice exhibit no difference in adult hippocampal progenitor proliferation and survival. Further, the number of immature newborn neurons, labeled using stage-specific developmental markers within the hippocampal neurogenic niche, was also unaltered in Dbh -/- mice. In contrast, the noradrenergic neurotoxin DSP-4, which had previously been shown to reduce adult hippocampal neurogenesis in rats, also resulted in a decline in hippocampal progenitor proliferation in C57/Bl6N mice. These findings indicate that pharmacological lesioning of noradrenergic afferents in adulthood, but not the complete genetic loss of NE from birth, impairs adult hippocampal neurogenesis in mice.

neuroscience↗