Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats

Hank Peter Jedema, Bita Moghaddam

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

The effect of various classes of excitatory amino acid agonists on the release of dopamine in the medial prefrontal cortex (PFC) of awake rats was examined using intracerebral microdialysis. Local infusion of 20 μM α- amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), through the microdialysis probe, produced a significant increase of more than twofold in extracellular levels of dopamine. Application of 100 μM AMPA increased these levels nearly 15 fold. The AMPA/kainate receptor antagonist 6-cyano-7- nitroquinoxaline-2,3-di-one (CNQX) (50 μM) blocked the increase in dopamine release produced by 20 μM AMPA. Local infusion of kainate at concentrations of 5 and 20 μM increased dopamine release by nearly 150 and 500%, respectively. Local application of CNQX (50 μM) before 20 μM kainate significantly attenuated the stimulatory effect of kainate on dopamine levels. In contrast to AMPA and kainate, infusion of N-methyl-D-aspartate (NMDA) at 20 or 100 μM did not increase dopamine release. In fact, a trend toward a decrease in dopamine release was evident after 100 μM NMDA. The present study indicates that the in vivo release of dopamine in the PFC is facilitated by AMPA and kainate receptors. This modulation is more profound than that previously reported in the basal ganglia. The lack of an excitatory effect of NMDA is in agreement with recent reports that the NMDA receptor may inhibit indirectly dopaminergic neurotransmission in the PFC.

Original languageEnglish (US)
Pages (from-to)1448-1453
Number of pages6
JournalJournal of Neurochemistry
Volume66
Issue number4
StatePublished - Apr 1996
Externally publishedYes

Fingerprint

Excitatory Amino Acids
Prefrontal Cortex
Rats
Dopamine
Modulation
Kainic Acid
N-Methylaspartate
6-Cyano-7-nitroquinoxaline-2,3-dione
Kainic Acid Receptors
Microdialysis
Excitatory Amino Acid Agonists
Basal Ganglia
N-Methyl-D-Aspartate Receptors
Synaptic Transmission
propionic acid
bucide

Keywords

  • α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid
  • Dopamine
  • Glutamate
  • Microdialysis
  • N-Methyl-D- aspartate
  • Prefrontal cortex

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats. / Jedema, Hank Peter; Moghaddam, Bita.

In: Journal of Neurochemistry, Vol. 66, No. 4, 04.1996, p. 1448-1453.

Research output: Contribution to journalArticle

@article{5526e99d52084a7282f050a75815de2f,
title = "Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats",
abstract = "The effect of various classes of excitatory amino acid agonists on the release of dopamine in the medial prefrontal cortex (PFC) of awake rats was examined using intracerebral microdialysis. Local infusion of 20 μM α- amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), through the microdialysis probe, produced a significant increase of more than twofold in extracellular levels of dopamine. Application of 100 μM AMPA increased these levels nearly 15 fold. The AMPA/kainate receptor antagonist 6-cyano-7- nitroquinoxaline-2,3-di-one (CNQX) (50 μM) blocked the increase in dopamine release produced by 20 μM AMPA. Local infusion of kainate at concentrations of 5 and 20 μM increased dopamine release by nearly 150 and 500{\%}, respectively. Local application of CNQX (50 μM) before 20 μM kainate significantly attenuated the stimulatory effect of kainate on dopamine levels. In contrast to AMPA and kainate, infusion of N-methyl-D-aspartate (NMDA) at 20 or 100 μM did not increase dopamine release. In fact, a trend toward a decrease in dopamine release was evident after 100 μM NMDA. The present study indicates that the in vivo release of dopamine in the PFC is facilitated by AMPA and kainate receptors. This modulation is more profound than that previously reported in the basal ganglia. The lack of an excitatory effect of NMDA is in agreement with recent reports that the NMDA receptor may inhibit indirectly dopaminergic neurotransmission in the PFC.",
keywords = "α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid, Dopamine, Glutamate, Microdialysis, N-Methyl-D- aspartate, Prefrontal cortex",
author = "Jedema, {Hank Peter} and Bita Moghaddam",
year = "1996",
month = "4",
language = "English (US)",
volume = "66",
pages = "1448--1453",
journal = "Journal of Neurochemistry",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats

AU - Jedema, Hank Peter

AU - Moghaddam, Bita

PY - 1996/4

Y1 - 1996/4

N2 - The effect of various classes of excitatory amino acid agonists on the release of dopamine in the medial prefrontal cortex (PFC) of awake rats was examined using intracerebral microdialysis. Local infusion of 20 μM α- amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), through the microdialysis probe, produced a significant increase of more than twofold in extracellular levels of dopamine. Application of 100 μM AMPA increased these levels nearly 15 fold. The AMPA/kainate receptor antagonist 6-cyano-7- nitroquinoxaline-2,3-di-one (CNQX) (50 μM) blocked the increase in dopamine release produced by 20 μM AMPA. Local infusion of kainate at concentrations of 5 and 20 μM increased dopamine release by nearly 150 and 500%, respectively. Local application of CNQX (50 μM) before 20 μM kainate significantly attenuated the stimulatory effect of kainate on dopamine levels. In contrast to AMPA and kainate, infusion of N-methyl-D-aspartate (NMDA) at 20 or 100 μM did not increase dopamine release. In fact, a trend toward a decrease in dopamine release was evident after 100 μM NMDA. The present study indicates that the in vivo release of dopamine in the PFC is facilitated by AMPA and kainate receptors. This modulation is more profound than that previously reported in the basal ganglia. The lack of an excitatory effect of NMDA is in agreement with recent reports that the NMDA receptor may inhibit indirectly dopaminergic neurotransmission in the PFC.

AB - The effect of various classes of excitatory amino acid agonists on the release of dopamine in the medial prefrontal cortex (PFC) of awake rats was examined using intracerebral microdialysis. Local infusion of 20 μM α- amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), through the microdialysis probe, produced a significant increase of more than twofold in extracellular levels of dopamine. Application of 100 μM AMPA increased these levels nearly 15 fold. The AMPA/kainate receptor antagonist 6-cyano-7- nitroquinoxaline-2,3-di-one (CNQX) (50 μM) blocked the increase in dopamine release produced by 20 μM AMPA. Local infusion of kainate at concentrations of 5 and 20 μM increased dopamine release by nearly 150 and 500%, respectively. Local application of CNQX (50 μM) before 20 μM kainate significantly attenuated the stimulatory effect of kainate on dopamine levels. In contrast to AMPA and kainate, infusion of N-methyl-D-aspartate (NMDA) at 20 or 100 μM did not increase dopamine release. In fact, a trend toward a decrease in dopamine release was evident after 100 μM NMDA. The present study indicates that the in vivo release of dopamine in the PFC is facilitated by AMPA and kainate receptors. This modulation is more profound than that previously reported in the basal ganglia. The lack of an excitatory effect of NMDA is in agreement with recent reports that the NMDA receptor may inhibit indirectly dopaminergic neurotransmission in the PFC.

KW - α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid

KW - Dopamine

KW - Glutamate

KW - Microdialysis

KW - N-Methyl-D- aspartate

KW - Prefrontal cortex

UR - http://www.scopus.com/inward/record.url?scp=0030010363&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030010363&partnerID=8YFLogxK

M3 - Article

C2 - 8627297

AN - SCOPUS:0030010363

VL - 66

SP - 1448

EP - 1453

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

IS - 4

ER -