Amino Acid Receptors in CNS. II. GABA in Supraspinal Regions

  • J. S. Kelly
  • P. M. Beart
Part of the Handbook of Psychopharmacology book series (HBKPS, volume 4)


By the early 1960s (see reviews by Elliott and Jasper, 1959; Krnjević, 1964; Curtis and Watkins, 1965), GAB A had been shown both by the use of evoked potentials and single cell recording techniques and by the application of drugs to single cells by microiontophoresis to have a powerful inhibitory action on the majority of neurons encountered in the more accessible parts of mammalian brain and spinal cord (Hayashi, 1956; Purpura et al., 1959; Curtis and Phillis, 1958; Curtis et al., 1959; Krnjević and Phillis, 1963a). Furthermore, during the previous decade GAB A had become established as the most likely mediator of inhibition at the crustacean neuromuscular junction (Kravitz et al., 1963; Takeuchi and Takeuchi, 1965; Otsuka et al., 1966), and its presence and that of enzymes capable of its production and destruction in the mammalian brain had been confirmed (see review by Roberts and Eidelberg, 1960; Tapia, Chap. 1, this volume). It was therefore surprising to find in the mid-1960s that the contention that GABA might fulfill the role of the inhibitory transmitter in the mammalian nervous system was still being hotly debated in reviews for by Krnjević (1964) and against by Curtis and Watkins (1965). Later these two groups, with others, resolved their differences, at least in part, by adopting two quite different strategies.


Purkinje Cell Pyramidal Tract Mitral Cell Inhibitory Transmitter Synaptic Inhibition 
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Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • J. S. Kelly
    • 1
  • P. M. Beart
    • 2
  1. 1.MRC Neurochemical Pharmacology Unit, Department of PharmacologyMedical SchoolCambridgeEngland
  2. 2.Neurology ResearchChildren’s Hospital Medical CenterBostonUSA

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