PubMed · 8480321
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V L Voith. 1993. Behaviour problems in cats.. https://pubmed.ncbi.nlm.nih.gov/8480321/
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Gonadal steroid hormones regulate sexually dimorphic development of brain functions and behaviors. Their nuclear receptors offer the opportunity to relate molecular events in neurons to simple instinctive mammalian behaviors. We have determined the role of estrogen receptor (ER) activation by endogenous estrogen in the development of male-typical behaviors by the use of transgenic estrogen-receptor-deficient (ERKO) mice. Surprisingly, in spite of the fact that they are infertile, ERKO mice showed normal motivation to mount females but they achieved less intromissions and virtually no ejaculations. Aggressive behaviors were dramatically reduced and male-typical offensive attacks were rarely displayed by ERKO males. Moreover, ER gene disruption demasculinized open-field behaviors. In the brain, despite the evident loss of functional ER protein, the androgen-dependent system appears to be normally present in ERKO mice. Together, these findings indicate that ER gene expression during development plays a major role in the organization of male-typical aggressive and emotional behaviors in addition to simple sexual behaviors.
In Syrian hamsters, vasopressin (AVP) controls a form of scent marking called flank marking. Microinjection and lesion studies have identified several components of the neural circuit controlling this behavior. Microinjection of AVP into the medial preoptic-anterior hypothalamus (MPOA-AH), lateral septal nucleus (LS), bed nucleus of stria terminalis (BNST), and periaqueductal gray (PAG) stimulates an intense bout of flank marking. Lesions of areas such as the MPOA-AH and the LS inhibit flank marking. Other studies employing Fos immunocytochemistry suggest that the central amygdala (Ce) might be a component of this neural circuit. The purpose of the present study was to assess the significance of the Ce in regulation of AVP-induced flank marking. In Expt. 1A, the Ce of hamsters were either lesioned with ibotenic acid or sham-lesioned. In Expt. 1B, the Ce of hamsters were either lesioned electrolytically or sham-lesioned. All lesions were made bilaterally. One week later, hamsters were microinjected with AVP into the MPOA-AH and immediately tested for flank marking. In Expt. 2, the hamsters were microinjected with AVP into the Ce and were immediately tested for flank marking. Ibotenic lesions of the Ce reduced flank marking and electrolytic lesions completely inhibited flank marking in response to AVP microinjected into the MPOA-AH. Sham-lesions or lesions placed in other areas of the amygdala resulted in intense bouts of AVP-induced flank marking and flank grooming. No flank marking or flank grooming was observed in response to AVP microinjected into the Ce. These data indicate that the Ce plays a critical role in AVP-induced flank marking, although flank marking is not induced by AVP within the Ce itself.
The effects of amygdala lesions on passive avoidance of drinking (dPA) and social interactions in a resident-intruder test were examined in two experiments that utilized different lines of Long-Evans hooded rats. The lesions were fairly well restricted to the rostral half of the central nucleus (rACe), or the cholinergically richly innervated basolateral nucleus (ABL) or the medial nucleus (AMe) of the amygdala. In both experiments, dPA deficits indicating disturbances in fear conditioning or fear expression were found with ABL and rACe lesions. The rACe lesions produced a greater deficit. AMe lesions caused no dPA deficit at all, which contrasts with the mild PA deficits reported by others employing larger lesions extending to the cortical nucleus and, perhaps, damaging the central nucleus. Social behavior was not affected by the lesions in any clear manner. In rats from a long-standing home colony, rACe lesions increased a behavior of plowing and kicking the wood-chip cage bedding during social encounters, and AMe lesions increased lateral defense behaviors. Both effects are paradoxical, suggesting increased anxiety in the fear-deficient rACe rats and increased defense with AMe lesions, despite several previous reports of decreased defense. In the second experiment, rats purchased from a supplier showed no lesion effects during social interactions; like the control group, all three lesion groups exhibited increases in offense associated with cohabitation with a female. The ABL lesions, particularly, had no effect comparable to the decreased offense recently reported to occur following neurotoxin lesions.