News & Events
Special Issue of Physiology & Behavior highlights developmental effects of alcohol.
A Closer Look at
Dave Werner's Research
DEARC Call for Pilot Proposals
Letter of Intent due: January 15, 2016
Proposals due: February 15, 2016
Research Society on Alcoholism
39th Annual Meeting
June 25 – 29, 2016
New Orleans, Louisiana
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- Pilot Project 1: Maternal Care Influence in Offspring Ethanol Sensitivity
PI: Nicole M. Cameron (firstname.lastname@example.org))
- Pilot Project 2: Ethanol withdrawal-induced alterations in coping strategy across ontogeny
PI: Tamara Fitzwater (email@example.com)
- Pilot Project 3: : Impact of Prenatal Ethanol on the Anxiety Circuit
PI: Marvin Diaz (firstname.lastname@example.org)
Pilot Project 1: Maternal Care Influence in Offspring Ethanol Sensitivity
This study aims to investigate maternal care programming of alcohol use in the rat. Specifically, we will study the effects of natural variations in maternal care on sedative/hypnotic effects of alcohol at different doses at postnatal days 30, 50 and 90 in male and female offspring. We will also investigate changes in the γ-aminobutyric acid (GABA) subunit expression in brain regions associated with alcohol sensitivity, such as hippocampus, medial prefrontal cortex and nucleus accubens. Lastly we will use next-generation sequencing to compare the effects of maternal care received on DNA methylation of the promoter region of the GABAA receptor subunits shown to be associated with the variation of sensitivity in our model. This pilot is expected to clarify the role of early life on alcohol sensitivity. It will also improve our understanding of epigenetic programming of the GABAergic system.
Pilot Project 2: Ethanol withdrawal-induced alterations in coping strategy across ontogeny
Early developmental exposure to alcohol is a risk factor that has been shown to be important to the etiology of alcoholism. Identification of contributors to excessive alcohol use during adolescence is therefore of critical importance, with previous work using rodent models having demonstrated that an adolescent-associated insensitivity to ethanol may be a permissive factor that permits adolescents to consume excessive quantities of alcohol. The hypothesis of my pilot proposal is that withdrawal from ethanol will result in a disruption of coping behavior among adult rats, and that these ethanol withdrawal-related alterations will be attenuated during adolescence, thus also contributing to alcohol abuse during adolescence. To test this hypothesis, behavioral assays (e.g., forced-swim and defensive probe-burying) will be used to characterize ontogenetic alterations in coping behavior during ethanol withdrawal following either acute or chronic exposure. Additionally, patterns of neural activation in response to these stressors, ethanol, or stress plus ethanol exposure will be examined across development. Findings from these studies will provide important information for more targeted studies using regional inactivation, as well as site-specific microinjections, to identify neural regions critical for age-related alterations in ethanol withdrawal and coping behavior.
Pilot Project 3: Impact of Prenatal Ethanol on the Anxiety Circuit
One of the most common disabilities resulting from prenatal alcohol exposure (PAE) is anxiety, which is evident from infancy through adulthood. However, the extent of anxiety-like behaviors and the neurobiological adaptations that arise from PAE are not known. This pilot project will focus on adolescence, a high-risk/stress developmental period, following PAE on gestational day 12 (a model known to induce social anxiety that is being used in Main Project 5). Specifically, Aim 1 will assess a variety of generalized anxiety-like behaviors using a battery of anxiety assays – elevated plus maze, light/dark box, open field, and novelty-induced hypophagia – in both males and females. Aim 2 will investigate the GABAergic system within the medial subnucleus of the central amygdala (CeM), a key structure involved in the expression of anxiety-like behaviors. Specifically, we will utilize patch-clamp electrophysiology to measure alterations in phasic and tonic GABAA-mediated currents, with an emphasis on α1-containing GABAA receptors. To corroborate functional changes, immunohistochemical techniques will be used to visualize changes in α1 expression within the CeM. These findings will give us insight into the neurobiological and neurophysiological mechanisms in a key brain structure that may underlie anxiety-like responses resulting from fetal alcohol exposure.