Central lateral thalamic neurons receive noxious visceral mechanical and chemical input in rats.
Thalamic intralaminar and medial nuclei participate mainly in affective and motivational aspects of pain processing. Unique to the present study were identification and characterization of spontaneously active neurons in the central lateral nucleus (CL) of the intralaminar thalamus, which were found to respond only to viscerally evoked noxious stimuli in animals under pentobarbital anesthesia. Responses to noxious colorectal distention, intrapancreatic bradykinin, intraperitoneal dilute acetic acid, and greater splanchnic nerve electrical stimulation were characterized. Electrophysiological recordings revealed activity in most CL neurons (93%) was excited (69%) or inhibited (31%) in response to noxious visceral stimulation of visceral nerves. Expression of c-Fos observed in CL nucleus after intensive visceral stimulation confirmed the activation. However, excited CL neurons did not have somatic fields, except in 3 of 43 (7%) CL neurons tested for responses to somatic stimulation (innocuous brush and noxious pinch). Intrathecal administration of morphine significantly reduced the increased responses of CL neurons to colorectal and pancreatic stimuli and was naloxone reversible. High-level thoracic midline dorsal column (DC) myelotomy also dramatically reduced responses, identifying the DC as a major route of travel from the spinal cord for CL input, in addition to input traveling ventromedially in the spinothalamic tract identified anatomically in a previous study. Spinal cord and lower brain stem cells providing input to medial thalamus were mapped after stereotaxic injections of a retrograde dye. These data combined with our previous data suggest that the CL nucleus is an important component of a medial visceral nociceptive system that may mediate attentional, affective, endocrine, motor, and autonomic responses to noxious visceral stimuli.
Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX, USA.
Yong
Y
Ren
Liping
L
Zhang
Ying
Y
Lu
Hong
H
Yang
Karin N
KN
Westlund
D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000473:pathology; D000818:Animals; D001920:Bradykinin / Q000009:adverse effects; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D010146:Pain / Q000473:pathology* / Q000503:physiopathology*; D010183:Pancreatic Ducts / Q000294:innervation; D010812:Physical Stimulation / Q000009:adverse effects; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000166:cytology*; D014665:Vasodilator Agents / Q000009:adverse effects; D014781:Viscera / Q000294:innervation*; D014966:Xanthenes / Q000378:metabolism
D016760:Proto-Oncogene Proteins c-fos; D014665:Vasodilator Agents; D014966:Xanthenes; D009020:Morphine; C034657:Texas red; D001920:Bradykinin