Effect of pre- or postnatal exposure to ethanol on the total number of neurons in the principal sensory nucleus of the trigeminal nerve: cell proliferation and neuronal death.
Early exposure to ethanol reduces the number of neurons in many CNS structures in vivo. The present study determined whether such reductions are caused by the death of neurons. Three groups of ethanol-treated rats were prepared: those exposed to ethanol from gestational day (G) 11 to G19 (during the period of neuronal generation and migration), from postnatal day (P) 4 to P12 (during the period of synaptogenesis), or from P31 to P39 [after the mature structure and function of neurons in the principal sensory nucleus (PSN) of the trigeminal nerve was established]. During these times, pregnant dams or pups were fed a liquid ethanol-containing diet that produced peak blood ethanol concentrations of 137-157 mg/dl. The number of PSN neurons in mature rats exposed to ethanol pre- or postnatally was determined using stereological procedures. The number of PSN neurons was also calculated for rats pair-fed an isocaloric liquid control diet or fed chow and water and libitum. The volume of the PSN was not affected by pre- or postnatal ethanol exposure. The number of PSN neurons, however, was significantly affected by ethanol exposure in a time-dependent manner. Prenatal exposure lead to a 27.1% decrease in neuronal number. Early postnatal exposure led to a smaller decrease (-15.1%), and late postnatal exposure had no affect on the number of PSN neurons. These data show not only that ethanol directly depresses the proliferation of neuronal precursors, but also that ethanol causes the death of neurons during the period of synaptogenesis.