Effects of Prenatal Exposure to Ethanol on the Number of Axons in the Pyramidal Tract of the Rat

Abstract

We examined the effect of gestational ethanol exposure on the number of axons in the caudal pyramidal tract. Between gestational day (G) 6 and G21, inclusive, pregnant rats were fed a liquid ethanol-containing diet (Et), an isocaloric liquid control diet (Ct), or a diet of chow and water (Ch). On postnatal day 30, the offspring of these rats were killed and their caudal medullas were processed for electron microscopy. The overall size of the pyramidal tract and the space occupied by the axons was smaller in the Et-treated rats than in the Ct-treated rats. The myelinated axons were smaller and the myelin was thinner in the Et-treated rats than in the Ct-treated rats. These decreases produced an ethanol-induced increase in the density of axons in the pyramidal tract. In particular, the density of myelinated axons (but not nonmyelinated axons) was greater in Et-treated rats. The net result was that the estimated number of axons in the pyramidal tracts of the Et-treated rats was not significantly different than the number in the Ch- and Ct-treated rats. The present data demonstrate that ethanol does not affect the absolute number of axons in the pyramidal tract. As a result of the ethanol-induced microencephaly, however, the data translate into a relative increase in the number of pyramidal tract axons. This relative increase matches the ethanol-induced increase in the density of corticospinal projection neurons that may result from the retention of a developmentally exuberant projection.

In Utero Ethanol Exposure Causes Mitochondrial Dysfunction, Which Can Result in Apoptotic Cell Death in Fetal Brain: A Potential Role for 4‐Hydroxynonenal

“…*p Ͻ 0.05 compared with control values with no HNE exposure. cell dendrites, causes abnormal projections of granule cell axons, and alters proliferation of precursor cells in the cerebral cortex (Barnes and Walker, 1981;Miller, 1995Miller, , 1996Miller and Al-Rabiai, 1994). In vivo studies with animal models have shown that short-term ethanol intake during the brain growth spurt interferes with normal brain growth Napper and West, 1995) and permanently reduces the number of neurons in various brain regions.…”

Number of axons in the corpus callosum of the mature Macaca nemestrina: Increases caused by prenatal exposure to ethanol

“…Prenatal exposure to ethanol induces an increase (1) in the number of callosal projection neurons in the somatosensory cortex of the rat (Miller, 1997), (2) in the number of corticospinal projection neurons in somatosensory and motor cortices (Miller, 1987), and (3) in the number of their descending axons in the lower pyramidal tract (Miller and Al-Rabiai, 1994). Recent evidence shows that ethanol treatment promotes axonal growth by cultured hippocampal neurons (Clamp and Lindsley, 1998).…”

“…The connectivity of cortical neurons is also affected by ethanol exposure. The scope of dendritic trees (Shapiro et al, 1984;Pentney et al, 1984;Fabregues et al, 1985;, the morphology of dendritic spines (Stoltenburg-Didinger and Spohr, 1983;, the density of cortical efferents (Miller and Al-Rabiai, 1994), and cortical synaptology (Al-Rabiai and Miller, 1989) are altered.…”

Astrocytes protect neurons from ethanol‐induced oxidative stress and apoptotic death

“…Several in vivo and in vitro studies have shown multiple adverse effects of ethanol on the developing brain's constituent cells in these areas (West et al, 1984;West, 1990, 1991;Miller and Kuhn, 1995;Miller, 1996a,b), including a loss of both neurons and glia (Miller and Potempa, 1990). Prenatal ethanol exposure decreased hippocampal pyramidal cell populations, decreased spines on pyramidal cell dendrites, caused abnormal projections of granule cell axons, and altered proliferation of precursor cells in the cerebral cortex (Barnes and Walker, 1981;Miller and al-Rabiai, 1994;Kuhn, 1995, Miller, 1996a). Clearly, the timing and degree of ethanol exposure are critical in determining regional differences in cell loss (Maier et al, 1999) as well as those within specific populations of neurons (Ikonomidou et al, 2000).…”