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15th Symposium of the Center for Neuroendocrine Studies University of Massachusetts, Amherst

The Center for Neuroendocrine Studies at UMass, Amherst would like to announce our 15th Symposium entitled, "Promiscuous Molecules: Hormones, Immunity, and Evolution in the Brain" which will take place on Saturday, September 26th, 2015.
Call for applications for Poster Awards at the SBN annual meeting - deadline May 25

Poster Award applications are limited to presenters that conducted the research as undergraduate or graduate students...

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, May 29, 2015
Publication date: Available online 17 May 2015
Source:Hormones and Behavior

Author(s): Maya Frankfurt , Victoria Luine

Memory processing is presumed to depend on synaptic plasticity, which appears to have a role in mediating the acquisition, consolidation, and retention of memory. We have studied the relationship between estrogen, recognition memory, and dendritic spine density in the hippocampus and medial prefrontal cortex, areas critical for memory, across the lifespan in female rodents. The present paper reviews the literature on dendritic spine plasticity in mediating both short and long term memory, as well as the decreased memory that occurs with aging and Alzheimer’s Disease. It also addresses the role of acute and chronic estrogen treatment in these processes.

Friday, May 29, 2015
Publication date: May 2015
Source:Hormones and Behavior, Volume 71

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.

Friday, May 29, 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.

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