Different sensitivity of in vivo acetylcholine transmission to D-1 receptor stimulation in shell and core of nucleus accumbens

Citation
S. Consolo et al., Different sensitivity of in vivo acetylcholine transmission to D-1 receptor stimulation in shell and core of nucleus accumbens, NEUROSCIENC, 89(4), 1999, pp. 1209-1217
Citations number
52
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE
ISSN journal
03064522 → ACNP
Volume
89
Issue
4
Year of publication
1999
Pages
1209 - 1217
Database
ISI
SICI code
0306-4522(199904)89:4<1209:DSOIVA>2.0.ZU;2-B
Abstract
We investigated whether D-1 dopaminergic receptors modulate in vivo acetylc holine output in the shell and core areas of rat nucleus accumbens using th e microdialysis technique. Subcutaneous injection (1, 2 and 3 mg/kg) of the D-1 agonist SKF 82958 enhanced acetylcholine output in both areas of the n ucleus accumbens while the selective D-1 antagonist SCH 39166 (0.15 and 0.3 0 mg/kg, s.c.) lowered it. Both SKF 82958 and SCH 39166 were more effective in the shell than in the core region. The increase in acetylcholine releas e induced by SKF 82958 in the shell was tetrodotoxin-sensitive. The dopamin e release inducer d-amphetamine (1 and 2 mg/kg, s.c.) and the dopamine upta ke inhibitor cocaine (IO and 20 mg/kg, i.p.) dose-dependently raised acetyl choline release in the shell and core areas. The dopaminergic stimulants, l ike the direct-acting D-1 compounds, were more effective in the shell than in the core compartment of the nucleus accumbens. The acetylcholine increas es in the shell induced by d-amphetamine (2 mg/kg), cocaine (20 mg/kg) and SKF 82958 (3 mg/kg) were antagonized by the D-1 antagonists SCH 39166 (5 mu M) and SCH 23390 (10 mu M), applied locally by reverse dialysis. The results suggest that dopamine acting at the D-1 receptors exerts a toni c stimulatory control over the cholinergic function of the shell and core c ompartments of the nucleus accumbens with the shell being more strongly inf luenced. (C) 1999 IBRO. Published by Elsevier Science Ltd.