Southern California Conferences for Undergraduate Research

Southern California Conferences for Undergraduate Research

The Effects of Forced Exercise in a Model of Fetal Alcohol Syndrome

Authors:

Thuy Hua, Kerry Thompson

Mentor:

Kerry Thompson, Associated Professor of Molecular Biology and Neurology, Occidental College

Fetal Alcohol Syndrome (FAS) is a disorder caused by alcohol exposure in utero that can lead to neurological, behavioral and physical birth defects that follow the infant into adulthood. The term Fetal Alcohol Spectrum Disorder (FASD) has recently been adopted to describe a wider distribution of effects caused by alcohol exposure than previously appreciated. The well-established anatomical signs of FAS include short palpebral fissures, a flat mid-face, and a smooth philtrum. Severe cases will include neuronal losses that lead to microcephaly. Less sever/selective neuronal losses in FASD are thought to contribute to attention deficit, hyperactivity, social skills deficits, and motor dysfunction. Research in this area is important because it is estimated that nearly 8-10,000 infants are diagnosed with FAS per year in the United States. Similar negative effects can be produced by exposure to a wide range of sedative-hypnotic drugs such as sleeping pills, anesthesia, and anticonvulsant. Exposure of the developing nervous system to these drugs through the placenta is especially destructive in the third trimester when neurons are undergoing synaptogenesis. Recent studies have demonstrated that immature neurons exposed to sedative-hypnotic drugs at this critical period of development results in premature cell death. To model FAS, newborn Sprague-Dawley rats were treated with diazepam (30 mg/kg) or saline at post-natal day 10. At post-natal day 21 animals from each injection group were given either seven days of forced exercise or they were similarly handled but without exercise. The animals were subsequently tested using a battery of behavioral assays to determine if forced exercise could alleviate the expected deficits. Our data support the concept that exercise can attenuate diazepam-induced deficits in juvenile rats. The rats in the forced exercise group performed as well as the saline-induced group despite severe damage to the thalamus, hippocampus and piriform cortex caused by early diazepam exposure.


Presented by:

Thuy Hua, Kerry Thompson

Date:

Saturday, November 17, 2012

Time:

8:45 AM — 9:00 AM

Room:

Bell Tower 1726

Presentation Type:

Oral Presentation

Discipline:

Biology