This research was supported by Grant AA 05523 from the National Institute on Alcohol Abuse and Alcoholism (to J.RW).
Effects of Alcohol and Nicotine on Developing Olfactory Bulb: Loss of Mitral Cells and Alterations in Neurotransmitter Levels
Article first published online: 30 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 23, Issue 1, pages 18–25, January 1999
How to Cite
Chen, W.-J. A., Parnell, S. E. and West, J. R. (1999), Effects of Alcohol and Nicotine on Developing Olfactory Bulb: Loss of Mitral Cells and Alterations in Neurotransmitter Levels. Alcoholism: Clinical and Experimental Research, 23: 18–25. doi: 10.1111/j.1530-0277.1999.tb04019.x
The authors thank Dr. Thomas H. Champney for technical guidance in HPLC analysis and Mr. Scott G. Anderson for assistance in stereological cell counting. The HPLC equipment is part of the Neuroendocrine/Neurochemical Core Facility at the Department of Human Anatomy and Medical Neurobiology, Texas A&M University Health Science Center.
- Issue published online: 30 MAY 2006
- Article first published online: 30 MAY 2006
- Received for publication December 15, 1997; accepted October 6, 1998
- Mitral Cells;
- Developing Rats
Previous research from our laboratory has shown that [ethanol (EtOH)] exposure during the brain growth spurt is detrimental to olfactory bulb development. This study extends those findings by examining the effects of EtOH, nicotine (NIC), and the combination of these drugs (EtOH/NIC) on olfactory bulb mitral cell numbers, as well as on various major neurotransmitter levels in neonatal rats. An artificial rearing paradigm was used in the present studies. These artificially reared pups were given 4 g/kg/day of EtOH and/or 6 mg/kg/ day of NIC on postnatal day (PD) 4 to PD 9, except in the case of the acute neurochemistry study, in which the pups received treatment on PD 9 only. An artificially reared gastrostomy control group (GC) and a suckle control group were included. The mean total numbers of mitral cells in the EtOH and NIC groups were significantly reduced from that of the GC, as well as the volume of the left main olfactory bulb. There was no difference among any of the groups in mitral cell density. As for neurochemistry data, there was no difference in neurotransmitter levels among any of the groups in the repeat exposure regimen. There were, however, changes after the acute exposure (exposure on PD 9 only). Both serotonin and GABA levels were significantly increased only after NIC exposure. However, norepinephrine levels were significantly decreased after acute exposure in all three drug treatment groups, compared with that of the control group. Except for the GC control group, dopamine levels were not detected consistently after acute exposure to EtOH, NIC, or EtOH/NIC. Collectively, these findings demonstrate that exposure to EtOH or NIC individually during the brain growth spurt results in developmental deficits in the olfactory bulb, suggesting that both EtOH and NIC are neuroteratogens. Furthermore, this study demonstrated the capability of NIC to antagonize (protect) EtOH-induced mitral cell loss in the developing olfactory bulb.