Background: Ethanol exposure is a consistent and reliable producer of neuro
nal toxicity, especially during periods of enhanced neuronal vulnerability.
For rat cerebellar Purkinje cells, the postnatal period during the time of
the brain growth spurt exhibits the greatest vulnerability to ethanol. Ana
lyses of studies completed over more than 20 years provides sufficient deta
il to allow for the determination of the specific vulnerable window for eth
anol-induced loss of Purkinje cells.
Methods: Data reporting Purkinje cell counts after ethanol exposure were co
mpiled from 18 studies published since 1975. We conducted linear regression
analysis between peak blood ethanol concentration (BEC) and percent reduct
ion in Purkinje cells for the following individual postnatal (PN) days: PN4
, PN5, PN6, PN7, and PN8 or beyond (+). The slope of the regression and the
coefficients of determination (IZ) were the primary factors of interest. A
nalysis of variance of the regressions was conducted to identify whether th
e slopes were significantly different from zero, or from each other.
Results: Exposures involving the PN4-6 period demonstrated the greatest sig
nificance in the relationship between BEC and reduction of Purkinje cell nu
mber. No significant differences were identified between different ethanol
exposure techniques or for different Purkinje cell counting techniques. In
addition, the initial day of exposure and the duration of exposure were not
identified as critical variables.
Conclusions: The literature database, developed over the past 20 years is c
lear in its direction that studies designed to identify the ethanol-specifi
c mechanisms of Purkinje cell death are best designed to involve ethanol ex
posure during the vulnerable window of postnatal days 4-6.