title: Nociceptive afferents selectively modulate the cardiac component of the peripheral chemoreceptor reflex via actions within the solitary tract nucleus.
abstract: Our previous findings showed that the nucleus of the solitary tract (NTS) mediated part of the tachycardia evoked during somatic noxious stimulation. Here, we investigated the interaction between somatic nociceptor- and peripheral chemoreceptor-evoked cardiac changes. We sought to determine whether this interaction occurred within the NTS, the primary site of termination of chemoreceptor afferents. In a working heart-brainstem preparation of rat, mechanical noxious activation of a forelimb evoked a tachycardia of 17.5+/-3 (mean+/-S.E.M.) b.p.m., whereas sodium cyanide (7-30 microg) stimulation of peripheral chemoreceptors produced a sub-maximal bradycardia of -140+/-15 b.p.m. During nociceptor stimulation the sodium cyanide-evoked bradycardia was attenuated to -42.6+/-12 b.p.m. but could be prevented by a multiple bilateral NTS microinjection of bicuculline (i.e. -173+/-18 b.p.m.). Furthermore, the activity of NTS neurones responding to peripheral chemoreceptor stimulation increased from 2.8+/-1.3 to 9.4+/-1.9 Hz during sodium cyanide injection (n=7; P<0.01). The latter response was attenuated reversibly to 2.9+/-0.9 Hz during simultaneous stimulation of the brachial nerve. Pressure ejection of bicuculline abolished this inhibitory action of brachial-nerve stimulation on the chemoreceptor-evoked excitatory synaptic response. We conclude that somatic noxious stimulation attenuates the chemoreceptor reflex-evoked bradycardia via a GABA(A)ergic mechanism in the NTS.
authors.affiliation: Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK. p.boscan@bristol.ac.uk
authors.forename: P
authors.initials: P
authors.lastname: Boscan
authors.forename: J F R
authors.initials: JF
authors.lastname: Paton
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001919:Bradycardia / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D002628:Chemoreceptor Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004558:Electric Stimulation; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D006321:Heart / Q000294:innervation* / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009431:Neural Conduction / Q000502:physiology; D009619:Nociceptors / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010525:Peripheral Nerves / Q000502:physiology; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000378:metabolism; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D012966:Sodium Cyanide / Q000494:pharmacology; D017552:Solitary Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D012966:Sodium Cyanide