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Welcome from the President

SBN President Cheryl Sisk.

Welcome to the website of the Society for Behavioral Neuroendocrinology (SBN). Since 1996, the SBN has been promoting intellectual exchanges between scientists who have interests in the interactions of the nervous system and the endocrine system on behavior and in the influences of behavior and the environment on neuroendocrine systems. We are an inclusive society with a very diverse membership. Our members are interested in quite an array of behaviors – reproductive behavior, parental behaviors, social behaviors, eating and drinking, responses to stressors, learning and memory, aggression and more, as well as mental health. We are interested in a wide range of species, from simple organisms, like c. elegans to humans and everything in between. We are interested in interactions at the molecular, cellular, and organismic/behavioral level of investigation. We work in laboratories, as well as in the field. Many of our members study natural behaviors, which in turn shed light on behavioral disorders, which often have strong neuroendocrine components. This rich mixture of ideas and approaches can be seen in the Society’s journal, Hormones and Behavior , and can be enjoyed at our vibrant, annual meetings.

Upcoming Meetings

Become a Member of the SBN

The Society for Behavioral Neuroendocrinology offers four levels of eligibility for prospective members: Regular, Emeritus, Student, or Associate Memberships.

To see which membership class you qualify for, please review the membership eligibility requirements.

For additional information on SBN and the rules of membership, please see the SBN Bylaws.

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Elected Officers

PRESIDENT (2013-2015) Cheryl Sisk

PRESIDENT-ELECT (2013-2015) Elizabeth Adkins-Regan

PAST PRESIDENT (2013-2015) Jeffrey Blaustein

SECRETARY (2013-2015) Zuoxin Wang

TREASURER (2013-2016) Nancy Forger

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Hormones and Behavior

Friday, October 17, 2014
Publication date: Available online 13 October 2014
Source:Hormones and Behavior

Author(s): Núria Daviu , Raül Andero , Antonio Armario , Roser Nadal

In recent years, special attention is being paid to sex differences in susceptibility to disease. In this regard, there is evidence that male rats present higher levels of both cued and contextual fear conditioning than females. However, little is known about the concomitant hypothalamic-pituitary-adrenal (HPA) axis response to those situations which is critical in emotional memories. Here, we studied the behavioural and HPA responses of male and female Wistar rats to context fear conditioning using electric footshock as the aversive stimulus. Fear-conditioned rats showed a much greater ACTH and corticosterone response than those merely exposed to the fear conditioning chamber without receiving shocks. Moreover, males presented higher levels of freezing whereas HPA axis response was greater in females. Accordingly, during the fear extinction tests, female rats consistently showed less freezing and higher extinction rate, but greater HPA activation than males. Exposure to an open-field resulted in lower activity/exploration in fear-conditioned males, but not females, suggesting greater conditioned cognitive generalization in males than females. It can be concluded that important sex differences in fear conditioning are observed in both freezing and HPA activation, but the two set of variables are affected in the opposite direction: enhanced behavioural impact in males, but enhanced HPA responsiveness in females. Thus, the role of sex differences on fear-related stimuli may depend on the variables chosen to evaluate it, the greater responsiveness of the HPA axis in females perhaps being an important factor to be further explored.

Friday, October 17, 2014
Publication date: Available online 13 October 2014
Source:Hormones and Behavior

Author(s): Brian Kelly , Vanessa Maguire-Herring , Christian M. Rose , Heather E. Gore , Stephen Ferrigno , Melinda A. Novak , Agnès Lacreuse

Human aging is characterized by declines in cognition and fine motor function as well as improved emotional regulation. In men, declining levels of testosterone (T) with age have been implicated in the development of these age-related changes. However, studies examining the effects of T replacement on cognition, emotion and fine motor function in older men have not provided consistent results. Rhesus monkeys (Macaca mulatta) are excellent models for human cognitive aging and may provide novel insights on this issue. We tested 10 aged intact male rhesus monkeys (mean age=19, range 15-25) on a battery of cognitive, motor and emotional tasks at baseline and under low or high T experimental conditions. Their performance was compared to that of 6 young males previously tested in the same paradigm (Lacreuse et al., 2009; Lacreuse et al., 2010). Following a 4-week baseline testing period, monkeys were treated with a gonadotropin releasing hormone agonist (Depot Lupron, 200μg/kg) to suppress endogenous T and were tested on the task battery under a 4-week high T condition (injection of Lupron+T enanthate, 20mg/kg, n=8) or 4-week low T condition (injection of Lupron+oil vehicle, n=8) before crossing over to the opposite treatment. The cognitive tasks consisted of the Delayed Non-Matching-to-Sample (DNMS), the Delayed Response (DR), and the Delayed Recognition Span Test (spatial-DRST). The emotional tasks included an object Approach-Avoidance task and a task in which monkeys were played videos of unfamiliar conspecifics in different emotional context (Social Playbacks). The fine motor task was the Lifesaver task that required monkeys to remove a Lifesaver candy from rods of different complexity. T manipulations did not significantly affect visual recognition memory, working memory, reference memory or fine motor function at any age. In the Approach-Avoidance task, older monkeys, but not younger monkeys, spent more time in proximity of novel objects in the high T condition relative to the low T condition. In both age groups, high T increased watching time of threatening social stimuli in the Social Playbacks. These results suggest that T affects some aspects of emotional processing but has no effect on fine motor function or cognition in young or older male macaques. It is possible that the duration of T treatment was not long enough to affect cognition or fine motor function or that T levels were too high to improve these outcomes. An alternative explanation for the discrepancies of our findings with some of the cognitive and emotional effects of T reported in rodents and humans may be the use of a chemical castration, which reduced circulating gonadotropins in addition to T. Further studies will investigate whether the luteinizing hormone LH mediates the effects of T on brain function in male primates.

Friday, October 17, 2014
Publication date: Available online 7 October 2014
Source:Hormones and Behavior

Author(s): Danilo Alves Moraes , Daniel Paulino Venancio , Deborah Suchecki

Studies have shown a gradual reduction of sleep time in the general population, accompanied by increased food intake, representing a risk for developing obesity, type II diabetes and cardiovascular disease. Rats subjected to paradoxical sleep deprivation (PSD) exhibit feeding and metabolic alterations, both of which are regulated by the communication between peripheral signals and the hypothalamus. This study aimed to investigate the daily change of 96h of PSD-induced food intake, body weight, blood glucose, plasma insulin and leptin concentrations and the expression of their receptors in the hypothalamus of Wistar rats. Food intake was assessed during the light and dark phases and was progressively increased in sleep-deprived animals, during the light phase. PSD produced body weight loss, particularly on the first day, and decreased plasma insulin and leptin levels, without change in blood glucose levels. Reduced leptin levels were compensated by increased expression of leptin receptors in the hypothalamus, whereas no compensations occurred in insulin receptors. The present results on body weight loss and increased food intake replicate previous studies from our group. The fact that reduced insulin levels did not lead to compensatory changes in hypothalamic insulin receptors, suggests that this hormone may be, at least in part, responsible for PSD-induced dysregulation in energy metabolism.

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