| Prenatal ethanol exposure alters the postnatal development of the spontaneous electrical activity of dopamine neurons in the ventral tegmental area. | |
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MedLine Citation:
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PMID: 15207341 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Prenatal ethanol exposure causes a persistent reduction in the spontaneous electrical activity of dopamine (DA) neurons in the ventral tegmental area (VTA) in adult animals. Because DA neuron activity matures into adult pattern during postnatal development, it is possible that reduced activity in VTA DA neurons after prenatal ethanol exposure is caused by impaired postnatal development. This possibility was investigated in the present study using the in vivo extracellular single-unit recording and brain stimulation techniques. The results show an age-dependent decrease in the number of spontaneously active VTA DA neurons from 2 to 4 weeks of age in both the control and prenatal ethanol-exposed animals. In ethanol-exposed animals, the age-dependent decrease was more prominent after 3 weeks of age, resulting in lower numbers of spontaneously active VTA DA neurons in 4-week-old and adult animals. In both the control and ethanol-exposed animals, there were age-dependent increases in the firing rates and burst firing activity of VTA DA neurons after 2 weeks of age. Ethanol exposure led to slightly lower firing rates in 4-week-old and adult animals and did not impact the burst firing pattern in any age groups. There were no changes in axon conduction velocity and antidromic spike characteristics of VTA DA neurons. These results indicate that reduced activity of VTA DA neurons during adulthood after prenatal ethanol exposure does not begin prenatally. Instead, it is a result of impaired postnatal development manifested only when animals reach 4 weeks of age. These results suggest that early intervention may be an effective treatment strategy for attention deficit/hyperactivity disorder, a behavioral dysfunction related to the abnormalities of DA systems and often observed in children with fetal alcohol spectrum disorder. |
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Authors:
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K Choong; R Shen |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Neuroscience Volume: 126 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 2004 |
Date Detail:
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Created Date: 2004-06-21 Completed Date: 2004-10-08 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: United States |
Other Details:
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Languages: eng Pagination: 1083-91 Citation Subset: IM |
Copyright Information:
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Copyright 2004 IBRO |
Affiliation:
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Research Institute on Addictions, State University of New York at Buffalo, 1021 Main Street, Buffalo, NY 14203, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials
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drug effects,
physiology Age Factors Analysis of Variance Animals Central Nervous System Depressants / toxicity* Dopamine / metabolism* Electrophysiology / methods Ethanol / toxicity* Female Male Neurons / drug effects*, metabolism Nucleus Accumbens / drug effects, growth & development Pregnancy Prenatal Exposure Delayed Effects* Rats Rats, Sprague-Dawley Ventral Tegmental Area / cytology*, growth & development |
| Grant Support | |
ID/Acronym/Agency:
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AA12435/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Central Nervous System Depressants; 64-17-5/Ethanol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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