Modulation by nicotine on the genes expression of brain potassium, sodium and calcium channels / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 359-362, 2004.
Article
in Chinese
| WPRIM
| ID: wpr-330095
ABSTRACT
<p><b>AIM</b>Using GeneChip to analyze the changes in genes expression of brain potassium, sodium and calcium channels after chronic treatment with nicotine.</p><p><b>METHODS</b>Animals were treated with nicotine at the doses of 2.4 mg/kg sc. twice a day for 14 days. RNA was extracted from the whole brain samples and converted to double-stranded cDNA and then to biotinylated cRNA. The biotinylated cRNA was fragmented, and hybridized to GeneChip (Affymetrix Rat Neurobiology U34). The chips were scanned with a probe array scanner, and the data were analyzed with the Affymetrix Microarray Analysis Suite (MAS). The GeneChip data were confirmed u sing RT-PCR.</p><p><b>RESULTS</b>After treatment with chronic nicotine, transcripts of potassium, sodium and calcium channels showed altered expression. K+ channel outward rectifier K+ channel and Ca2(+)-activated K+ channel were down-regulated, other voltage-dependent K+ channel including Kv2.3r were up-regulated. Voltage-dependent Na+ channel beta2 subunit was increased, alpha subunit and beta1 subunit were decreased. Beta3 subunit of Ca2+ channel was up-regulated.</p><p><b>CONCLUSION</b>Chronic exposure to nicotine not only desensitized nicotinic receptors, but also effected genes expression, of important ion channels, such as sodium channels, potassium channels and calcium channels.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Brain
/
Calcium Channels
/
Potassium Channels
/
Sodium Channels
/
Gene Expression
/
Rats, Sprague-Dawley
/
Metabolism
/
Nicotine
Limits:
Animals
Language:
Chinese
Journal:
Chinese Journal of Applied Physiology
Year:
2004
Type:
Article
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