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Bosch, O. J., Nair, H. P., Ahern, T. H., Neumann, I. D., & Young, L. J. (2008). The CRF System Mediates Increased Passive Stress-Coping Behavior Following the Loss of a Bonded Partner in a Monogamous Rodent. Neuropsychopharmacology, 34(6), 1406–1415.
Abstract: Social relationships significantly influence physiology and behavior, including the hypothalamo–pituitary–adrenal axis, anxiety, and mental
health. Disruption of social bonds through separation or death often results in profound grieving, depression, and physical illness. As the
monogamous prairie vole forms enduring, selective pair bonds with the mating partner, they provide an animal model to study the
physiological consequences of pair bonding and, thus, the loss of the bonded partner. Male prairie voles were paired with a novel female
or male sibling. After 5 days, half of the males of each group were separated from the partner. Elevated plus-maze, forced swim, and tail
suspension tests were used to assess anxiety-like and passive stress-coping behaviors indicative of depressive-like behavior. Following 4
days of separation from the female but not the male partner, experimental males displayed increased passive stress-coping. This effect
was abolished by long-term intracerebroventricular infusion of a nonselective corticotropin-releasing factor (CRF) receptor antagonist
without disrupting the bond itself. Both CRF type 1 and 2 receptors were involved in the emergence of passive stress-coping behavior.
Furthermore, pairing with a female was associated with elevated CRF mRNA in the bed nucleus of the stria terminalis, and partner loss
elicited a pronounced increase in circulating corticosteroid and adrenal weight. We speculate that the CRF system may mediate an
aversive affect following separation from the female partner, which may facilitate proximity seeking between the pair-bonded individuals.
Hence, the prairie vole model may provide insights into brain mechanisms involved in the psychopathological consequences of partner
loss.
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Calcagnoli, F., Boer, S. F., Althaus, M., Boer, J. A., & Koolhaas, J. M. (2013). Antiaggressive activity of central oxytocin in male rats. Psychopharmacology, 229(4), 639–651.
Abstract: Rationale A substantial body of research suggests that the
neuropeptide oxytocin promotes social affiliative behaviors
in a wide range of animals including humans. However, its
antiaggressive action has not been unequivocally demonstrated
in male laboratory rodents.
Objective Our primary goal was to examine the putative
serenic effect of oxytocin in a feral strain (wild type
Groningen, WTG) of rats that generally show a much
broader variation and higher levels of intermale aggression
than commonly used laboratory strains of rats.
Methods Resident animals were intracerebroventricularly
(icv) administered with different doses of synthetic oxytocin
and oxytocin receptor antagonist, alone and in combination,
in order to manipulate brain oxytocin functioning and to
assess their behavioral response to an intruder.
Results Our data clearly demonstrate that acute icv administered
oxytocin produces dose-dependent and receptorselective
changes in social behavior, reducing aggression
and potentiating social exploration. These antiaggressive
effects are stronger in the more offensive rats. On the other
hand, administration of an oxytocin receptor antagonist
tends to increase (nonsignificantly) aggression only in
low–medium aggressive animals.
Conclusions These results suggest that transiently enhancing
brain oxytocin function has potent antiaggressive effects,
whereas its attenuation tends to enhance aggressiveness. In
addition, a possible inverse relationship between trait aggression
and endogenous oxytocinergic signaling is revealed.
Overall, this study emphasizes the importance of brain
oxytocinergic signaling for regulating intermale offensive aggression.
This study supports the suggestion that oxytocin
receptor agonists could clinically be useful for curbing heightened
aggression seen in a range of neuropsychiatric disorders
like antisocial personality disorder, autism, and addiction.
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Czeh, B., Muller-Keuker, J. I. H., Rygula, R., Abumaria, N., Hiemke, C., Domenici, E., et al. (2006). Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment. Neuropsychopharmacology, 32(7), 1490–1503.
Abstract: Profound neuroplastic changes have been demonstrated in various limbic structures after chronic stress exposure and antidepressant treatment in animal models of mood disorders. Here, we examined in rats the effect of chronic social stress and concomitant antidepressant treatment on cell proliferation in the medial prefrontal cortex (mPFC). We also examined possible hemispheric differences. Animals were subjected to 5 weeks of daily social defeat by an aggressive conspecific and received concomitant, daily, oral fluoxetine (10 mg/kg) during the last 4 weeks. Bromodeoxyuridine (BrdU) labeling and quantitative stereological techniques were used to evaluate the treatment effects on proliferation and survival of newborn cells in limbic structures such as the mPFC and the hippocampal dentate gyrus, in comparison with nonlimbic structures such as the primary motor cortex and the subventricular zone. Phenotypic analysis showed that neurogenesis dominated the dentate gyrus, whereas in the mPFC most newborn cells were glia, with smaller numbers of endothelial cells. Chronic stress significantly suppressed cytogenesis in the mPFC and neurogenesis in the dentate gyrus, but had minor effect in nonlimbic structures. Fluoxetine treatment counteracted the inhibitory effect of stress. Hemispheric comparison revealed that the rate of cytogenesis was significantly higher in the left mPFC of control animals, whereas stress inverted this asymmetry, yielding a significantly higher incidence of newborn cells in the right mPFC. Fluoxetine treatment abolished hemispheric asymmetry in both control and stressed animals. These pronounced changes in gliogenesis after chronic stress exposure may relate to the abnormalities of glial cell numbers reported in the frontolimbic areas of depressed patients.
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