title: Interactive effect of alcohol and nicotine on developing cerebellum: an investigation of the temporal pattern of alcohol and nicotine administration.
abstract: BACKGROUND
  Among individuals who use alcohol and tobacco products, pregnant women represent a unique subpopulation that generates a greater concern because of the toxic effects of alcohol and nicotine (from cigarettes and tobacco products) on the health of both the pregnant woman and her fetus. Therefore, it is imperative to understand the interactive effects of these two substances on the fetus. Previously, we found that concurrent exposure to alcohol and nicotine did not result in the loss of greater numbers of Purkinje cells compared with each drug treatment alone, possibly as a result of a nicotine-mediated decline in peak blood alcohol concentration (BAC). The present study tested the validity of this hypothesis.
  
  
  METHODS
  On postnatal day (PD) 4, Sprague-Dawley rat pups were assigned to five groups, GC (no alcohol [ALC], no nicotine [NIC]), ALC (4 g/kg/day), NIC (6 mg/kg/day), ALC/NIC (ALC and NIC given concurrently), or ALC-NIC (NIC administered 6 hr after ALC exposure). These rat pups were reared in an artificial-rearing apparatus from PDs 4 to 9, and the cerebellar tissues were obtained on PD 10. The total number of cerebellar Purkinje cells in the vermis was estimated using stereological methods.
  
  
  RESULTS
  The results showed that alcohol significantly reduced Purkinje cell numbers. The coexposure of alcohol and nicotine did not lead to further reduction in Purkinje cell number regardless of administration method, concurrent or sequential. However, alcohol and nicotine administered concurrently but not sequentially significantly lowered the BAC.
  
  
  CONCLUSIONS
  These findings suggest that the lack of increased Purkinje cell loss after the coexposure of alcohol and nicotine is independent of nicotine's ability to lower the BAC. An alternative hypothesis might be that alcohol and nicotine target the same subpopulation of Purkinje cells; therefore, no additional Purkinje cells were lost from the coexposure of these two drugs.
authors.affiliation: Department of Human Anatomy & Medical Neurobiology, College of Medicine, The Texas A&M University System Health Science Center, College Station, TX 77843, USA. wjchen@tamu.edu
authors.forename: Wei-Jung A
authors.initials: WJ
authors.lastname: Chen
authors.forename: Lindsey K
authors.initials: LK
authors.lastname: Harle
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects / Q000254:growth & development*; D004347:Drug Interactions; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D009929:Organ Size / Q000187:drug effects; D011689:Purkinje Cells / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D002492:Central Nervous System Depressants; D018722:Nicotinic Agonists; D000431:Ethanol; D009538:Nicotine