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Cholecystokinin and Neuroendocrine Secretion
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
Joseph G. Verbalis, Edward M. Stricker
Another potential mechanism that should be considered involves interactions of CCK with dopaminergic systems. Lordosis behavior is increased in rats following either dopamine-depleting brain lesions (Caggiula et al., 1979a) or treatment with drugs blocking central dopamine receptors (Everitt et al., 1975; Caggiula et al., 1979b). Because some studies have suggested that CCK-8 can depress potassium-stimulated release of dopamine from caudate nucleus slices in vitro (Hökfelt et al., 1985), these data suggest the possibility that some of the effects of CCK on lordosis behavior could result from presynaptic inhibition of central dopaminergic activity. This again emphasizes the necessity to consider potential interactive effects of a peptide as widely distributed in the brain as CCK.
Genetic Contributions to the Sexual Differentiation of Behavior
Published in Akira Matsumoto, Sexual Differentiation of the Brain, 2017
Despite the difficulties summarized above, there has been some success with genetic analyses of the simplest forms of mammalian reproductive and aggressive behaviors. In particular, these studies built upon substantial structures of knowledge about the mechanisms of lordosis behavior, studied at the neuroanatomical, neurophysiological, and neurochemical levels, accompanied by many studies of hormone-dependent messenger RNA fluctuations.1,2 Consistent with neuroendocrine findings, the gene for the classical estrogen receptor, ERα, is absolutely required for lordosis behavior (Figure 2.3).3 Instead of performing normal reproductive behaviors, estrogen receptor knockout (ERKO) female mice refuse to allow stud males to mount and intromit properly and instead show high frequencies of aggressive behaviors.
Perinatal Sex Steroid Exposure, Brain Morphology, and Neuroendocrine and Behavioral Functions
Published in Takao Mori, Hiroshi Nagasawa, Toxicity of Hormones in Perinatal Life, 2020
Y. Arai, A. Matsumoto, K. Yamanouchi, M. Nishizuka
In behavioral defeminization of male rats, for example, it has been proposed that testosterone inhibits the neonatal development of a lordosis facilitation center located in the ventromedial hypothalamus. Testosterone implants in this region have been reported to be most effective in eliminating lordosis behavior in adulthood.8 However, the surgical transection of descending fibers (presumably of septal origin) just above the anterior commissure has been found to potentiate lordosis in normal males.9, 10 As in normal females, lesions in the pontine central gray abolish lordosis in those males receiving the surgical transection of the dorsal extrahypothalamic descending fibers.11 These findings indicate that the neural mechanisms for lordosis expression are still left intact or only slightly affected by the organizational action of neonatal testicular androgen in male rats. This is hard to reconcile with a view that neonatal testicular androgen destroys the neural mechanism for facilitation of lordosis. Instead, behavioral defeminization in normal male rats seems to be associated with the development of a strong forebrain lordosis-inhibiting system. In normal female rats, the inhibitory system is easily disinhibited by circulating ovarian hormones. However, the inhibition of this system in males is much stronger than in females, being insensitive to any hormonal priming to induce lordosis in males.12 In fact, lordosis cannot be seen in adult male rats unless the inhibitory system is removed surgically by cutting the descending fibers. Therefore, the organizational action of androgen seems to build in a strong inhibitory neural circuit in the lordosis-regulating system.
An Exploratory Study on the Central Nervous Correlates of Sexual Excitation and Sexual Inhibition
Published in The Journal of Sex Research, 2020
K. Unterhorst, H. Gerwinn, A. Pohl, C. Kärgel, C. Massau, I. Ristow, J. Kneer, T. Amelung, H. Walter, K. Beier, M. Walter, B. Schiffer, T. H. C. Kruger, A. Stirn, J. Ponseti
The hypothalamus, which is part of the brain’s dopamine system (Pfaus, 2009), has been associated with sexual arousal in a variety of studies (e.g., Arnow et al., 2002; Ferretti et al., 2005; Karama et al., 2002). In addition, Pfaus (2009) suggested that it plays a central role in the excitatory system of sexual desire. This has been shown in the animal model as well. Hypothalamic protein synthesis seems to be essential for the induction of lordosis behavior in female rats (Parsons, Rainbow, Pfaff, & McEwen, 1982). Lordosis describes the lowering of the forelimbs, raising of the hips, and ventral arching of the back in female rats as a sign of sexual receptiveness. Because of this association between the hypothalamus, mating behavior, and sexual arousal, we expected to find a correlation between hypothalamic brain response and SES scores.