Modulation by nicotine on the genes expression of brain potassium, sodium and calcium channels.
- Author:
Xiu-Lan SUN
1
;
Yue LIU
;
Gang HU
;
Hai WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain; drug effects; metabolism; Calcium Channels; drug effects; metabolism; Gene Expression; Male; Nicotine; pharmacology; Potassium Channels; drug effects; metabolism; Rats; Rats, Sprague-Dawley; Sodium Channels; drug effects; metabolism
- From: Chinese Journal of Applied Physiology 2004;20(4):359-362
- CountryChina
- Language:Chinese
-
Abstract:
AIMUsing GeneChip to analyze the changes in genes expression of brain potassium, sodium and calcium channels after chronic treatment with nicotine.
METHODSAnimals 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.
RESULTSAfter 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.
CONCLUSIONChronic 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.
