UCL logo

UCL Discovery

UCL home » Library Services » Electronic resources » UCL Discovery

THE NOCICEPTOR SENSITIZATION BY BRADYKININ DOES NOT DEPEND ON SYMPATHETIC NEURONS

KOLTZENBURG, M; KRESS, M; REEH, PW; (1992) THE NOCICEPTOR SENSITIZATION BY BRADYKININ DOES NOT DEPEND ON SYMPATHETIC NEURONS. NEUROSCIENCE , 46 (2) 465 - 473.

Full text not available from this repository.

Abstract

Nociceptive primary afferents develop an increased responsiveness in inflamed tissue. The aim of this neurophysiological investigation was to study the sensitivity changes of cutaneous nociceptors following application of the algesic inflammatory mediator bradykinin and to examine a possible contribution of the sympathetic nervous system. Single unit recordings were obtained in a skin-nerve in vitro preparation from unmyelinated nociceptive afferents supplying the hairy skin of intact or of chronically sympathectomized rats. In preparations from intact skin, mechano-heat-sensitive C-fibres responding to superfusion of the receptive fields with 10-mu-M bradykinin for 1 min were sensitized to heat stimulation 2 min later. On average, the threshold dropped by 5.0-degrees-C, the maximal discharge frequency increased by 34% and the temperature eliciting this peak discharge dropped by 5.6-degrees-C. This resulted in a leftward shift and an increased slope of the stimulus-response function indicating sensitization. In surgically sympathectomized animals, 52% of the nociceptive afferents were activated by bradykinin which is not different from normal controls. In sympathectomized animals neither the reduction of the mean threshold (4.6-degrees-C) nor the increase of the peak discharge frequency (48%) differed significantly from intact controls. The change of the stimulation-response function following bradykinin application was virtually identical in intact and sympathectomized preparations. Moreover, bradykinin increased the heat discharge of individual fibres by a factor of 2.1 in intact and 1.9 in sympathectomized animals, respectively. In both preparations the increased responsiveness of the nociceptors was short-lived and had resolved 7 min after chemical stimulation.We conclude that the inflammatory mediator bradykinin can excite unmyelinated nociceptive afferents supplying the rat hairy skin and causes a sensitization for subsequent heat stimulation. Following sympathectomy there is no significant change of these responses, indicating that the sympathetic nervous system does not contribute appreciably to the bradykinin-induced sensitization of nociceptors.

Type: Article
Title: THE NOCICEPTOR SENSITIZATION BY BRADYKININ DOES NOT DEPEND ON SYMPATHETIC NEURONS
Keywords: POLYMODAL NOCICEPTORS, NORADRENALINE HYPERALGESIA, NEUROGENIC INFLAMMATION, AFFERENT-FIBERS, RAT SKIN, ACTIVATION, RABBIT, STIMULATION, CAPSAICIN, RESPONSIVENESS
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences
URI: http://discovery.ucl.ac.uk/id/eprint/116305
Downloads since deposit
0Downloads
Download activity - last month
Download activity - last 12 months
Downloads by country - last 12 months

Archive Staff Only

View Item View Item