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Sustained enhancement of AMPA receptor- and NMDA receptor-mediated currents induced by dopamine D1/D5 receptor activation in the hippocampus: an essential role of postsynaptic Ca2+.
Hippocampus. 2000; 10(1):57-63.H

Abstract

The dopaminergic system in the limbic system, particularly the D1/D5 receptor (D1/D5r), is important for certain forms of learning and memory, such as reinforcement learning, as well as the acute development of behavioral sensitization to psychostimulants such as cocaine and methamphetamine. Here, whole-cell patch-clamp recordings of evoked excitatory postsynaptic currents (EPSCs) mediated by ionotropic glutamate receptors were made from pyramidal neurons in the CA1 area of rat hippocampal slices. Activation of the D1/D5r by a selective D1/D5r agonist (+/-)-6-chloro-PB hydrobromide (SKF 81297; 3-100 microM) concentration-dependently induced a delayed-onset, sustained enhancement of EPSCs. The D1/D5r-induced effect was blocked by a selective D1/D5r antagonist (+)SCH 23390 hydrochloride (5 microM). Furthermore, the D1/D5r-induced effect involved a sustained enhancement of both the pharmacologically isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate receptor-(AMPAr-) and N-methyl-D-asparate receptor- (NMDAr-) mediated EPSCs, respectively. Such persistently enhanced AMPAr- and NMDAr-mediated EPSCs were also associated with significant increases in the normalized amplitudes of the decay times of the isolated EPSCs. Blockade of NMDAr activation failed to prevent the induction of D1/D5r-induced sustained enhancement, suggesting the independence of the D1/D5r-induced effect on NMDAr activation. A rise of postsynaptic calcium was required for the induction of D1/D5r-induced sustained enhancement, being abolished by loading cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N '-tetracetic acid (BAPTA; 10 mM). Studies indicated that the D1/D5r activation induced a sustained enhancement of both the AMPAr-and NMDAr-mediated EPSCs in the hippocampus. Moreover, a rise in postsynaptic Ca2+ was necessary for triggering the D1/D5r-induced effect in the hippocampus, although the NMDAr-dependent mechanisms, such as the calcium entry via the NMDA channels, were not.

Authors+Show Affiliations

Yang SN
Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan, Republic of China. snyang@ndmc1.ndmctsgh.edu.tw

MeSH

6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsBenzazepinesCalciumChelating AgentsDopamine AgonistsEgtazic AcidExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsHippocampusIn Vitro TechniquesMembrane PotentialsPatch-Clamp TechniquesRatsRats, Sprague-DawleyReceptors, AMPAReceptors, Dopamine D1Receptors, Dopamine D5Receptors, N-Methyl-D-Aspartate

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10706217

Citation

Yang, S N.. "Sustained Enhancement of AMPA Receptor- and NMDA Receptor-mediated Currents Induced By Dopamine D1/D5 Receptor Activation in the Hippocampus: an Essential Role of Postsynaptic Ca2+." Hippocampus, vol. 10, no. 1, 2000, pp. 57-63.
Yang SN. Sustained enhancement of AMPA receptor- and NMDA receptor-mediated currents induced by dopamine D1/D5 receptor activation in the hippocampus: an essential role of postsynaptic Ca2+. Hippocampus. 2000;10(1):57-63.
Yang, S. N. (2000). Sustained enhancement of AMPA receptor- and NMDA receptor-mediated currents induced by dopamine D1/D5 receptor activation in the hippocampus: an essential role of postsynaptic Ca2+. Hippocampus, 10(1), 57-63.
Yang SN. Sustained Enhancement of AMPA Receptor- and NMDA Receptor-mediated Currents Induced By Dopamine D1/D5 Receptor Activation in the Hippocampus: an Essential Role of Postsynaptic Ca2+. Hippocampus. 2000;10(1):57-63. PubMed PMID: 10706217.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sustained enhancement of AMPA receptor- and NMDA receptor-mediated currents induced by dopamine D1/D5 receptor activation in the hippocampus: an essential role of postsynaptic Ca2+. A1 - Yang,S N, PY - 2000/3/8/pubmed PY - 2000/4/15/medline PY - 2000/3/8/entrez SP - 57 EP - 63 JF - Hippocampus JO - Hippocampus VL - 10 IS - 1 N2 - The dopaminergic system in the limbic system, particularly the D1/D5 receptor (D1/D5r), is important for certain forms of learning and memory, such as reinforcement learning, as well as the acute development of behavioral sensitization to psychostimulants such as cocaine and methamphetamine. Here, whole-cell patch-clamp recordings of evoked excitatory postsynaptic currents (EPSCs) mediated by ionotropic glutamate receptors were made from pyramidal neurons in the CA1 area of rat hippocampal slices. Activation of the D1/D5r by a selective D1/D5r agonist (+/-)-6-chloro-PB hydrobromide (SKF 81297; 3-100 microM) concentration-dependently induced a delayed-onset, sustained enhancement of EPSCs. The D1/D5r-induced effect was blocked by a selective D1/D5r antagonist (+)SCH 23390 hydrochloride (5 microM). Furthermore, the D1/D5r-induced effect involved a sustained enhancement of both the pharmacologically isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate receptor-(AMPAr-) and N-methyl-D-asparate receptor- (NMDAr-) mediated EPSCs, respectively. Such persistently enhanced AMPAr- and NMDAr-mediated EPSCs were also associated with significant increases in the normalized amplitudes of the decay times of the isolated EPSCs. Blockade of NMDAr activation failed to prevent the induction of D1/D5r-induced sustained enhancement, suggesting the independence of the D1/D5r-induced effect on NMDAr activation. A rise of postsynaptic calcium was required for the induction of D1/D5r-induced sustained enhancement, being abolished by loading cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N '-tetracetic acid (BAPTA; 10 mM). Studies indicated that the D1/D5r activation induced a sustained enhancement of both the AMPAr-and NMDAr-mediated EPSCs in the hippocampus. Moreover, a rise in postsynaptic Ca2+ was necessary for triggering the D1/D5r-induced effect in the hippocampus, although the NMDAr-dependent mechanisms, such as the calcium entry via the NMDA channels, were not. SN - 1050-9631 UR - https://www.unboundmedicine.com/medline/citation/10706217/Sustained_enhancement_of_AMPA_receptor__and_NMDA_receptor_mediated_currents_induced_by_dopamine_D1/D5_receptor_activation_in_the_hippocampus:_an_essential_role_of_postsynaptic_Ca2+_ L2 - https://doi.org/10.1002/(SICI)1098-1063(2000)10:1<57::AID-HIPO6>3.0.CO;2-0 DB - PRIME DP - Unbound Medicine ER -