5-Hydroxytryptamine Inhibits Glutamatergic Synaptic Transmission in Rat Corticostriatal Brain Slice.
- Author:
Hyeong Seok CHO
1
;
Se Joon CHOI
;
Ki Jung KIM
;
Hyun Ho LEE
;
Seong Yun KIM
;
Young Jin CHO
;
Ki Wug SUNG
Author Information
1. Department of Pharmacology, MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea. sungkw@catholic.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Striatum;
5-Hydoxytrptamine;
Spontaneous EPSC;
Synaptic transmission
- MeSH:
Animals;
Bicuculline;
Brain*;
Cerebral Cortex;
Excitatory Postsynaptic Potentials;
gamma-Aminobutyric Acid;
Glutamic Acid;
Kinetics;
Memory;
N-Methylaspartate;
Neurotransmitter Agents;
Patch-Clamp Techniques;
Raphe Nuclei;
Rats*;
Serotonin*;
Synapses;
Synaptic Transmission*
- From:The Korean Journal of Physiology and Pharmacology
2005;9(5):255-262
- CountryRepublic of Korea
- Language:English
-
Abstract:
Striatum is involved in the control of movement and habitual memory. It receives glutamatergic input from wide area of the cerebral cortex as well as an extensive serotonergic (5-hydroxytryptamine, 5-HT) input from the raphe nuclei. In our study, the effects of 5-HT on synaptic transmission were studied in the rat corticostriatal brain slice using in vitro whole-cell recording technique. 5-HT inhibited the amplitude as well as frequency of spontaneous excitatory postsynaptic currents (sEPSC) significantly, and neither gamma-aminobutyric acid (GABA) A receptor antagonist bicuculline (BIC), nor N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonovaleric acid (AP-V) could block the effect of 5-HT. In the presence non-NMDA receptor antagonist, 2, 3-dioxo-6-nitro-1, 2, 3, 4-tetrahydrobenxo[f] quinoxaline-7-sulfonamide (NBQX), the inhibitory effect of 5-HT was blocked. We also figured out that 5-HT change the channel kinetics of the sEPSC. There was a significant increase in the rise time during the 5-HT application. Our results suggest that 5-HT has an effect on both pre- and postsynaptic site with decreasing neurotransmitter release probability of glutamate and decreasing the sensitivity to glutamate by increasing the rise time of non-NMDA receptor mediated synaptic transmission in the corticostriatal synapses.
