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The 2016 Society of Behavioral Neuroendocrinology Annual Meeting in Montreal, Quebec, Canada, has been changed to August 7 – 10, 2016.
FABBS Advocacy Update: Federal Funding for FY 2016

Negotiators reached an agreement last night on an omnibus bill to fund the federal government for the remainder of the fiscal year...

Welcome from the President

SBN President Cheryl Sisk.

I am delighted and honored to be your new President. SBN is a wonderful organization that provides significant benefits to its members. I look forward to helping the society meet your interests and needs in science and professional development, and I encourage you to share your ideas about how SBN can best serve you.

—Elizabeth Adkins-Regan

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 (2015-2017) Elizabeth Adkins-Regan

PRESIDENT-ELECT (2015-20175) Rae Silver

PAST PRESIDENT (2015-2017) Cheryl Sisk

SECRETARY (2015-2017) Colin John Saldanha

TREASURER (2013-2016) Nancy Forger

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Hormones and Behavior

Tuesday, February 09, 2016
Publication date: April 2016
Source:Hormones and Behavior, Volume 80

Author(s): Lydie Naulé, Clarisse Marie-Luce, Caroline Parmentier, Mariangela Martini, Christelle Albac, Anne-Charlotte Trouillet, Matthieu Keller, Hélène Hardin-Pouzet, Sakina Mhaouty-Kodja

Estradiol derived from neural aromatization of gonadal testosterone plays a key role in the perinatal organization of the neural circuitry underlying male sexual behavior. The aim of this study was to investigate the contribution of neural estrogen receptor (ER) β in estradiol-induced effects without interfering with its peripheral functions. For this purpose, male mice lacking ERβ in the nervous system were generated. Analyses of males in two consecutive tests with a time interval of two weeks showed an effect of experience, but not of genotype, on the latencies to the first mount, intromission, pelvic thrusting and ejaculation. Similarly, there was an effect of experience, but not of genotype, on the number of thrusts and mating length. Neural ERβ deletion had no effect on the ability of males to adopt a lordosis posture in response to male mounts, after castration and priming with estradiol and progesterone. Indeed, only low percentages of both genotypes exhibited a low lordosis quotient. It also did not affect their olfactory preference. Quantification of tyrosine hydroxylase- and kisspeptin-immunoreactive neurons in the preoptic area showed unaffected sexual dimorphism of both populations in mutants. By contrast, the number of androgen receptor- and ERα-immunoreactive cells was significantly increased in the bed nucleus of stria terminalis of mutant males. These data show that neural ERβ does not play a crucial role in the organization and activation of the neural circuitry underlying male sexual behavior. These discrepancies with the phenotype of global ERβ knockout models are discussed.

Tuesday, February 09, 2016
Publication date: April 2016
Source:Hormones and Behavior, Volume 80

Author(s): Chul Ju Hwang, Dong-Young Choi, Yu Yeon Jung, Young-Jung Lee, Jae Suk Yun, Ki-Wan Oh, Sang-Bae Han, Seikwan Oh, Mi Hee Park, Jin Tae Hong

Approximately, 7–10 million people in the world suffer from Parkinson's disease (PD). Recently, increasing evidence has suggested the protective effect of estrogens against nigrostriatal dopaminergic damage in PD. In this study, we investigated whether estrogen affects 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced behavioral impairment in estrogen receptor alpha (ERα)-deficient mice. MPTP (15mg/kg, four times with 1.5-h interval)-induced dopaminergic neurodegeneration was evaluated in ERα wild-type (WT) and knockout (KO) mice. Larger dopamine depletion, behavioral impairments (Rotarod test, Pole test, and Gait test), activation of microglia and astrocytes, and neuroinflammation after MPTP injection were observed in ERα KO mice compared to those in WT mice. Immunostaining for tyrosine hydroxylase (TH) after MPTP injection showed fewer TH-positive neurons in ERα KO mice than WT mice. Levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC, metabolite of dopamine) were also lowered in ERα KO mice after MPTP injection. Interestingly, a higher immunoreactivity for monoamine oxidase (MAO) B was found in the substantia nigra and striatum of ERα KO mice after MPTP injection. We also found an increased activation of p38 kinase (which positively regulates MAO B expression) in ERα KO mice. In vitro estrogen treatment inhibited neuroinflammation in 1-methyl-4-phenyl pyridium (MPP+)-treated cultured astrocyte cells; however, these inhibitory effects were removed by p38 inhibitor. These results indicate that ERα might be important for dopaminergic neuronal survival through inhibition of p38 pathway.

Tuesday, February 09, 2016
Publication date: March 2016
Source:Hormones and Behavior, Volume 79

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