Premium
Acute and Long‐Term P urkinje Cell Loss Following a Single Ethanol Binge During the Early Third Trimester Equivalent in the Rat
Author(s) -
Idrus Nirelia M.,
Napper Ruth M. A.
Publication year - 2012
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2012.01743.x
Subject(s) - binge drinking , apoptosis , medicine , endocrinology , cerebellum , programmed cell death , ethanol , physiology , alcohol , biology , biochemistry , alcohol consumption
Background In the rat, binge‐like ethanol ( EtOH ) exposure during the early neonatal period (a developmental period equivalent to the human third trimester) can result in a permanent deficit of cerebellar P urkinje cells ( P cells). However, the consequences of a moderate binge alcohol exposure on a single day during this postnatal period have not been established. This is an issue of importance as many pregnant women binge drink periodically at social drinking levels. This study aimed to identify both the acute and long‐term effects of exposure to a single alcohol binge that achieved a mean peak blood EtOH concentration of approximately 250 mg/dl during early postnatal life using a rat model of fetal alcohol spectrum disorders. Methods Acute apoptotic P cell death 10 hours after a moderate dose binge EtOH exposure from postnatal days ( PD s) 0 to 10 was assessed using active caspase‐3 immunolabeling. Acute P cell apoptosis was quantified in cerebellar vermal lobules I–X using the physical disector method. Long‐term effects were assessed at PD 60 using stereological methods to determine total P cell numbers in the vermis, lobule III, and lobule IX, following a moderate dose binge EtOH exposure at PD s 0, 2, or 4. Results Acute apoptosis was induced by EtOH on PDs 1 to 8 in a time and lobular‐dependent manner. For EtOH exposure on PD 2, significant long‐term P cell loss occurred in lobule III . EtOH exposure on PD 4 resulted in significant long‐term P cell loss throughout the entire vermis. Conclusions These results indicate that a single, early EtOH episode of moderate dose can create significant and permanent Pcell loss in the developing cerebellum.