Abstract

Alcohol is known to cause selective neuronal degeneration. In the hippocampus, pyramidal neurons are selectively vulnerable to alcohol, especially during withdrawal. In addition, in males, alcohol acutely decreases circulating testosterone(T) levels. Recent evidence suggests that T can be neuroprotective. Therefore, alcohol-related reduction in circulating T may contribute to the pyramidal cell's vulnerability during alcohol withdrawal. The goal of this project is to assess the contribution of lowered testosterone levels, which accompany alcohol consumption, to alcohol withdrawal-related neurotoxicity.
Specific aim 1 will address the ability of DHT (a highly active form of T) to attenuate toxicity to cultured hippocampal pyramidal cells following alcohol withdrawal.
Specific aim 2 will address the same question in vivo.
Specific aim 3 will address the specific molecular mechanism by which DHT is attenuating neurotoxicity following alcohol withdrawal. The information gained from this research will be-valuable in understanding the mechanisms by which alcohol is causing specific neuronal degeneration.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31AA005461-02
Application #
2545099
Study Section
Biochemistry, Physiology and Medicine Subcommittee (ALCB)
Project Start
1998-02-28
Project End
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
2
Fiscal Year
1997
Total Cost
Indirect Cost

  Institution

Name
Loyola University Chicago
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
791277940
City
Maywood
State
IL
Country
United States
Zip Code
60153