Whereas the adolescent brain is a major target for gonadal hormones, our understanding of hormonal influences on adolescent neural and behavioral development remains limited. These experiments investigated how variations in the timing of testosterone (T) exposure, relative to adolescence, alters the strength of steroid-sensitive neural circuits underlying social behavior in male Syrian hamsters. Experiment 1 simulated early, on-time, and late pubertal development by gonadectomizing males on postnatal d 10 and treating with SILASTIC brand T implants for 19 d before, during, or after adolescence. T treatment before or during, but not after, adolescence facilitated mating behavior in adulthood. In addition, preadolescent T treatments most effectively increased mating behavior overall, indicating that the timing of exposure to pubertal hormones contributes to individual differences in adult behavior. Experiment 2 examined the effects of preadolescent T treatment on behavior and brain regional volumes within the mating neural circuit of juvenile males (i.e. still preadolescent). Although preadolescent T treatment did not induce reproductive behavior in juvenile males, it did increase volumes of the bed nucleus of the stria terminalis, sexually dimorphic nucleus, posterodorsal medial amygdala, and posteroventral medial amygdala to adult-typical size. In contrast, juvenile anterodorsal medial amygdala and ventromedial hypothalamus volumes were not changed by preadolescent T treatment yet differed significantly in volume from adult controls, suggesting that further maturation of these brain regions during adolescence is required for the expression of male reproductive behavior. Thus, adolescent maturation of social behavior may involve both steroid-independent and -dependent processes, and adolescence marks the end of a postnatal period of sensitivity to steroid-dependent organization of the brain.

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The medial amygdala plays a key role in regulating adult social behavior and undergoes structural changes during puberty that may be driven by gonadal hormone secretion during this developmental period. The current study sought to investigate potential organizational effects of testosterone during puberty, activational effects of testosterone in adulthood, and any interactions on regional volume and neuronal number of the medial amygdala. Male Syrian hamsters either did or did not experience endogenous testosterone during pubertal brain development, and then received either testosterone-filled or blank capsules during adulthood two weeks before tissue collection. The results show that pubertal testosterone has long-term organizational effects on volume of specific subregions of the medial amygdala such that the presence of pubertal testosterone resulted in 1) decreased volume of the anterior ventral amygdala and, to a lesser extent, the anterior dorsal medial amygdala; 2) increased volume of the posterior dorsal medial amygdala. Both effects were independent of the presence of testosterone during adulthood. Pubertal testosterone also decreased neuronal number in the anterior dorsal medial amygdala, suggesting a possible mechanism by which pubertal testosterone decreases volume in this subregion. In addition, there was a significant interaction between pubertal and adult testosterone, such that testosterone in adulthood increased the number of neurons in the posterior ventral medial amygdala only in males that did not experience endogenous pubertal testosterone. In conclusion, pubertal testosterone organizes the medial amygdala in a subregion-specific manner, which may contribute to the maturation of adult-typical social behavior.

Cocaine exposure during pregnancy can impact brain development and have long-term behavioral consequences. The present study examined the lasting consequences of prenatal cocaine (PN-COC) exposure on the performance of cognitive tasks and dendritic spine density in adult male and female rats. From gestational day 8 to 20, dams were treated daily with 30 mg/kg (ip) of cocaine HCl or saline. At 62 days of age, offspring were tested consecutively for anxiety, locomotion, visual memory and spatial memory. PN-COC exposure significantly increased anxiety in both sexes. Object recognition (OR) and placement (OP) tasks were used to assess cognitive function. Behavioral tests consisted of an exploration trial (T1) and a recognition trial (T2) that were separated by an inter-trial delay of varying lengths. Male PN-COC subjects displayed significantly less time investigating new objects or object location during T2 in both OR and OP tasks. By contrast, female PN-COC subjects exhibited impairments only in OR and only at the longest inter-trial delay interval. In addition, gestational cocaine increased dendritic spine density in the prefrontal cortex and nucleus accumbens in both genders, but only females had increased spine density in the CA1 region of the hippocampus. These data reveal that in-utero exposure to cocaine results in enduring alterations in anxiety, cognitive function and spine density in adulthood. Moreover, cognitive deficits were more profound in males than in females. Keywords sex differences; synaptic plasticity; prefrontal cortex; hippocampus; visual memory; spatial memory Cocaine abuse during pregnancy is recognized as a major social problem (G. A. Richardson, 1998; L. T. Singer et al., 2002). Clinical reports reveal an adverse relationship between Corresponding Author: Kaliris Salas-Ramirez, Department of Physiology and Pharmacology, 138th St and Convent Ave, New York, NY 10031, Tel: 212-650-8255; Fax: 212-650-7726; ksalasram@ccny.cuny.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2011 September 1. Less is known about gender-specific effects of gestational cocaine exposure, even though the effects of cocaine exposure in adulthood are sex-dependent in both rodents and humans (S. M. Evans and R. W. Foltin, 2009). For example, adult female subjects self-administer psychostimulants at lower doses than do males, drug use escalates more rapidly to dependence, and females are at greater risk for relapse following withdrawal than males (J. B. Becker and M. Hu, 2008). Fe...