PubMed · 16102827
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Iain S McGregor, Robert Adamec, Newton S Canteras, Robert J Blanchard, D Caroline Blanchard. 2005-08-15. Defensive behavior.. https://doi.org/10.1016/j.neubiorev.2005.05.004
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Behavioral differences can evolve rapidly in allopatry, but little is known about the neural bases of such changes. Allopatric populations of Amargosa pupfish (Cyprinodon nevadensis) vary in aggression and courtship behaviors in the wild. Two of these wild populations were recently found to differ in brain expression of arginine vasotocin (AVT)--a peptide hormone shown previously to modulate aggression in pupfish. These populations have been isolated for less than 4000 years, so it remained unclear whether the differences in behavior and neural AVT phenotype were evolved changes or plastic responses to ecologically dissimilar habitats. Here, I tested whether these population differences have a genetic basis by examining how aggressive behavior and neural AVT phenotype responded to ecologically relevant variation in salinity (0.4 ppt or 3 ppt) and temperature (stable or daily fluctuating). Pupfish from Big Spring were more aggressive than pupfish from the Amargosa River when bred and reared under common laboratory conditions. Morphometric analysis of preoptic AVT immunoreactivity showed that the populations differed in how the AVT system responded to salinity and temperature conditions, and revealed that this plasticity differed between parvocellular and magnocellular AVT neuron groups. Both populations also showed relationships between neural AVT phenotype and aggression in the rearing environment, although populations differed in how aggression related to variation in magnocellular AVT neuron size. Together, these results demonstrate that the pupfish populations have diverged in how physical and social conditions affect the AVT system, and provide evidence that the AVT system can evolve quickly to ecologically dissimilar environments.
The anxiogenic neuropeptide, corticotropin-releasing factor (CRF), has a complex effect on intermale aggression. CRF receptor 1 (CRFR1) is the primary receptor for CRF and in this study, we examined in detail isolation-induced intermale aggression in CRFR1 deficient mice. All mice contained a mixed 50:50 inbred/outbred background to improve aggressive performance. Mice were isolated for 4 weeks prior to 2 consecutive days of aggression testing using the resident-intruder paradigm. Mice were also tested for anxiety on the elevated plus maze. Relative to littermate wild-type (WT) controls, CRFR1-mutant mice exhibited normal levels of intermale aggression over the 2 test days in terms of percentage showing aggression, number of attacks, time aggressive, and latency to first attack. In terms of sites of attacks on intruders, CRFR1-deficient mice attacked the ventral portion of the mid-section (including belly) significantly less frequently than WT males on test day 1, but these differences did not reach significance on test day 2. No other differences in sites of attacks were observed. Tail rattling also did not differ between groups. Importantly, KO males showed decreased anxiety relative to WT mice (consistent with previous reports) as evidenced by spending significantly more time on the open arms and significantly less time on the closed arms of the elevated plus maze. Plus maze performance did not correlate with any measure of levels of aggression, suggesting a dissociation between altered levels of anxiety and aggressive performance. Taken together, the results suggest that the activation CRFR1 is not necessary for the normal production of isolation-induced intermale aggression.
In this review we critically examine the data on functions of the estrogen receptor beta (ERbeta) in both behavior and neuroendocrinology. The influence of estradiol via the ERbeta has been assessed using several methods: estrogen receptor knockout mice, specific ERbeta selective agonists, and phytoestrogens which preferentially bind to ERbeta rather than ERalpha. The behavior for which a solid database and consensus is forming is anxiety; activation of ERbeta reduces anxiety on a number of tasks and in several species. Moreover, the relationship between ERbeta and serotonin may be critical for the regulation of this behavior by estradiol. There have been very few studies on learning and memory but the little we know suggests that ERbeta is involved in visuospatial learning; in its absence learning is inhibited. Recent work has suggested a unique function for ERbeta in sexual differentiation; its activation in male neonates may promote defeminization of sexual behavior. Several neurotransmitter-containing neurons in the rat paraventricular nucleus coexpress ERbeta including; vasopressin, oxytocin, prolactin, and to a lesser extent corticotrophin releasing hormone. Given the potential for ERbeta to interact with these important neurotransmitters and its co-expression in gonadotropin releasing hormone neurons it is surprising how normal the hypothalamic-pituitary-adrenal and -gonadal axes appear to be in ERbeta knockout mice. Either this represents a species difference (the neuroanatomy has been conducted in the rat) or compensatory actions of ERalpha or other mechanisms. Exciting avenues for future research include; in vivo interactions between ERalpha and ERbeta, actions of non-estrogenic ligands with ERbeta, and the role of ERbeta in sexual differentiation.