Dopamine Modulates Corticostriatal Synaptic Transmission through Both D1 and D2 Receptor Subtypes in Rat Brain.
- Author:
Hyun Ho LEE
1
;
Se Joon CHOI
;
Ki Jung KIM
;
Hyeong Seok CHO
;
Seong Yun KIM
;
Ki Wug SUNG
Author Information
1. Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea. sungkw@catholic.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Dopamine;
Population Spike;
Striatum;
Rat
- MeSH:
Animals;
Brain*;
Corpus Callosum;
Dopamine*;
Learning;
Memory;
Neocortex;
Rats*;
Substantia Nigra;
Sulpiride;
Synaptic Transmission*;
Thalamus
- From:The Korean Journal of Physiology and Pharmacology
2005;9(5):263-268
- CountryRepublic of Korea
- Language:English
-
Abstract:
Striatum has important roles in motor control, habitual learning and memory. It receives glutamatergic inputs from neocortex and thalamus, and dopaminergic inputs from substantia nigra. We examined effects of dopamine (DA) on the corticostriatal synaptic transmission using in vitro extracellular recording technique in rat brain corticostriatal slices. Synaptic responses were elicited by stimulation of cortical glutamatergic inputs on the corpus callosum and recorded in the dorsal striatum. Corticostriatal population spike (PS) amplitudes were decreased (39.4+/-7.9%) by the application of 100microM DA. We applied receptor subtype specific agonists and antagonists and characterized the modulation of corticostriatal synaptic transmission by different DA receptor subtypes. D2 receptor agonist (quinpirole), antagonist (sulpiride), and D1 receptor antagonist (SKF 83566), but not D1 receptor agonist (SKF 38393), induced significantly the reduction of striatal PS. Pretreatment neither with SKF 83566 nor sulpiride significantly affected corticostriatal synaptic inhibition by DA. However, the inhibition of DA was completely blocked by pretreatment with mixed solution of both SKF 83566 and sulpiride. These results suggest that DA inhibits corticostriatal synaptic transmission through both D1 and D2 receptors in concert with each other.
