A Comparison of Axonal and Somatodendritic Dopamine Release Using In Vivo Dialysis

Authors

  • Peter W. Kalivas,

    Corresponding author
    1. Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington, U.S.A.
      Address correspondence and reprint requests to Dr. P. Kalivas at Department of VCAPP, Washington State University, Pullman, WA 99164-6520, U.S.A.
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  • Patricia Duffy

    1. Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington, U.S.A.
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Address correspondence and reprint requests to Dr. P. Kalivas at Department of VCAPP, Washington State University, Pullman, WA 99164-6520, U.S.A.

Abstract

Abstract: The release of endogenous dopamine from the axon terminal field in the nucleus accumbens and from the A10 dopamine cell bodies of conscious rats was measured using intracranial dialysis. Release of dopamine from both areas was calcium-dependent and markedly inhibited by the presence of the D2 agonist, quinpirole, in the dialysis buffer. However, the addition of tetrodotoxin to the buffer produced less of a decrease in dopamine in the A10 region than in the nucleus accumbens. When dopamine release was examined by substituting K+ for Na+ or by adding amphetamine to the buffer, the evoked release was significantly less in the A10 region than in the nucleus accumbens. Likewise, enhanced extracellular dopamine following blockade of reuptake by nomifensine addition to the dialysis buffer was not as great in the A10 region as in the nucleus accumbens. These data argue that, in general, axonal and somatodendritic dopamine release are regulated by similar factors, although somatodendritic release is less influenced by action potential generation and less responsive to some releasing agents.

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