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Effects of Short‐ and Long‐Term Nicotine Treatment on Intracellular Calcium and Tyrosine Hydroxylase Gene Expression
Author(s) -
SABBAN ESTHER L.,
GUEORGUIEV VOLODIA D.
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04430.x
Subject(s) - tyrosine hydroxylase , nicotine , tyrosine 3 monooxygenase , chemistry , endocrinology , tyrosine phosphorylation , medicine , gene expression , phosphorylation , signal transduction , calcium in biology , stimulation , tyrosine , catecholamine , calcium , dopamine , pharmacology , biology , gene , biochemistry
A bstract : It is important to determine how the signaling pathways for the short‐term effects of nicotine (catecholamine secretion, phosphorylation of tyrosine hydroxylase) differ from those required for changes in gene expression. Our aim was to distinguish the pathways involved in short‐ and long‐term nicotinic stimulation. PC12 cells were treated with several concentrations of nicotine from 10 μM to 1 mM. All elicited a rapid and transient rise in [Ca 2+ ] i , which was concentration dependent. After several minutes of continued exposure, a second smaller sustained rise in [Ca 2+ ] i was only observed with intermediate concentrations of nicotine (50‐200 μM). This sustained rise was not observed in cells pretreated with α‐bungarotoxin (α‐BTX). α‐BTX also prevented the elevation of tyrosine hydroxylase mRNA by nicotine. The effects of brief and prolonged treatment with nicotine on the signaling pathways involved in changes in [Ca 2+ ] i and induction of tyrosine hydroxylase gene expression are summarized. The results indicate that nicotine may elicit different signaling pathways depending on the concentration. The sustained elevation of [Ca 2+ ] i via activation of α7 nAChRs is proposed as the mechanism leading to increased tyrosine hydroxylase gene expression.