[Abstract Title]. - Society for Neuroscience

Disclosures: Q. Yan, None; S. Yan, None.
Poster
257. Alcohol Intake and Preference
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 257.5/Z22
Topic: C.16.a. Alcohol
Support: William Evans Visiting Fellowship Fund of the University of Otago
University of Delaware Funds
Title: Neonatal one-day binge-like ethanol exposure results in the loss of neurons in the
CA1/CA3 subfields of rat hippocampus
Authors: C. E. SCHNELL 1 , R. M. A. NAPPER 2 , *A. Y. KLINTSOVA 1 ;
1 Psychology, Univ. Delaware, Newark, DE; 2 Univ. of Otago, Dunedin, New Zealand
Abstract: A single binge exposure to ethanol via intragastric intubation on postnatal day four
(PD4) results in significant apoptotic cell death in the hippocampus of the rat 10 hours after
ethanol delivery. This study reports the long-term effects of a binge-like ethanol exposure on
PD4 on the number of neurons in CA1 and CA3 subfields of the hippocampus. On PD4, Long
Evans male and female rat pups were divided between three treatment conditions: alcoholexposed
(AE), pups received intubations of ethanol in milk substitute (4.5g/kg of ethanol in two
feeds two hours apart); sham-intubated (SI), pups were intubated as for AE but no fluid was
delivered; and suckle control (SC), pups remained with the dam. On PD50, animals were
anesthetized and transcardially perfused with fixative. Using unbiased stereology (estimation of
total cell number using optical fractionator on a systematic random set of every 10 th horizontal
section through the entire hippocampus) the total neuron number in CA1 and CA3 hippocampal
regions was estimated. There was a significant effect of postnatal treatment on the total number
of CA1 neurons (F=8.48; p=0.003). Post-hoc comparison revealed that AE animals had lower
number of neurons in the CA1 subfield of hippocampus than SC (p=0.002) and SI rats (p=0.05).
Importantly, data also indicated a negative correlation between the peak blood alcohol
concentration, measured on PD4 after the second AE intubation, and the total number of CA1
neurons on PD50 (r = - .45). Preliminary data showed a trend toward a deficit in CA3 neurons as
a result of postnatal ethanol exposure (F=2.95, p=0.088). This data demonstrates that even a
single binge ethanol exposure during the brain growth spurt can result in permanent brain
damage.