[Abstract Title]. - Society for Neuroscience

Authors: *E. JUNG 1 , D.-S. KIM 2 , K.-S. KIM 3 , J. KIM 4 , I. SHIM 5 ;
1 Depart of Integrative Med., The Catho Univ. of korea, seoul, Republic of Korea; 2 Korea
Advanced Inst. of Sci. and Technol., Daejeon, Republic of Korea; 3 Dept. of Integrative Med.,
4 Inst. of Med. Sci., The Catholic Univ. of Korea, Seoul, Republic of Korea; 5 The Catholic Univ.
of Korea, Dept. of Integrative Med, Republic of Korea
Abstract: Dopamine (DA) regulates motor function by influencing GABA level in the basal
ganglia. GABAergic cells in the basal ganglia have DA receptors which divide into two main
branches, D1 family (comprising the D1 and D5 subtype) and the D2 family (comprising the D2,
D3, and D4 subtypes). In order to establish the functional role of the different DA subtypes on
GABAergic system in basal ganglia, D1 selective agonist (SKF 38393) and D2 selective agonist
(Quinpirole) were administered to mice. Motor activity was assessed for 60 min immediately
after the injection of DA agonists SKF 38393 and Quinpirole (0,1,5,10 mg/kg). Mice were
sacrificed after behavior test and the brains were dissected into region of the basal ganglia for
analysis of GABA level with HPLC. Mice treated with D1 and D2 agonists showed significant
increase in locomotor activity. In the analysis of GABA level measured by using HPLC-coupled
with fluorescence detector, D1 agonist increased GABA level in the striatum and GPi whereas
D2 agonist decreased its level in the same region. Our results suggest that two type of DA
receptors differencially regulate motor function by regulating each GABA level of the basal
ganglia.
Disclosures: E. Jung , None; D. Kim, None; K. Kim, None; J. Kim, None; I. Shim, None.
Poster
274. Basal Ganglia: Transmitters and Neuromodulation II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 274.20/JJ15
Topic: D.15.a. Transmitters and neuromodulation
Support: CONACyT Grant 50427Q
Title: D4 receptors inhibit depolarization-induced [ 3 H]GABA release from pallido-nigral
terminals
Authors: J. ACOSTA 1 , A. SIERRA 1 , *R. ESCARTIN-PEREZ 2 , D. ERLIJ 3 , J. ACEVES 1 , B.
FLORAN 1 ;
1 CINVESTAV-IPN, Mexico DF, Mexico; 2 Lab. Eating Neurobiol, Univ. Natl. Autonoma
Mexico, Tlalnepantla, Mexico; 3 Sunny Dowstate Med. Center, State Univ. of NY, New York,
NY