Many peptides, when released as chemical messengers within the brain, have powerful influences on complex behaviours. Most strikingly, vasopressin and oxytocin, once thought of as circulating hormones whose actions were confined to peripheral organs, are now known to be released in the brain where they play fundamentally important roles in social behaviours1. In humans, disruptions of these peptide systems have been linked to several neurobehavioural disorders, including Prader-Willi syndrome, affective disorders, and obsessive-compulsive disorder, and polymorphisms of the vasopressin V1a receptor have been linked to autism2,3. Here we report that the rat olfactory bulb contains a large population of interneurones which express vasopressin, that blocking the actions of vasopressin in the olfactory bulb impairs the social recognition abilities of rats, and that vasopressin agonists and antagonists can modulate the processing of information by olfactory bulb neurones. The findings indicate that social information is processed in part by a vasopressin system intrinsic to the olfactory system.

TitleRapid inhibition of female sexual behavior by gonadotropin-inhibitory hormone (GnIH). Abstract Gonadotropin-releasing hormone (GnRH) is largely responsible for the initiation of sexual behaviors; one form of GnRH activates a physiological cascade causing gonadal growth and gonadal steroid feedback to the brain, and another form is thought to act as a neurotransmitter to enhance sexual receptivity. In contrast to GnRH, gonadotropin-inhibitory hormone (GnIH) inhibits gonadotropin release. The distribution of GnIH in the avian brain suggests that it has not only hypophysiotropic actions but also unknown behavioral actions. GnIH fibers are present in the median eminence (ME) and are in apparent contact with chicken GnRH (cGnRH)-I and -II neurons and fibers. In birds, cGnRH-I regulates pituitary gonadotropin release, whereas cGnRH-II enhances copulation solicitation in estradiol-primed females exposed to male song. In the present study, we determined the effects of GnIH administered centrally to female white-crowned sparrows. A physiological dose of GnIH reduced circulating LH and inhibited copulation solicitation, without affecting locomotor activity. Using rhodaminated GnIH, putative GnIH binding sites were seen in the ME close to GnRH-I fiber terminals and in the midbrain on or close to GnRH-II neurons. These data demonstrate direct effects of GnIH upon reproductive physiology and behavior, possibly via separate actions on two forms of GnRH.

In male song sparrows (Melospiza melodia), territorial challenges during the breeding season can rapidly increase circulating levels of testosterone (T). During the non-breeding season, male song sparrows are highly aggressive, but the gonads are regressed and plasma T levels are non-detectable and unaffected by territorial challenges. The pro-hormone dehydroepiandrosterone (DHEA) is elevated in song sparrow plasma and brain during the non-breeding season and may be locally converted to sex steroids in the brain to regulate aggression. The enzyme 3β-hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD) converts DHEA to androstenedione (AE) using the cofactor NAD+, and this is a critical rate-limiting step. We predicted that brain 3β-HSD activity varies seasonally and is rapidly modulated by aggressive challenges. In the first study, brain 3β-HSD activity was highest in the non-breeding season in specific regions. In the second study, a simulated territorial challenge rapidly increased aggressive behavior in non-breeding song sparrows. Brain 3β-HSD activity, when measured without exogenous NAD+, increased by ∼250 to 500% in telencephalic regions of challenged subjects. When brain 3β-HSD activity was measured with exogenous NAD+, these effects of territorial challenges were not observed. These data suggest that territorial challenges rapidly increase endogenous NAD+levels or increase 3β-HSD activity specifically within a NAD-rich subcellular compartment. Together, these two studies suggest a shift from systemic to local sex steroid signaling in the non-breeding season. Local steroid signaling produces high spatial and temporal specificity of steroid signals and avoids the costs of high systemic T levels during the non-breeding season.

Free-living male song sparrows experience three annually repeating life history stages associated with differential expression of sex steroid-dependent reproductive and aggressive behavior. In the breeding stage, they display reproductive and aggressive behavior and have elevated circulating testosterone levels. During molt, males show little or no aggression and no reproductive behavior, and have basal levels of circulating testosterone. In the non-breeding stage, they display high levels of aggression and no reproductive behavior, and have basal levels of circulating testosterone. In order to understand more fully the neural regulation of seasonal aggressive and reproductive behavior, birds were collected during all three life history stages, and levels of neural aromatase, androgen receptor (AR), and estrogen receptor alpha (ERalpha) and beta (ERbeta) mRNA expression were measured. Breeding males had the highest levels of aromatase expression in both the preoptic area (POA) and medial preoptic area/medial bed nucleus of the stria terminalis (mPOA/BSTm), and the highest AR expression levels in the POA, consistent with the well-established role these regions play in the regulation of male reproductive behavior. Aromatase expression in the ventromedial nucleus of the hypothalamus (VMH) was higher during breeding and non-breeding compared with molt, suggesting that the VMH may play a role in the estrogen-dependent regulation of aggression in this species. AR expression also varied in medial HVC and pvMSt, a newly described periventricular region in the medial striatum. ERalpha and ERbeta mRNA expression did not vary seasonally in any brain region examined, suggesting that estrogen-dependent changes in behavior are mediated by differences in neural estrogen synthesis.

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