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Abstract: 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 releas

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Author

Z. Jian Yu; Lynn Wecker

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

1994

Language

EN

Field

Neuroscience (Life Sciences)