Autonomic control of sensory responsiveness.
This paper discusses some recent evidence concerned with interactions between the sympathetic nervous system and sensory processing. There is some evidence for a direct inhibitory influence of sympathetic nerves on C-fibre somatic afferents. However, the effects are often masked by other actions which are secondary to sympathetically induced local vascular changes. In addition, in certain pathological pain states sympathetic activity does appear to enhance activity in C-fibres. Centrally induced changes in sensory responsiveness and in the pattern of ongoing sympathetic activity are fundamental components of certain behavioural states, such as aggression or sleep. Even though these changes occur in concert, there is as yet no unequivocal evidence for a common central control mechanism. The central control of the sympathetic outflow and sensory afferent input appear to be mediated independently. In contrast, increased visceral afferent input to the central nervous system, e.g. from cardiopulmonary baroreceptors, may lead to a decreased responsiveness to noxious input indirectly by enhancing centrally the activity in descending pain control pathways.
Lovick
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D000222:Adaptation, Physiological; D000344:Afferent Pathways / Q000502:physiology*; D006801:Humans; D008526:Medulla Oblongata / Q000502:physiology; D010147:Pain Measurement; D010487:Periaqueductal Gray / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*