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Opioids II pp 3–20Cite as

Brainstem Mechanisms of Pain Modulation: Anatomy and Physiology

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Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 104 / 2))

Abstract

Opioids relieve pain through actions upon the nervous system. Under certain circumstances, for example, inflammation, opioids may act locally upon peripheral tissues (see Chap. 34). However, systemically administered opioids produce analgesia primarily through a direct action on receptors in the central nervous system (CNS). Direct evidence on this point is provided by clinical studies demonstrating that, compared with systemic administration, lower doses are required to produce analgesia when opioids are given intracerebroventricularly (Lazorthes et al. 1988) or intraspinally (see Chap. 33). Animal studies in which opioids were microinjected into the CNS confirm these clinical observations (Yaksh et al. 1988; Chap. 32) and extend them by demonstrating reversal of the antinociceptive effect of systemically administered opioids by direct application of opioid antagonists at CNS sites (Azami et al. 1982; Dickenson et al. 1979; Yeung and Rudy 1980). This chapter will review what is known of the CNS circuitry underlying the painrelieving action of exogenously administered opioids.

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Authors
  1. H. L. Fields
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Editors and Affiliations

  1. Abteilung Neuropharmakologie, Max-Planck-Institut für Psychiatrie, Am Klopferspitz 18, W-8033, Martinsried, Germany

    Albert Herz

  2. Mental Health Research Institute, School of Medicine, University of Michigan, 205 Zina Pitcher, 48109, Ann Arbor, MI, USA

    Huda Akil

  3. Medical Center, School of Medicine, New York University, 550 First Avenue, 10016, New York, NY, USA

    Eric J. Simon

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© 1993 Springer-Verlag Berlin Heidelberg

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Fields, H.L. (1993). Brainstem Mechanisms of Pain Modulation: Anatomy and Physiology. In: Herz, A., Akil, H., Simon, E.J. (eds) Opioids II. Handbook of Experimental Pharmacology, vol 104 / 2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77540-6_1

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