Premium
Dopamine Agonist‐Mediated Inhibition of Acetylcholine Release in Rat Striatum Is Modified by Thyroid Hormone Status
Author(s) -
Foley P. B.,
Crocker A. D.
Publication year - 1993
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 - 10.1111/j.1471-4159.1993.tb03591.x
Subject(s) - apomorphine , medicine , endocrinology , agonist , quinpirole , chemistry , dopamine receptor d2 , sch 23390 , raclopride , acetylcholine , dopamine receptor , dopamine , receptor , biology
K + ‐evoked acetyl[ 3 H]choline ([ 3 H]ACh) release was inhibited in a concentration‐dependent manner by apomorphine and the D 2 agonist quinpirole in striatal slices prepared from euthyroid and hypothyroid rats. However, there was a significant increase in the maximum inhibition observed with both agonists in the hypothyroid compared with the euthyroid group, which paralleled the increased D 2 agonist sensitivity reported for stereotyped behavior. The D 2 antagonist raclopride decreased, and the D, antagonist SCH 23390 increased, the inhibition of [ 3 H]ACh release by apomorphine, confirming an inhibitory role for D 2 receptors and an opposing role for D 1 receptors. Because there is no difference in D 1 or D 2 receptor concentration between the euthyroid and hypothyroid groups, it is suggested that thyroid hormone modulation of D 2 receptor sensitivity affects a receptor‐mediated event. Following intrastriatal injection of pertussis toxin (PTX), apomorphine no longer inhibited [ 3 H]ACh release. In fact, increased [ 3 H]‐ ACh release was observed, an effect reduced by SCH 23390, providing evidence that D 1 receptors enhance [ 3 H]‐ ACh release, and confirming that a PTX‐sensitive G protein mediates the D 2 response. As it has been reported that thyroid hormones modulate G protein expression, this mechanism may underlie their effect on dopamine agonist‐ mediated inhibition of ACh.