Behavioral and neurobiological consequences of social subjugation during puberty in golden hamsters

In golden hamsters, offensive aggression is facilitated by vasopressin and inhibited by serotonin. We tested whether these neurotransmitter systems respond to modifications resulting from the stress of threat and attack (i.e., social subjugation) during puberty. Male golden hamsters were weaned at postnatal day 25 (P25), exposed daily to aggressive adults from P28 to P42, and tested for offensive aggression as young adults (P45). The results showed a context-dependent alteration in aggressive behavior. Subjugated animals were more likely to attack younger and weaker intruders than nonsubjugated controls. Conversely, subjugated animals were less likely to attack animals of similar size and age. After testing, the animals were killed, and their brains were collected to determine whether these behavioral changes are underlined by changes in the vasopressin and serotonin systems. Social subjugation resulted in a 50% decrease in vasopressin levels within the anterior hypothalamus, a site involved in the regulation of aggression. Furthermore, whereas the density of vasopressin-immunoreactive fibers within the area was not significantly altered in subjugated animals, the number of serotonin-immunoreactive varicosities within the anterior hypothalamus and lateral septum was 20% higher in subjugated animals than in their controls. These results establish puberty as a developmental period sensitive to environmental stressors. Furthermore, the results show that changes in the vasopressin and serotonin systems can correlate with behavioral alterations, supporting the role of these two neurotransmitters in the regulation of aggression

Vasopressin/serotonin interactions in the anterior hypothalamus control aggressive behavior in golden hamsters

Studies in several species of rodents show that arginine vasopressin (AVP) acting through a V1A receptor facilitates offensive aggression, i.e., the initiation of attacks and bites, whereas serotonin (5-HT) acting through a 5-HT1B receptor inhibits aggressive responding. One area of the CNS that seems critical for the organization of aggressive behavior is the basolateral hypothalamus, particularly the anterior hypothalamic region. The present studies examine the neuroanatomical and neurochemical interaction between AVP and 5-HT at the level of the anterior hypothalamus (AH) in the control of offensive aggression in Syrian golden hamsters. First, specific V1A and 5-HT1B binding sites in the AH are shown by in vitro receptor autoradiography. The binding for each neurotransmitter colocalizes with a dense field of immunoreactive AVP and 5-HT fibers and putative terminals. Putative 5-HT synapses on AVP neurons in the area of the AH are identified by double-staining immunocytochemistry and laser scanning confocal microscopy. These morphological data predispose a functional interaction between AVP and 5-HT at the level of the AH. When tested for offensive aggression in a resident/intruder paradigm, resident hamsters treated with fluoxetine, a selective 5-HT reuptake inhibitor, have significantly longer latencies to bite and bite fewer times than vehicle-treated controls. Conversely, AVP microinjections into the AH significantly shorten the latency to bite and increase biting attacks. The action of microinjected AVP to increase offensive aggression is blocked by the pretreatment of hamsters with fluoxetine. These data suggest that 5-HT inhibits fighting, in part, by antagonizing the aggression-promoting action of the AVP system

Localization of sites for estradiol priming of progesterone-facilitated sexual receptivity in female guinea pigs

The studies described in this dissertation were designed to examine certain aspects of the neuronal networks controlling sexual receptivity facilitated by estradiol and progesterone in female guinea pigs. In particular, the first part of this thesis was designed to localize discrete sites within the mediobasal hypothalamus (MBH) where local activation by estradiol is sufficient to induce responsiveness to progesterone-facilitated sexual receptivity. Implants localized within the rostroventral ventrolateral hypothalamus (rostro-ventral VLH) were sufficient to induce responsiveness to progesterone. Using immunocytochemistry for progestin receptors, the same implants were found to induce progestin receptors within the same area. The second part of this thesis was focussed on the description of afferent connections to the rostro-ventral VLH, and the identification of some of these afferents as originating from estradiol-sensitive neurons. Using retrograde tracing techniques, afferents to the rostro-ventral VLH were observed throughout the forebrain and the midbrain, particularly within the medial preoptic nucleus, bed nucleus of the stria terminalis, anterior hypothalamus, amygdala, and lateral parabrachial nucleus. Using immunoreactivity to label neurons containing estrogen receptors, retrogradely labelled neurons were found is most areas highlighted by immunolabelling. Furthermore, within some areas, particularly within the medial preoptic nucleus, medial amygdala, and bed nucleus of the stria terminalis, retrogradely labelled neurons were also immunoreactive to estrogen receptors. The third part of this thesis was designed to study connections between estrogen receptor-rich hypothalamic areas. Interestingly, the results show that neurons within the estrogen receptor-poor ventromedial nucleus were connected to estrogen receptor-immunoreactive neurons in estrogen receptor-rich areas such as the rostro-ventral VLH, suggesting that this nucleus integrates estrogen-dependent hypothalamic functions. In conclusion, the present results point to a discrete part of the hypothalamus as a site of action for estradiol and progesterone in the facilitation of sexual receptivity. Furthermore, this area is connected to a network of estrogen-sensitive neurons integrating several sensory functions involved in the behavior. Finally, this estrogen-dependent function might be integrated with other estrogen-dependent functions at the level of the hypothalamus