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2015 Elections

2015 SBN Executive Committee Elections held from 04/06/2015-05/08/2015. Eligible members cast your vote now for the President-Elect and Secretary!
Seeking nominations for Chair of the SBN Website Committee

We are now soliciting nominations (self or otherwise) for chairperson of the SBN Website Committee. Read more...

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.

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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

Saturday, April 18, 2015
Publication date: Available online 11 April 2015
Source:Hormones and Behavior

Author(s): Philip M. Sinnett , Michael R. Markham

Energetic demands of social communication signals can constrain signal duration, repetition, and magnitude. The metabolic costs of communication signals are further magnified when they are coupled to active sensory systems that require constant signal generation. Under such circumstances, metabolic stress incurs additional risk because energy shortfalls could degrade sensory system performance as well as the social functions of the communication signal. The weakly electric fish Eigenmannia virescens generates electric organ discharges (EODs) that serve as both active sensory and communication signals. These EODs are maintained at steady frequencies of 200-600Hz throughout the lifespan, and thus represent a substantial metabolic investment. We investigated the effects of metabolic stress (food deprivation) on EOD amplitude (EODa) and EOD frequency (EODf) in E. virescens and found that only EODa decreases during food deprivation and recovers after restoration of feeding. Cortisol did not alter EODa under any conditions, and plasma cortisol levels were not changed by food deprivation. Both melanocortin hormones and social challenges caused transient EODa increases in both food-deprived and well-fed fish. Intramuscular injections of leptin increased EODa in food-deprived fish but not well-fed fish, identifying leptin as a novel regulator of EODa and suggesting that leptin mediates EODa responses to metabolic stress. The sensitivity of EODa to dietary energy availability likely arises because of the extreme energetic costs of EOD production in E. virescens and also could reflect reproductive strategies of iteroparous species that reduce social signaling and reproduction during periods of stress to later resume reproductive efforts when conditions improve.

Saturday, April 18, 2015
Publication date: April 2015
Source:Hormones and Behavior, Volume 70

Author(s): Tertia D. Purves-Tyson , Danny Boerrigter , Katherine Allen , Katerina Zavitsanou , Tim Karl , Vanezha Djunaidi , Kay L. Double , Reena Desai , David J. Handelsman , Cynthia Shannon Weickert

Although sex steroids are known to modulate brain dopamine, it is still unclear how testosterone modifies locomotor behaviour controlled, at least in part, by striatal dopamine in adolescent males. Our previous work suggests that increasing testosterone during adolescence may bias midbrain neurons to synthesise more dopamine. We hypothesised that baseline and amphetamine-induced locomotion would differ in adult males depending on testosterone exposure during adolescence. We hypothesised that concomitant stimulation of estrogen receptor signaling, through a selective estrogen receptor modulator (SERM), raloxifene, can counter testosterone effects on locomotion. Male Sprague-Dawley rats at postnatal day 45 were gonadectomised (G) or sham-operated (S) prior to the typical adolescent testosterone increase. Gonadectomised rats were either given testosterone replacement (T) or blank implants (B) for six weeks and sham-operated (i.e. intact or endogenous testosterone group) were given blank implants. Subgroups of sham-operated, gonadectomised and gonadectomised/testosterone-replaced rats were treated with raloxifene (R, 5mg/kg) or vehicle (V), daily for the final four weeks. There were six groups (SBV, GBV, GTV, SBR, GBR, GTR). Saline and amphetamine-induced (1.25mg/kg) locomotion in the open field was measured at PND85. Gonadectomy increased amphetamine-induced locomotion compared to rats with endogenous or with exogenous testosterone. Raloxifene increased amphetamine-induced locomotion in rats with either endogenous or exogenous testosterone. Amphetamine-induced locomotion was negatively correlated with testosterone and this relationship was abolished by raloxifene. Lack of testosterone during adolescence potentiates and testosterone exposure during adolescence attenuates amphetamine-induced locomotion. Treatment with raloxifene appears to potentiate amphetamine-induced locomotion and to have an opposite effect to that of testosterone in male rats.

Saturday, April 18, 2015
Publication date: March 2015
Source:Hormones and Behavior, Volume 69

Author(s): Audrey Davis , Emily Abraham , Erin McEvoy , Sarah Sonnenfeld , Christine Lewis , Catherine S. Hubbard , E. Kurt Dolence , James D. Rose , Emma Coddington

In rough-skinned newts, Taricha granulosa, exposure to an acute stressor results in the rapid release of corticosterone (CORT), which suppresses the ability of vasotocin (VT) to enhance clasping behavior. CORT also suppresses VT-induced spontaneous activity and sensory responsiveness of clasp-controlling neurons in the rostromedial reticular formation (Rf). The cellular mechanisms underlying this interaction remain unclear. We hypothesized that CORT blocks VT-enhanced clasping by interfering with V1a receptor availability and/or VT-induced endocytosis. We administered a physiologically active fluorescent VT conjugated to Oregon Green (VT–OG) to the fourth ventricle 9min after an intraperitoneal injection of CORT (0, 10, 40μg/0.1mL amphibian Ringers). The brains were collected 30min post-VT–OG, fixed, and imaged with confocal microscopy. CORT diminished the number of endocytosed vesicles, percent area containing VT–OG, sum intensity of VT–OG, and the amount of VT-V1a within each vesicle; indicating that CORT was interfering with V1a receptor availability and VT-V1a receptor-mediated endocytosis. CORT actions were brain location-specific and season-dependent in a manner that is consistent with the natural and context-dependent expression of clasping behavior. Furthermore, the sensitivity of the Rf to CORT was much higher in animals during the breeding season, arguing for ethologically appropriate seasonal variation in CORT's ability to prevent VT-induced endocytosis. Our data are consistent with the time course and interaction effects of CORT and VT on clasping behavior and neurophysiology. CORT interference with VT-induced endocytosis may be a common mechanism employed by hormones across taxa for mediating rapid context- and season-specific behavioral responses.

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