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A scholar, mentor, colleague, and friend.
20th Annual Meeting Call for Proposals

We now seek proposals for symposia and keynote speakers for the 18th Annual Meeting of the SBN.

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

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

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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

Friday, October 09, 2015
Publication date: Available online 9 October 2015
Source:Hormones and Behavior

Author(s): Ruth Feldman

Research on the neurobiology of attachment, pioneered by scholars in the generation that followed the discovery of social bonding, examined the biological basis of mammalian parenting through systematic experiments in animal models and their application to theories on human attachment. This paper argues for the need to construct a theory on the neurobiology of human attachment that integrates findings in animal models with human neuroscience research to formulate concepts based on experimental, not only extrapolative data. Rosenblatt's (2003) three characteristics of mammalian parenting – rapid formation of attachment, behavioral synchrony, and mother-offspring attachment as basis of social organization – are used to guide discussion on mammalian-general versus human-specific attributes of parental care. These highlight specific components of attachment in rodents, primates, and humans that chart the evolution from promiscuous, nest-bound, olfactory-based bonds to exclusive, multi-sensory, and representation-based attachments. Following, three continua are outlined in parental behavior, hormones, and brain, each detailing the evolution from rodents to humans. Parental behavior is defined as a process of trophallaxis – the reciprocal multisensory exchange that supports approach orientation and enables collaboration in social species – and includes human-specific features that enable behavioral synchrony independent of tactile contact. The oxytocin system incorporates conserved and human-specific components and is marked by pulsatile activity and dendritic release that reorganize neural networks on the basis of species-specific attachment experiences. Finally, the subcortical limbic circuit underpinning mammalian mothering extends in humans to include multiple cortical networks implicated in empathy, mentalizing, and emotion regulation that enable flexible, goal-directed caregiving. I conclude by presenting a philosophical continuum from Hobbes to Lorenz, which illustrates how research on the neurobiology of attachment can put in the forefront the social-collaborative elements in human nature and afford a new perspective on the mind-brain polarity.

Friday, October 09, 2015
Publication date: Available online 5 October 2015
Source:Hormones and Behavior

Author(s): Sarah A. Johnson, Angela B. Javurek, Michele S. Painter, Mark R. Ellersieck, Thomas H. Welsh, Luísa Camacho, Sherry M. Lewis, Michelle M. Vanlandingham, Sherry A. Ferguson, Cheryl S. Rosenfeld

Bisphenol A (BPA) is a ubiquitous industrial chemical used in the production of a wide variety of items. Previous studies suggest BPA exposure may result in neuro-disruptive effects; however, data are inconsistent across animal and human studies. As part of the Consortium Linking Academic and Regulatory Insights on BPA Toxicity (CLARITY-BPA), we sought to determine whether female and male rats developmentally exposed to BPA demonstrated later spatial navigational learning and memory deficits. Pregnant NCTR Sprague–Dawley rats were orally dosed from gestational day 6 to parturition, and offspring were directly orally dosed until weaning (postnatal day 21). Treatment groups included a vehicle control, three BPA doses (2.5μg/kg/day—[2.5], 25μg/kg/day—[25], and 2500μg/kg/day—[2500]) and a 0.5μg/kg/day ethinyl estradiol (EE)-reference estrogen dose. At adulthood, 1/sex/litter was tested for seven days in the Barnes maze. The 2500 BPA group sniffed more incorrect holes on day 7 than those in the control, 2.5 BPA, and EE groups. The 2500 BPA females were less likely than control females to locate the escape box in the allotted time (p value=0.04). Although 2.5 BPA females exhibited a prolonged latency, the effect did not reach significance (p value=0.06), whereas 2.5 BPA males showed improved latency compared to control males (p value=0.04), although the significance of this result is uncertain. No differences in serum testosterone concentration were detected in any male or female treatment groups. Current findings suggest developmental exposure of rats to BPA may disrupt aspects of spatial navigational learning and memory.

Friday, October 09, 2015
Publication date: Available online 3 October 2015
Source:Hormones and Behavior

Author(s): Deepika Pandey, Sugato Banerjee, Mahua Basu, Nibha Mishra

Tamoxifen (TMX) is a selective estrogen receptor modulator (SERM) used in the treatment of breast cancer. Earlier studies show its neuroprotection via regulating apoptosis, microglial functions, and synaptic plasticity. TMX also showed memory enhancement in ovariectomized mice, and protection from amyloid induced damage in hippocampal cell line. These reports encouraged us to explore the role of TMX in relevance to Alzheimer's disease (AD). We report here, the effect of TMX treatment a) on memory, and b) levels of neurotransmitters (acetylcholine (ACh) and dopamine (DA)) in breeding-retired-female mice injected with beta amyloid1-42 (Aβ1-42). Mice were treated with TMX (10mg/kg, i.p.) for 15days. In Morris water maze test, the TMX treated mice escape latency decreased during training trials. They also spent longer time in the platform quadrant on probe trial, compared to controls. In Passive avoidance test, TMX treated mice avoided stepping on the shock chamber. This suggests that TMX protects memory from Aβ induced toxicity. In frontal cortex, ACh was moderately increased, with TMX treatment. In striatum, dopamine was significantly increased, 3,4-Dihydroxyphenylacetic acid (DOPAC) level and DOPAC/DA ratio was decreased post TMX treatment. Therefore, TMX enhances spatial and contextual memory by reducing dopamine metabolism and increasing ACh level in Aβ1-42 injected-breeding-retired-female mice.

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