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Research ArticleNEUROPHARMACOLOGY

Alterations in Responses of Ventral Pallidal Neurons to Excitatory Amino Acids after Long-Term Dopamine Depletion

Michael S. Turner, Laurence Mignon and T. Celeste Napier
Journal of Pharmacology and Experimental Therapeutics April 2002, 301 (1) 371-381; DOI: https://doi.org/10.1124/jpet.301.1.371
Michael S. Turner
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Laurence Mignon
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T. Celeste Napier
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Abstract

The present study explored the possibility that excitatory amino acid (EAA) sensitivity within the ventral pallidum (VP) is altered by long-term removal of dopamine (DA). Electrophysiological experiments were conducted in chloral hydrate-anesthetized rats 21 to 28 days after they received unilateral substantia nigra injections of the dopaminergic toxin 6-hydroxydopamine (6-OHDA). VP neurons increased firing at low microiontophoretic ejection currents of the EAA agonistsN-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); however, high currents decreased action potential amplitude and rapidly caused cessation of neuronal firing. These responses likely reflected the induction of depolarization block for they were reversed by coiontophoresis of the hyperpolarizing transmitter γ-aminobutyric acid (GABA) at ejection current levels that normally suppressed firing. The ability of NMDA and AMPA to induce such inactivation was greater in the VP of 6-OHDA-lesioned hemispheres, but unchanged in reserpinized rats, verifying that the alterations in responding to NMDA were the result of chronic, rather than acute, DA removal. The adaptations do not appear to be the consequence of a diminished GABAergic tone for the ability of bicuculline to increase firing (due to blocking a tonic GABAergic input) was not changed. However, low ejection currents of GABA that were insufficient to alter firing rate greatly attenuated the ability of NMDA to induce an apparent depolarization inactivation when coiontophoresed with NMDA onto VP neurons of the lesioned, but not the unlesioned, hemisphere. These studies show that chronic DA removal altered the EAA-induced amplitude-decreasing (i.e., the apparent depolarization inactivation) effects in VP neurons in the absence of a decrease in GABAergic tone.

Footnotes

  • ↵1 Present address: Department of Neurology, Reed Neurological Research Center, UCLA School of Medicine, Los Angeles, CA 90095.

  • This work was supported by U.S. Public health Service Grant MH11607 (to M.S.T. and T.C.N.), and by the M.D./Ph.D. and Neuroscience graduate programs at Loyola University Chicago.

  • Abbreviations:
    EAA
    excitatory amino acid
    PD
    Parkinson's Disease
    DA
    dopamine
    STN
    subthalamic nucleus
    GPi
    internal segment of globus pallidus
    VP
    ventral pallidum
    NMDA
    N-methyl-d-aspartate
    AMPA
    α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid
    GABA
    γ-aminobutyric acid
    6-OHDA
    6-hydroxydopamine
    HPLC-EC
    high-performance liquid chromatography with electrochemical detection
    ANOVA
    analysis of variance
    ISI
    interspike interval
    CNQX
    6-cyano-2,3-dihydroxy-7-nitroquinoxaline
    AP-5
    2-amino-5-phosphopentanoic acid
    GPe
    external segment of globus pallidus
    • Received August 30, 2001.
    • Accepted January 8, 2002.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 301 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 301, Issue 1
1 Apr 2002
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Research ArticleNEUROPHARMACOLOGY

Alterations in Responses of Ventral Pallidal Neurons to Excitatory Amino Acids after Long-Term Dopamine Depletion

Michael S. Turner, Laurence Mignon and T. Celeste Napier
Journal of Pharmacology and Experimental Therapeutics April 1, 2002, 301 (1) 371-381; DOI: https://doi.org/10.1124/jpet.301.1.371

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Research ArticleNEUROPHARMACOLOGY

Alterations in Responses of Ventral Pallidal Neurons to Excitatory Amino Acids after Long-Term Dopamine Depletion

Michael S. Turner, Laurence Mignon and T. Celeste Napier
Journal of Pharmacology and Experimental Therapeutics April 1, 2002, 301 (1) 371-381; DOI: https://doi.org/10.1124/jpet.301.1.371
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