Alcohol and nutritional control treatments during neurogenesis in rat brain reduce total neuron number in locus coeruleus, but not in cerebellum or inferior olive.
Although a significant amount of progress has been made during the past two decades in determining the effects of alcohol on brain development, there is still a gap in the literature in terms of when the neurons in the brain are more or less vulnerable to the deleterious effects of alcohol. Using a rat model system, we examined the effect of alcohol on the development of three brain regions after exposure to alcohol only during the period of neurogenesis of each specific region. Our working hypothesis was that all three regions would be equally vulnerable to alcohol-induced reductions in neuron number after exposure during neurogenesis. The Purkinje cells of the cerebellum and the neurons of the locus coeruleus and inferior olive were chosen for examination because of their functional relation to the neuroanatomical circuit for motor coordination and gait, which is disrupted in children exposed to alcohol during gestation. Groups of timed-pregnant Sprague-Dawley rats were administered alcohol or nutritional control substitute daily by gavage during the period of neurogenesis for each region, or they were given no treatments. On postnatal day 10, neuron counts were derived from the three regions of the offspring brains by using stereological cell-counting techniques. The number of neurons in the locus coeruleus was reduced in both the alcohol- and nutritional control-treated groups relative to findings for the normal control group. There was no similar reduction in neuron number in the Purkinje cells of the cerebellum, nor in the neurons of the inferior olive, among the treatment groups. These results demonstrate that the period of neurogenesis is not a uniformly vulnerable period for the three brain regions tested, and the findings support the suggestion of a possible avenue for examining the underlying explanation for why some regions are more vulnerable than other regions during various phases of neuronal development.
Maier
Susan E
SE
Human Anatomy and Medical Neurobiology, Room 228 Reynolds Medical Building, College of Medicine, 1114 TAMU, The Texas A&M University System Health Science Center, College Station, TX 77843-1114, USA. smaier@medicine.tamu.edu
West
James R
JR
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001835:Body Weight / Q000502:physiology; D001921:Brain / Q000166:cytology / Q000187:drug effects / Q000196:embryology*; D001923:Brain Chemistry / Q000187:drug effects; D002452:Cell Count; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects / Q000196:embryology*; D004326:Drinking / Q000502:physiology; D004435:Eating / Q000502:physiology; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D005260:Female; D066298:In Vitro Techniques; D008098:Litter Size / Q000187:drug effects; D008125:Locus Coeruleus / Q000166:cytology / Q000187:drug effects / Q000196:embryology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D009847:Olivary Nucleus / Q000166:cytology / Q000187:drug effects / Q000196:embryology*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D015430:Weight Gain / Q000187:drug effects
D002492:Central Nervous System Depressants; D000431:Ethanol; D009638:Norepinephrine