γ-Aminobutyric acid (GABA) was discovered at the beginning of the century (Ackerman and Kutscher, 1910), and, shortly after it was first detected in mammalian brain in 1950 (Awapara et al., 1950; Roberts and Frankel, 1950; Udenfriend, 1950), an extract of mammalian brain and spinal cord was shown to contain a factor, ’Factor P, which inhibited the stretch receptor neurone (a single sensory cell with its dendrites entwined in a fine muscle bundle) of the crayfish (Florey, 1954). Through fractional crystallisation of bovine brain Factor I, GABA was shown to be the most active component in terms of its inhibitory activity on the stretch receptor neurone (Bazemore et al., 1957). Following some controversy over the role of GABA as a neurotransmitter, Kravitz and colleagues demonstrated GABA to be present in lobster inhibitory neurones, where it is synthesised, accumulated and released (Kravitz, 1967), and this work will be described later in this chapter. By the early 1970s it was thought that GABA might be the universal transmitter of junctional neuromuscular inhibition in all invertebrate phyla from nematodes to arthropods (though not molluscs), and it was also thought to be involved in the CNS of crustaceans, insects and possibly molluscs (see Gerschenfeld, 1973; Pichon, 1974; Callec, 1974). However, the evidence for this was virtually all electrophysiological, and despite the early studies on GABA involving invertebrate tissues, the bulk of the biochemistry of GABAergic neurotransmission has been elucidated in mammalian tissues.


Gaba Receptor Gaba Concentration Gaba Uptake Succinic Semialdehyde Nipecotic Acid 
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