Do androgen receptors contribute to the expression of sex differences in the brain?

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Inputs from the olfactory bulb terminate in the medial amygdaloid nucleus (MA) neurons and then project to the medial preoptic area (MPOA) in male rats or the ventromedial hypothalamus (VMH) in female rats. The MPOA in male rats and the VMH in female rats are the center of sexual desire. To understand the effects of gonadal hormones on the MA and MPOA neurons, intracellular recordings were made from these neurons in mouse brain slice preparations. The mean resting membrane potential and input resistance were -68 ± 7 mV and 76 ± 46 MΩ in the MA neurons and -68 ± 10 mV and 140 ± 113MΩ in the MPOA neurons, respectively. The mean threshold and the amplitude of the spike were -54Ω4mV and 73±7mV in the MA neurons and -55±3mV and 74±3mV in the MPOA neurons, respectively. No difference existed between the resting and active membrane properties between male and female mice. The fast excitatory postsynaptic potentials (fast EPSPs) were mainly mediated by AMPA/kainate type glutamate receptors in both male and female mice. The fast inhibitory postsynaptic potentials (fast IPSPs) were mediated by γ-aminobutylic acid (GABA) A receptors in the MA neurons. The administration of 17β-estradiol (1 nM) augmented the amplitude in the fast EPSP and reduced it in the fast IPSP in both the MA and MPOA neurons in male and female mice. In the MA neurons, the administration of testosterone (100 nM) augmented the amplitude of fast EPSP in male mice, but reduced it in female mice. These results suggest that testosterone augments the excitatory responses induced by inputs to the MA neurons in male mice and then transmits information to the center of sexual desire, but in female mice testosterone induces the opposite responses.