Presynaptic Inhibition: Transmitter and Ionic Mechanisms

Abstract

Publisher Summary This chapter discusses the pharmacology and ionic mechanism of presynaptic inhibition in both invertebrates and vertebrates. For invertebrates, the chapter mainly focuses on crustacean nervous system. Pharmacological and anatomical studies suggest that the inhibition results from the release of gamma-aminobutyric acid (GABA) from axo-axonic synapses. There is evidence that in mammalian CNS presynaptic fibers may have GABA receptors even though they do not receive axo-axonic synapses. In addition, electrical stimulation of these presynaptic fibers results in the activation of these receptors, presumably due to the diffusion of GABA from remote synapses. This raises the possibility that presynaptic inhibition might occur in regions that do not contain axo-axonic synapses. In vertebrates, there is evidence that GABA, at least on the cell bodies of primary afferents, increases chloride permeability. At the crustacean neuromuscular junction (NMJ) the increased conductance of the motor nerve terminal results in a reduction in spike amplitude and/or a block in impulse invasion into the terminal that reduces the number of quanta released per stimulus. The major difference in the presynaptic action of GABA in vertebrate primary afferents and in the crustacean NMJ is that in the former, the increased chloride conductance results in a large depolarization.