TY - JOUR
T1 - Regulation of striatal dopamine release by metabotropic glutamate receptors
AU - Verma, Anita
AU - Moghaddam, Bita
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1998/3
Y1 - 1998/3
N2 - In vivo microdialysis in conscious rats was used to assess the effect of metabotropic glutamate receptor stimulation on striatal dopamine release. Local application of the metabotropic glutamate agonist (±)-trans-1- aminocyclopentane-1,3-dicarboxylic acid (ACPD), via a microdialysis probe, produced a concentration-dependent response: infusion of 50 μM ACPD did not produce a significant effect on extracellular dopamine levels, while application of 100 μM or 500 μM ACPD increased dopamine release by approximately 50% or 100%, respectively. To examine the contribution of impulse flow and multisynaptic mechanisms to the ACPD-induced increase in dopamine release, 500 μM ACPD were coapplied with 2 μM tetrodotoxin (TTX). An increase in extracellular dopamine levels was observed after the application of 500 μM ACPD, despite the presence of TTX. To further study the actions of metabotropic glutamate receptor-stimulation on terminal release characteristics of dopamine, the effect of ACPD on 40 mM K+- stimulated dopamine release was investigated. It was found that application of ACPD reduces dopamine release in response to K+ stimulation. These data suggest that during basal conditions, metabotropic glutamate receptor activation facilitates striatal dopamine release, possibly through presynaptic, impulse-independent mechanisms. However, during conditions of hyperstimulation, activation of metabotropic receptors, in contrast to ionotropic receptors, reduces excess dopamine release.
AB - In vivo microdialysis in conscious rats was used to assess the effect of metabotropic glutamate receptor stimulation on striatal dopamine release. Local application of the metabotropic glutamate agonist (±)-trans-1- aminocyclopentane-1,3-dicarboxylic acid (ACPD), via a microdialysis probe, produced a concentration-dependent response: infusion of 50 μM ACPD did not produce a significant effect on extracellular dopamine levels, while application of 100 μM or 500 μM ACPD increased dopamine release by approximately 50% or 100%, respectively. To examine the contribution of impulse flow and multisynaptic mechanisms to the ACPD-induced increase in dopamine release, 500 μM ACPD were coapplied with 2 μM tetrodotoxin (TTX). An increase in extracellular dopamine levels was observed after the application of 500 μM ACPD, despite the presence of TTX. To further study the actions of metabotropic glutamate receptor-stimulation on terminal release characteristics of dopamine, the effect of ACPD on 40 mM K+- stimulated dopamine release was investigated. It was found that application of ACPD reduces dopamine release in response to K+ stimulation. These data suggest that during basal conditions, metabotropic glutamate receptor activation facilitates striatal dopamine release, possibly through presynaptic, impulse-independent mechanisms. However, during conditions of hyperstimulation, activation of metabotropic receptors, in contrast to ionotropic receptors, reduces excess dopamine release.
KW - ACPD
KW - Excitatory amino acids
KW - Microdialysis
KW - Schizophrenia
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U2 - 10.1002/(SICI)1098-2396(199803)28:3<220::AID-SYN5>3.0.CO;2-C
DO - 10.1002/(SICI)1098-2396(199803)28:3<220::AID-SYN5>3.0.CO;2-C
M3 - Article
C2 - 9488507
AN - SCOPUS:0031910849
SN - 0887-4476
VL - 28
SP - 220
EP - 226
JO - Synapse
JF - Synapse
IS - 3
ER -