scholarly journals Characterization of upper thoracic spinal neurons receiving noxious cardiac and/or somatic inputs in diabetic rats

2011 ◽  
Vol 165 (2) ◽  
pp. 168-177 ◽  
Author(s):  
Marie Louise M. Ghorbani ◽  
Chao Qin ◽  
Mingyuan Wu ◽  
Jay P. Farber ◽  
Majid Sheykhzade ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Spinal Neurons ◽  
Thoracic Spinal ◽  
Upper Thoracic

scholarly journals Characterization of upper thoracic spinal neurons responding to esophageal distension in diabetic rats

2009 ◽  
Vol 145 (1-2) ◽  
pp. 27-34 ◽  
Author(s):  
Chao Qin ◽  
Marie L.M. Ghorbani ◽  
Mingyuan Wu ◽  
Jay P. Farber ◽  
Jianxing Ma ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Spinal Neurons ◽  
Thoracic Spinal ◽  
Upper Thoracic

Axonal projection patterns of ventrolateral medullospinal sympathoexcitatory neurons

1985 ◽  
Vol 53 (6) ◽  
pp. 1551-1566 ◽  
Author(s):  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Gray Matter ◽  
Sympathetic Nerve ◽  
Action Potentials ◽  
Spinal Neurons ◽  
Spinal Segment ◽  
Axonal Conduction ◽  
Thoracic Spinal ◽  
Branching Patterns ◽  
Reflex Activation ◽  
Upper Thoracic

We studied the following properties of cat ventrolateral medullary (VLM) neurons that projected to the thoracic spinal cord: the relationship between their spontaneous activity and that in the inferior cardiac postganglionic sympathetic nerve, their responses to baroreceptor-reflex activation, their axonal conduction velocities, the funicular trajectories of their axons, the likely sites of termination of their axons, and their axonal branching patterns. Microstimulation in the second thoracic spinal segment (T2) antidromically activated 67 VLM neurons (as determined with time-controlled collision of spontaneous and evoked action potentials), whose activity was correlated to inferior cardiac sympathetic nerve discharge (as determined with spike-triggered averaging). We tested the effect of baroreceptor-reflex activation on the firing rate of 20 of these VLM-spinal neurons. Because the firing rate decreased in each instance, these neurons apparently subserved a sympathoexcitatory function. The axonal branching patterns of 51 VLM-spinal sympathoexcitatory neurons were studied. Thirty-four neurons were antidromically activated by stimulation in the T2 gray matter and in more caudal thoracic spinal segments (T11 and/or T6). In each case, the antidromic response evoked by stimulation in the T2 gray matter was due to activation of an axonal branch rather than the main axon (via current spread to the white matter). This was demonstrated with tests that included time-controlled collision of the action potentials initiated by stimulation in T2 and a more caudal thoracic spinal segment. Some VLM-spinal axons that projected to T11 branched in T6 as well as in T2. These data indicate that some VLM-spinal neurons exerted widespread excitatory influences on sympathetic outflow. Seventeen VLM sympathoexcitatory neurons that innervated the T2 gray matter could not be antidromically activated by stimulation in T5, T6, and T11 despite an extensive search at each level. Thus the axonal projections of some VLM-spinal neurons were restricted to upper thoracic segments. Antidromic mapping in T2 revealed that the axons of VLM sympathoexcitatory neurons coursed through the dorsolateral or ventrolateral funiculus to innervate the region of the intermediolateral nucleus. Mean axonal conduction velocity was 3.5 +/- 0.3 m/s. Those VLM-spinal axons restricted to upper thoracic segments generally were located dorsally and/or medially to those that innervated widely separated thoracic segments. The discharges of 35 other VLM neurons that were antidromically activated by T2 stimulation were not related to sympathetic nerve activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Urinary bladder and hindlimb stimuli inhibit T1-T6 spinal and spinoreticular cells

1990 ◽  
Vol 258 (1) ◽  
pp. R10-R20 ◽  
Author(s):  
S. F. Hobbs ◽  
U. T. Oh ◽  
T. J. Brennan ◽  
M. J. Chandler ◽  
K. S. Kim ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Inhibitory Effect ◽  
Afferent Input ◽  
Spinal Neuron ◽  
Spinal Neurons ◽  
Lumbosacral Spinal Cord ◽  
Thoracic Spinal ◽  
Excitatory Responses ◽  
Upper Thoracic ◽  
Alpha Chloralose

Upper thoracic spinal neurons are primarily excited by cardiopulmonary spinal afferent input but are excited and inhibited by splanchnic afferent input. These data suggest that the greater the number of segments between a spinal neuron and spinal afferent input the greater the probability that the afferent input will inhibit the spinal neuron. Based on this idea we hypothesized that visceral (urinary bladder) and somatic (hindlimb) afferent input would inhibit upper thoracic spinal neurons. To test this hypothesis the activities of 69 spinal and 27 spinoreticular tract neurons in 45 alpha-chloralose-anesthetized cats were studied. Only neurons excited by both visceral and somatic thoracic afferent input were studied. Urinary bladder distension (UBD) inhibited 48 (50%), excited 6 (6%), and did not affect 41 (43%) of these neurons. Also, UBD inhibited the excitatory responses of these cells to noxious visceral and somatic stimuli. Hindlimb pinch also inhibited greater than 50% of the neurons. These data indicate that visceral and somatic afferent input to the lumbosacral spinal cord inhibits the activity of upper thoracic neurons. This inhibitory effect may play a role in localization of sensory and motor responses to noxious stimuli.

scholarly journals Cross-organ sensitization of thoracic spinal neurons receiving noxious cardiac input in rats with gastroesophageal reflux

2010 ◽  
Vol 298 (6) ◽  
pp. G934-G942 ◽  
Author(s):  
Chao Qin ◽  
Anna P. Malykhina ◽  
Ann M. Thompson ◽  
Jay P. Farber ◽  
Robert D. Foreman
Keyword(s):  
Gastroesophageal Reflux ◽  
Gastroesophageal Junction ◽  
Gastric Fundus ◽  
Control Group ◽  
Sprague Dawley ◽  
Spinal Neurons ◽  
Thoracic Spinal ◽  
Afferent Fibers ◽  
Excitatory Responses ◽  
Upper Thoracic

Gastroesophageal reflux (GER) frequently triggers or worsens cardiac pain or symptoms in patients with coronary heart disease. This study aimed to determine whether GER enhances the activity of upper thoracic spinal neurons receiving noxious cardiac input. Gastric fundus and pyloric ligations as well as a longitudinal myelotomy at the gastroesophageal junction induced acute GER in pentobarbital-anesthetized, paralyzed, and ventilated male Sprague-Dawley rats. Manual manipulations of the stomach and lower esophagus were used as surgical controls in another group. At 4–9 h after GER surgery, extracellular potentials of single neurons were recorded from the T3 spinal segment. Intrapericardial bradykinin (IB) (10 μg/ml, 0.2 ml, 1 min) injections were used to activate cardiac nociceptors, and esophageal distensions were used to activate esophageal afferent fibers. Significantly more spinal neurons in the GER group responded to IB compared with the control group (69.1 vs. 38%, P < 0.01). The proportion of IB-responsive neurons in the superficial laminae of GER animals was significantly different from those in deeper layers (1/8 vs. 46/60, P < 0.01); no difference was found in control animals (7/25 vs. 20/46, P > 0.05). Excitatory responses of spinal neurons to IB in the GER group were greater than in the control group [32.4 ± 3.5 impulses (imp)/s vs. 13.3 ± 2.3 imp/s, P < 0.01]. Forty-five of 47 (95.7%) neurons responded to cardiac input and ED, which was higher than the control group (61.5%, P < 0.01). These results indicate that acute GER enhanced the excitatory responses of thoracic spinal neurons in deeper laminae of the dorsal horn to noxious cardiac stimulus.

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