Sex differences in the neural circuit that mediates female sexual receptivity - PubMed (original) (raw)
Review
Sex differences in the neural circuit that mediates female sexual receptivity
Loretta M Flanagan-Cato. Front Neuroendocrinol. 2011 Apr.
Abstract
Female sexual behavior in rodents, typified by the lordosis posture, is hormone-dependent and sex-specific. Ovarian hormones control this behavior via receptors in the hypothalamic ventromedial nucleus (VMH). This review considers the sex differences in the morphology, neurochemistry and neural circuitry of the VMH to gain insights into the mechanisms that control lordosis. The VMH is larger in males compared with females, due to more synaptic connections. Another sex difference is the responsiveness to estradiol, with males exhibiting muted, and in some cases reverse, effects compared with females. The lack of lordosis in males may be explained by differences in synaptic organization or estrogen responsiveness, or both, in the VMH. However, given that damage to other brain regions unmasks lordosis behavior in males, a male-typical VMH is unlikely the main factor that prevents lordosis. In females, key questions remain regarding the mechanisms whereby ovarian hormones modulate VMH function to promote lordosis.
Copyright © 2011 Elsevier Inc. All rights reserved.
Figures
FIGURE 1
Working model of the cell types in the VL-VMH, including their dendritic arbors, axonal targets and possible connections between them. A) The ER-containing neurons (gold) are known to release glutamate as their neurotransmitter and may serve as local interneurons. Other neurons (purple) exhibit estradiol-induced increases in dendritic spines. A third cell type (blue) sends descending projections to the periaqueductal gray (PAG) to affect behavior. All three cell types extend long dendrites into the lateral fiber field, which includes axonal fibers containing a variety of peptides and transmitters.
FIGURE 2
Summary of our current understanding of the neuron types in the VMH. Several lines of evidence indicate that the ERα-containing neurons are largely separate from the PAG-projecting neurons. Various markers have been co-localized with the ERα-containing neurons. The available evidence suggests that there is a third cell type, that is, non-ERα-containing neurons and non-PAG-projecting neurons. Although several features may be attributed to these neurons, it is not yet known if this represents a single cell type. Abbreviations: Enkephalin, Enk; Estrogen receptor-α; ERα; Neuronal nitrous oxide synthase, nNOS; Oxytocin receptor, OTR; Vesicular glutamate transporter 2, vGlut2. References: [75; 81; 82; 83; 84; 85; 94; 102; 103; 104; 109].
FIGURE 3
Working model of the mechanisms of sexual differentiation in the VMH. Testosterone acts on androgen receptors, which in turn upregulate the enzyme aromatase. Aromatase allows the conversion of testosterone to estradiol, and many masculinizing effects then are mediated by estrogen receptors. ER-α is certainly a critical receptor, but other estrogen receptors are likely to participate as well. Membrane-based actions may mediate the sex differences in dendrite morphology, which lead to permanent sex differences in synaptic organization. In parallel, developmental effects of estrogen receptors may modify the chromatin to permanently alter the responsiveness to sex hormones in adult hood.
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