PRESYNAPTIC MODULATION OF SENSORY AFFERENTS IN THE INVERTEBRATE AND VERTEBRATE NERVOUS-SYSTEM

1. Ultrastructural examination of the central terminals of sensory afferent neurons in both invertebrates and vertebrates demonstrates that the synapses that form the substrate for presynaptic inhibition and facilitation are almost universally present. 2. Presynaptic modulation of afferent input acts in many ways which tailor the inflow of sensory information to the behaviour of the animal, effectively providing a means of turning this on and off, or of combining information of the same or different modalities to refine responsiveness or clarify ambiguity. 3. Presynaptic modulation may act in several different roles on the same afferent. 4. A comparison of the mechanisms of presynaptic inhibition in different animals demonstrates the likelihood of a variety of common mechanisms, several of which may act simultaneously on the same terminal. These include changes in the conductance of the afferent membrane to Cl-, K+ and Ca2+ ions, in addition to less well understood mechanisms that directly affect transmitter release. 5. A single transmitter can produce several effects on a terminal through the same or different receptors. 6. Ultrastructural studies of afferent terminals reveal that only a proportion of boutons on a given afferent may receive presynaptic input and that this may depend on the region of the nervous system in which these are found or on the identity of the postsynaptic neurons contacted, 7. The synaptic relationships of afferent terminals can be complex. In invertebrates different types of presynaptic neuron may interact synaptically, as may postsynaptic dendrites in vertebrates. 8. Axons presynaptic to afferent terminals in vertebrates frequently synapse also with dendrites postsynaptic to the afferents. 9. In both invertebrates and vertebrates reciprocal interactions between afferents and postsynaptic neurons are seen. 10. Ultrastructural immunocytochemistry reveals the likely dominance of GABA as an agent of presynaptic inhibition but also demonstrates the possible presence of other transmitters some of whose roles are less completely understood.