Document Detail


Chronic nicotine selectively enhances alpha4beta2* nicotinic acetylcholine receptors in the nigrostriatal dopamine pathway.
MedLine Citation:
PMID:  19812319     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
These electrophysiological experiments, in slices and intact animals, study the effects of in vivo chronic exposure to nicotine on functional alpha4beta2* nAChRs in the nigrostriatal dopaminergic (DA) pathway. Recordings were made in wild-type and alpha4 nicotinic acetylcholine receptor (nAChR) subunit knock-out mice. Chronic nicotine enhanced methyllycaconitine citrate hydrate-resistant, dihydro-beta-erythroidine hydrobromide-sensitive nicotinic currents elicited by 3-1000 mum ACh in GABAergic neurons of the substantia nigra pars reticulata (SNr), but not in DA neurons of the substantia nigra pars compacta (SNc). This enhancement leads to higher firing rates of SNr GABAergic neurons and consequently to increased GABAergic inhibition of the SNc DA neurons. In the dorsal striatum, functional alpha4* nAChRs were not found on the neuronal somata; however, nicotine acts via alpha4beta2* nAChRs in the DA terminals to modulate glutamate release onto the medium spiny neurons. Chronic nicotine also increased the number and/or function of these alpha4beta2* nAChRs. These data suggest that in nigrostriatal DA pathway, chronic nicotine enhancement of alpha4beta2* nAChRs displays selectivity in cell type and in nAChR subtype as well as in cellular compartment. These selective events augment inhibition of SNc DA neurons by SNr GABAergic neurons and also temper the release of glutamate in the dorsal striatum. The effects may reduce the risk of excitotoxicity in SNc DA neurons and may also counteract the increased effectiveness of corticostriatal glutamatergic inputs during degeneration of the DA system. These processes may contribute to the inverse correlation between tobacco use and Parkinson's disease.
Authors:
Cheng Xiao; Raad Nashmi; Sheri McKinney; Haijiang Cai; J Michael McIntosh; Henry A Lester
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  29     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-08     Completed Date:  2009-11-10     Revised Date:  2014-09-13    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  12428-39     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Dopamine / secretion
Drug Administration Schedule
Evoked Potentials
GABA Agents / administration & dosage
Glutamic Acid / secretion
Mice
Mice, Inbred C57BL
Neurons / drug effects
Nicotine / administration & dosage*
Patch-Clamp Techniques
Receptors, Nicotinic / drug effects*
Substantia Nigra / cytology,  drug effects*,  metabolism*
Up-Regulation
Grant Support
ID/Acronym/Agency:
AG033954/AG/NIA NIH HHS; DA17279/DA/NIDA NIH HHS; MH53631/MH/NIMH NIH HHS; R01 AG033954/AG/NIA NIH HHS; R01 AG033954-01A1/AG/NIA NIH HHS; R01 DA017279/DA/NIDA NIH HHS; R01 DA017279-01A1/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/GABA Agents; 0/Receptors, Nicotinic; 0/nicotinic receptor alpha4beta2; 3KX376GY7L/Glutamic Acid; 54-11-5/Nicotine; VTD58H1Z2X/Dopamine
Comments/Corrections

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