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From early psychophysical studies a variety of exogenous and endogenous substances have been found to induce pain and hyperalgesia, that is, to be algogenic. To study the underlying mechanisms several behavioural and reflex models have been developed in animals. However, it has been difficult to differentiate between peripheral and central mechanisms. Single-fibre recordings provided a tool for isolating the contributions of primary afferents. Controlled application of defined mediator concentrations became feasible allowing for the investigation of the direct effects on nociceptive nerve endings. These sensory terminals, however, comprise receptive membrane sections, action potential generator region(s), and conductive zones of the axon, each of which could be the target of a chemical mediator. To differentiate these would require intracellular recording of the membrane potential or currents; this is not achievable due to the submicroscopic size of nociceptive nerve endings and their embedding in the tissue. Considering the cell soma in dissociated sensory ganglion cultures to be a model of its receptive ending, valuable information can be obtained from patch-clamp recordings of chemically mediated membrane effects.

This chapter covers the following aspects which are relevant to the role of N-methyl-d-aspartate (NMDA) receptors in spinal neurotransmission: the involvement of NMDA receptors and the co-agonist glycine site in long duration spinal reflexes elicited from dorsal roots; the relationship between glutamatergic and peptidergic transmission from primary afferent C fibres; and the selective depression of NMDA-receptive excitatory pathways by analgesic and myorelaxant drugs. It has been reported that long duration synaptic potentials in spinal preparations are a property of early development because in rats older than ten days, synaptic potentials are of much shorter duration than in younger rats. However, such comparisons between spinal root recordings from animals of different ages should be cautiously interpreted.

The study of peripheral mechanisms of pain was greatly advanced by the technique of microneurography. This technique not only makes possible experiments on human volunteers instead of on guinea-pigs, but also adds a psychophysical dimension to electrophysiology, since human volunteers are able to describe their stimulus-induced sensations while primary afferent units are recorded. This chapter discusses the insights into the peripheral neural mechanisms of pain and hyperalgesia recently gained by microneurography. The most abundant and probably the most important class of nociceptor units in the skin are unmyelinated (C) fibres, and hence most of this review is dedicated to this fibre class. The myelinated fibres contributing to withdrawal reflexes and pain, which are generally slowly conducting Αδ fibres, are also considered. Mechanisms of hyperalgesia involving low-threshold mechanoreceptor units and central nervous plasticity are briefly discussed.

The vestibulo-ocular reflexes help to stabilize the visual image on the retina, and the vestibulocollic (vestibular neck) reflexes play a role in restoring the head position in space during head movements. The vestibular nucleus neurons play a crucial role in both reflex pathways. It was observed that individual vestibular relay neurons receive inputs from two to three semicircular canal pairs, or from canals and otolith organs, when natural stimuli were applied in alert cats. However, according to observations in anesthetized cats, it has been considered that the primary afferent fibers from each semicircular canal have their own target neurons in the vestibular nuclei.