Latest News

SBN Encourages NIH to Support Inclusion of Both Sexes in Biomedical Research

In response to NIH's request of information, Rae Silver and the rest of SBN's Public Relations Committee
James McKeen Cattell Fund Fellowships Support for Extending Sabbaticals

James McKeen Cattell Fund "Fellowships" provide support for the science and the application of psychology through supplementary sabbatical awards. Click the title for more information.

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

Tuesday, November 25, 2014
Publication date: Available online 20 November 2014
Source:Hormones and Behavior

Author(s): Shu-Chen Chu , Pei-Ni Chen , Ying-Jui Ho , Ching-Han Yu , Yih-Shou Hsieh , Dong-Yih Kuo

Amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibition of neuropeptide Y (NPY)-containing neurons in the hypothalamus. This study examined whether hypothalamic cocaine- and amphetamine-regulated transcript (CART)-containing neurons and NPY Y1 receptor (Y1R) were involved in the action of AMPH. Rats were treated daily with AMPH for four days, and changes in feeding behavior and expression levels of NPY, CART, and POMC were assessed and compared. The results showed that both feeding behavior and NPY expression decreased during AMPH treatment, with the biggest reduction occurring on day 2. By contrast, the expression of CART and melanocortin 3 receptor (MC3R), a member of the POMC neurotranamission, increased with the maximum response on day 2, directly opposite to the NPY expression results. The intracerebroventricular infusion of NPY antisense or Y1R inhibitor both modulated AMPH-induced anorexia and the expression levels of MC3R and CART. The results suggest that in the hypothalamus both POMC- and CART-containing neurons participate in regulating NPY-mediated appetite control during AMPH treatment. These results may advance the knowledge of molecular mechanism of anorectic drugs.

Tuesday, November 25, 2014
Publication date: Available online 11 November 2014
Source:Hormones and Behavior

Author(s): Mary K. Holder , Shaun S. Veichweg , Jessica A. Mong

Methamphetamine (METH) is a psychomotor stimulant strongly associated with increases in sexual drive and impulsive sexual behaviors that often lead to unsafe sexual practices. In women METH users, such practices have been associated with increases in unplanned pregnancies and sexually transmitted diseases. Despite this significant heath concern, the neural mechanisms underlying this drug-sex association are not known. We previously established a rodent model of METH-facilitated female sexual behavior in which estradiol and progesterone interact with METH to increase motivational components of female behavior and neuronal activation in the posterodorsal medial amygdala (MePD) (Holder et al., 2010; Holder and Mong, 2010). The current study more directly examines the mechanisms underlying the drug-sex interaction. Here, we hypothesize that METH-induced increases in MePD dopamine signaling bridge the METH-hormone interaction. In support of this hypothesis, we found that excitotoxic lesions targeted to the MePD attenuated the METH-induced increases in proceptive behavior. Furthermore, infusion of a D1 agonist into the MePD increased proceptive behavior, while infusion of a D1 antagonist blocked the ability of METH to increase proceptive behaviors. Additionally, we found that METH-treatment increased progesterone receptor (PR)- immunoreactivity in the MePD, suggesting an interaction between dopamine and progesterone signaling. Indeed, infusions of the PR antagonist, RU486, prevented METH-induced increases in sexual behavior. Thus, taken together, the current findings suggest dopamine in the MePD modulates enhanced sexual motivation via an amplification of progesterone signaling and contributes to a better understanding of the neurobiology of drug-enhanced sexual behaviors.

Tuesday, November 25, 2014
Publication date: November 2014
Source:Hormones and Behavior, Volume 66, Issue 5



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