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Chronic Nicotine Administration Differentially Affects Neurotransmitter Release from Rat Striatal Slices
Author(s) -
Yu Z. Jian,
Wecker Lynn
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.63010186.x
Subject(s) - nicotine , neurotransmitter , acetylcholine , endocrinology , medicine , dopamine , chemistry , saline , liberation , serotonin , cholinergic , pharmacology , biology , central nervous system , receptor , biochemistry , in vitro
The objective of these experiments was to determine whether the chronic administration of nicotine, at a dose regimen that increases the density of nicotine binding sites, alters the nicotine‐induced release of [ 3 H]dopamine ([ 3 H]DA), [ 3 H]norepinephrine ([ 3 H]NE), [ 3 H]serotonin ([ 3 H]5‐HT), or [ 3 H]acetylcholine ([ 3 H]ACh) from rat striatal slices. For these experiments, rats received subcutaneous injections of either saline or nicotine bitartrate [1.76 mg (3.6 µmol)/kg, dissolved in saline] twice daily for 10 days, and neurotransmitter release was measured following preloading of the tissues with [ 3 H]DA, [ 3 H]NE, [ 3 H]5‐HT, or [ 3 H]choline. Chronic nicotine administration did not affect the accumulation of tritium by striatal slices, the basal release of radioactivity, or the 25 m M KCl‐evoked release of neurotransmitter. Superfusion of striatal slices with 1, 10, and 100 µ M nicotine increased [ 3 H]DA release in a concentration‐dependent manner, and release from slices from nicotine‐injected animals was significantly ( p < 0.05) greater than release from saline‐injected controls; release from the former increased to 132, 191, and 172% of release from the controls following superfusion with 1, 10, and 100 µ M nicotine, respectively. Similarly, [ 3 H]5‐HT release increased in a concentration‐related manner following superfusion with nicotine, and release from slices from nicotine‐injected rats was significantly ( p < 0.05) greater than that from controls. [ 3 H]5‐HT release from slices from nicotine‐injected rats evoked by superfusion with 1 and 10 µ M nicotine increased to 453 and 217%, respectively, of release from slices from saline‐injected animals. The nicotine‐induced release of [ 3 H]NE from striatal slices was also concentration dependent but was unaffected by chronic nicotine administration. [ 3 H]ACh release from striatal slices could not be detected when samples were superfused with nicotine but was measurable when tissues were incubated with nicotine. The release of [ 3 H]ACh from slices from nicotine‐injected rats was significantly ( p < 0.05) less than release from controls and decreased to 36, 83, and 77% of control values following incubation with 1, 10, or 100 µ M nicotine, respectively. This decreased [ 3 H]ACh release could not be attributed to methodological differences because slices from nicotine‐injected rats incubated with nicotine exhibited an increased [ 3 H]DA release, similar to results from superfusion studies. In addition, it is unlikely that the decreased release of [ 3 H]ACh from striatal slices from nicotine‐injected rats was secondary to increased DA release because [ 3 H]ACh release from slices from hippocampus, which is not tonically inhibited by DA, also decreased significantly ( p < 0.05) in response to nicotine; hippocampal slices from nicotine‐injected rats incubated with 1 and 10 µ M nicotine decreased to 42 and 70%, respectively, of release from slices from saline‐injected animals. Results indicate that the chronic administration of nicotine increases the ability of nicotine to induce the release of [ 3 H]DA and [ 3 H]5‐HT and decreases the ability of nicotine to evoke the release of [ 3 H]ACh but does not alter the nicotine‐induced release of [ 3 H]NE from brain slices.