Failure of sympathetic stimulation to affect responsiveness of rabbit polymodal nociceptors

Abstract

The responses of polymodal nociceptors with unmyelinated (C) fibers of the rabbit's great auricular nerve were examined with and without intermittent stimulation of the ipsilateral cervical sympathetic trunk. The receptive field of each polymodal nociceptor was heated twice in a stepwise manner from 30 to 50 or 55 degrees C in 5 degree C steps. For each unit, one heating trial was a control trial and the other was accompanied by sympathetic stimulation. The order of the control and sympathetic stimulation trials and the maximum testing temperature were varied systematically among the units examined. The initial responses of polymodal nociceptors in the first heating trial in the presence of sympathetic stimulation were similar to the responses of units whose first heating was a control trial. Units whose receptive fields were tested to a maximum temperature of 50 degrees C in the first trial displayed enhanced responses to heat in their second trial (sensitization), while units tested initially to 55 degrees C responded less briskly during their second heating trial (depression). However, the occurrence of sympathetic stimulation in the second heating trials had no apparent effect on the responses to heat of sensitized or depressed elements. Alterations in the numbers of impulses, instantaneous frequency, or pattern of impulse activity of individual units could not be attributed to sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

What lies above and beyond the concept of “sympathetically maintained pain”?

“…Animal studies indicate that the activity of polymodal C afferent fibers is unaffected by sympathetic stimulation under normal conditions [28][29][30], but neural injury may induce a sensitivity to sympathetic/adrenergic stimulation. Thus, both electrical stimulation of the sympathetic trunk and administration of adrenoceptor agonists have been shown to elicit discharge from C nociceptors in several nerve injury models [31][32][33][34], possibly due to an increased expression of ci-adrenergic receptors on primary afferent neurons following nerve lesions [35].…”

Adrenergic Excitation of Cutaneous Pain Receptors Induced by Peripheral Nerve Injury

“…This association, and the relief that can be provided by interruption of the sympathetic nervous supply to the affected body region, have led to characterization of causalgia and its pain as a reflex sympathetic dystrophy (2). Injuryinduced interactions between sympathetic efferent postganglionic axons and cutaneous sensory fibers have been proposed as the basis of causalgic pain (1); however, sympathetic stimulation (SS) and sympathetic chemical mediators neither excite nor enhance the activity ofpain receptors (nociceptors, that is, noxious stimulus receptors) of normal skin (3). Because SS does increase the responsiveness of some sensory units associated with nonpainful cutaneous mechanoreception (3), some proposals suggest central neural processes rather than peripheral interactions between efferent sympa-thetic neurons and specific sensory receptors for pain as the basis for causalgia (2,4).…”

“…Injuryinduced interactions between sympathetic efferent postganglionic axons and cutaneous sensory fibers have been proposed as the basis of causalgic pain (1); however, sympathetic stimulation (SS) and sympathetic chemical mediators neither excite nor enhance the activity ofpain receptors (nociceptors, that is, noxious stimulus receptors) of normal skin (3). Because SS does increase the responsiveness of some sensory units associated with nonpainful cutaneous mechanoreception (3), some proposals suggest central neural processes rather than peripheral interactions between efferent sympa-thetic neurons and specific sensory receptors for pain as the basis for causalgia (2,4). We examined the influence nerve lesions have on the way nociceptors respond to sympathetic action, to darify the relation of presumed pain receptors to causalgia.…”

Overexpression of nerve growth factor in transgenic mice induces novel sympathetic projections to primary sensory neurons

“…Common underlying features of these syndromes are alterations in regional blood flow and perspiration and the ability of chemical or surgical sympathectomy to provide relief. These pathological interactions between sympathetic and sensory systems are remarkable in that sympathetic stimulation normally does not excite nociceptors or enhance painful stimuli (Shea and Perl, 1985;Roberts and Elardo, 1985;Barasi and Lyn, 1986;Sanjue and Jun, 1989). Therefore, sympathetically mediated hyperalgesia develops de nouo in individuals with these syndromes.…”