Responses and Afferent Pathways of C1–C2 Spinal Neurons to Cervical and Thoracic Esophageal Stimulation in Rats

2004 ◽  
Vol 91 (5) ◽  
pp. 2227-2235 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Chuanchau J. Jou ◽  
Robert D. Foreman
Keyword(s):  
Male Rats ◽  
Thoracic Esophagus ◽  
Spinal Neurons ◽  
Afferent Pathways ◽  
Dorsal Roots ◽  
Upper Cervical ◽  
Cervical Vagotomy ◽  
Bilateral Vagotomy ◽  
Extracellular Potentials ◽  
Stimulation Of

Because vagal and sympathetic inputs activate upper cervical spinal neurons, we hypothesized that stimulation of the esophagus would activate C1–C2 neurons. This study examined responses of C1–C2 spinal neurons to cervical and thoracic esophageal distension (CED, TED) and afferent pathways for CED and TED inputs to C1–C2 spinal neurons. Extracellular potentials of single C1–C2 spinal neurons were recorded in pentobarbital-anesthetized male rats. Graded CED or TED was produced by water inflation (0.1–0.5 ml) of a latex balloon. CED changed activity of 48/219 (22%) neurons; 34 were excited (E), 12 were inhibited (I), and 2 were E-I. CED elicited responses for 18/18 neurons tested after ipsilateral cervical vagotomy, for 12/14 neurons tested after bilateral vagotomy and for 9/11 neurons tested after bilateral vagotomy and C6–C7 spinal cord transection. TED changed activity of 31/190 (16%) neurons (28E, 3 I). Ipsilateral cervical vagotomy abolished TED-evoked responses of 5/12 neurons. Bilateral vagotomy eliminated responses of 2/4 neurons tested, and C6–C7 spinal transection plus bilateral vagotomy eliminated responses of 2/2 neurons. Thus inputs from CED to C1–C2 neurons most likely entered upper cervical dorsal roots, whereas inputs from TED were dependent on vagal pathways and/or sympathetic afferent pathways that entered the thoracic dorsal roots. These results supported a concept that C1–C2 spinal neurons play a role in integrating visceral information from cervical and thoracic esophagus.

Responses and Afferent Pathways of Superficial and Deeper C1–C2 Spinal Cells to Intrapericardial Algogenic Chemicals in Rats

2001 ◽  
Vol 85 (4) ◽  
pp. 1522-1532 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman
Keyword(s):  
Afferent Input ◽  
Vagal Afferents ◽  
Male Rats ◽  
Prostaglandin E ◽  
Joint Movement ◽  
Spinal Neurons ◽  
Afferent Pathways ◽  
Bilateral Vagotomy ◽  
Cardiac Afferents ◽  
Stimulation Of

Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C1–C2spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C1–C2 spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C1–C2 neurons. Extracellular potentials of single C1–C2 neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10− 3 M), bradykinin, histamine, serotonin, and prostaglandin E2(10− 5 M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C1–C2 spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input ( P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C1–C2 spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C6–C7 segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C1–C2 superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.

Inhalation of a pulmonary irritant modulates activity of lumbosacral spinal neurons receiving colonic input in rats

2007 ◽  
Vol 293 (5) ◽  
pp. R2052-R2058 ◽  
Author(s):  
Chao Qin ◽  
Robert D. Foreman ◽  
Jay P. Farber
Keyword(s):  
Afferent Input ◽  
Male Rats ◽  
Ammonia Vapor ◽  
Spinal Neurons ◽  
Afferent Fibers ◽  
Cervical Vagotomy ◽  
Nociceptive Pathway ◽  
Lower Airways ◽  
Increased Activity ◽  
Extracellular Potentials

The purpose of the present study was to determine whether an intraspinal nociceptive pathway from the lungs modulated activity of spinal neurons that also received afferent input from the colon. Extracellular potentials of single lumbosacral (L6–S2) spinal neurons were recorded in pentobarbital-anesthetized, paralyzed, and ventilated male rats. The lower airways and lungs were irritated by injecting ammonia vapor over a 30% NH4OH solution into the inspiratory line of the ventilator (0.5 ml, 20 s). Graded colorectal distension (CRD; 20–60 mmHg, 20 s) was produced by air inflation of a balloon. Inhaled ammonia (IA) altered activity of 31/51 (61%) lumbosacral spinal neurons responding to noxious CRD (60 mmHg, 20 s). In contrast, IA changed activity of 3/30 (10%) spinal neurons with somatic fields that did not respond to colorectal inputs. IA decreased activity of 16/31 (52%) spinal neurons and increased activity of the other 15 neurons with colorectal input. Multiple patterns of viscerovisceral convergent spinal neurons with excitatory and inhibitory responses to CRD and IA were observed; 87% (27/31) of the viscerovisceral convergent neurons also responded to innocuous and/or noxious stimuli of somatic fields. Bilateral cervical vagotomy abolished responses to IA in 2/8 tested neurons, indicating that the remaining 6 neurons had input originating from sympathetic afferent fibers. Rostral C1 spinal transection did not abolish inhibitory responses to IA in 4/4 neurons, but L2 transection eliminated inhibitory responses to IA in 3/3 neurons. These results indicated that irritation of the lower airways modulated activity of lumbosacral spinal neurons with colorectal input. It might contribute to intraspinal cross talk between the colon and lungs.

Responses of Medullary Dorsal Horn Neurons to Corneal Stimulation by CO2 Pulses in the Rat

1999 ◽  
Vol 82 (5) ◽  
pp. 2092-2107 ◽  
Author(s):  
Harumitsu Hirata ◽  
James W. Hu ◽  
David A. Bereiter
Keyword(s):  
Thalamic Nucleus ◽  
Receptive Fields ◽  
Male Rats ◽  
Cervical Cord ◽  
Type I ◽  
Type Ii ◽  
Upper Cervical ◽  
The Difference ◽  
Evoked Activity ◽  
Stimulation Of

Corneal-responsive neurons were recorded extracellularly in two regions of the spinal trigeminal nucleus, subnucleus interpolaris/caudalis (Vi/Vc) and subnucleus caudalis/upper cervical cord (Vc/C1) transition regions, from methohexital-anesthetized male rats. Thirty-nine Vi/Vc and 26 Vc/C1 neurons that responded to mechanical and electrical stimulation of the cornea were examined for convergent cutaneous receptive fields, responses to natural stimulation of the corneal surface by CO2 pulses (0, 30, 60, 80, and 95%), effects of morphine, and projections to the contralateral thalamus. Forty-six percent of mechanically sensitive Vi/Vc neurons and 58% of Vc/C1 neurons were excited by CO2 stimulation. The evoked activity of most cells occurred at 60% CO2 after a delay of 7–22 s. At the Vi/Vc transition three response patterns were seen. Type I cells ( n = 11) displayed an increase in activity with increasing CO2 concentration. Type II cells ( n = 7) displayed a biphasic response, an initial inhibition followed by excitation in which the magnitude of the excitatory phase was dependent on CO2 concentration. A third category of Vi/Vc cells (type III, n = 3) responded to CO2 pulses only after morphine administration (>1.0 mg/kg). At the Vc/C1 transition, all CO2-responsive cells ( n = 15) displayed an increase in firing rates with greater CO2 concentration, similar to the pattern of type I Vi/Vc cells. Comparisons of the effects of CO2 pulses on Vi/Vc type I units, Vi/Vc type II units, and Vc/C1 corneal units revealed no significant differences in threshold intensity, stimulus encoding, or latency to sustained firing. Morphine (0.5–3.5 mg/kg iv) enhanced the CO2-evoked activity of 50% of Vi/Vc neurons tested, whereas all Vc/C1 cells were inhibited in a dose-dependent, naloxone-reversible manner. Stimulation of the contralateral posterior thalamic nucleus antidromically activated 37% of Vc/C1 corneal units; however, no effective sites were found within the ventral posteromedial thalamic nucleus or nucleus submedius. None of the Vi/Vc corneal units tested were antidromically activated from sites within these thalamic regions. Corneal-responsive neurons in the Vi/Vc and Vc/C1 regions likely serve different functions in ocular nociception, a conclusion reflected more by the difference in sensitivity to analgesic drugs and efferent projection targets than by the CO2 stimulus intensity encoding functions. Collectively, the properties of Vc/C1 corneal neurons were consistent with a role in the sensory-discriminative aspects of ocular pain due to chemical irritation. The unique and heterogeneous properties of Vi/Vc corneal neurons suggested involvement in more specialized ocular functions such as reflex control of tear formation or eye blinks or recruitment of antinociceptive control pathways.

Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Single Unit Activity ◽  
Afferent Pathways ◽  
Sympathetic Control ◽  
Stellate Ganglia ◽  
Cervical Vagotomy ◽  
The Mean ◽  
Cardiac Receptors ◽  
Stimulation Of

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.

Chemical Activation of Cervical Cell Bodies: Effects on Responses to Colorectal Distension in Lumbosacral Spinal Cord of Rats

1999 ◽  
Vol 82 (6) ◽  
pp. 3423-3433 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman
Keyword(s):  
Spontaneous Activity ◽  
Chemical Activation ◽  
Male Rats ◽  
Evoked Responses ◽  
Colorectal Distension ◽  
Lumbosacral Spinal Cord ◽  
Cervical Cell ◽  
Upper Cervical ◽  
Excitatory Responses ◽  
Stimulation Of

We have shown that stimulation of cardiopulmonary sympathetic afferent fibers activates relays in upper cervical segments to suppress activity of lumbosacral spinal cells. The purpose of this study was to determine if chemical excitation (glutamate) of upper cervical cell bodies changes the spontaneous activity and evoked responses of lumbosacral spinal cells to colorectal distension (CRD). Extracellular potentials were recorded in pentobarbital-anesthetized male rats. CRD (80 mmHg) was produced by inflating a balloon inserted in the descending colon and rectum. A total of 135 cells in the lumbosacral segments (L6–S2) were activated by CRD. Seventy-five percent (95/126) of tested cells received convergent somatic input from the scrotum, perianal region, hindlimb, and tail; 99/135 (73%) cells were excited or excited/inhibited by CRD; and 36 (27%) cells were inhibited or inhibited/excited by CRD. A glutamate (1 M) pledget placed on the surface of C1–C2 segments decreased spontaneous activity and excitatory CRD responses of 33/56 cells and increased spontaneous activity of 13/19 cells inhibited by CRD. Glutamate applied to C6–C7 segments decreased activity of 10/18 cells excited by CRD, and 9 of these also were inhibited by glutamate at C1–C2 segments. Glutamate at C6–C7 increased activity of 4/6 cells inhibited by CRD and excited by glutamate at C1–C2 segments. After transection at rostral C1 segment, glutamate at C1–C2still reduced excitatory responses of 7/10 cells. Further, inhibitory effects of C6–C7 glutamate on excitatory responses to CRD still occurred after rostral C1transection but were abolished after a rostral C6transection in 4/4 cells. These data showed that C1–C2 cells activated with glutamate primarily produced inhibition of evoked responses to visceral stimulation of lumbosacral spinal cells. Inhibition resulting from activation of cells in C6–C7 segments required connections in the upper cervical segments. These results provide evidence that upper cervical cells integrate information that modulates activity of distant spinal neurons responding to visceral input.

scholarly journals Electrophysiology of Supramedullary Neurons in Spheroides maculatus

1959 ◽  
Vol 43 (1) ◽  
pp. 159-188 ◽  
Author(s):  
M. V. L. Bennett ◽  
S. M. Crain ◽  
H. Grundfest
Keyword(s):  
Action Potential ◽  
Cell Body ◽  
Cranial Nerves ◽  
Dorsal Surface ◽  
Compound Action Potential ◽  
Direct Stimulation ◽  
Afferent Pathways ◽  
Dorsal Roots ◽  
Indirect Stimulation ◽  
Stimulation Of

This series of three papers presents data on a system of neurons, the large supramedullary cells (SMC) of the puffer, Spheroides maculatus, in terms of the physiological properties of the individual cells, of their afferent and efferent connections, and of their interconnections. Some of these findings are verified by available anatomical data, but others suggest structures that must be sought for in the light of the demonstration that these cells are not sensory neurons. Analysis on so broad a scale was made possible by the accessibility of the cells in a compact cluster on the dorsal surface of the spinal cord. Simultaneous recordings were made intracellularly and extracellularly from individual cells or from several, frequently with registration of the afferent or efferent activity as well. The passive and active electrical properties of the SMC are essentially similar to those of other neurons, but various response characteristics have been observed which are related to different excitabilities of different parts of the neuron, and to specific anatomical features. The SMC produce spikes to direct stimuli by intracellular depolarization, or by indirect synaptic excitation from many afferent paths, including tactile stimulation of the skin. Responses that were evoked by intracellular stimulation of a single cell cause an efferent discharge bilaterally in many dorsal roots, but not in the ventral. Sometimes several distinct spikes occurred in the same root, and behaved independently. Thus, a number of axons are efferent from each neuron. They are large unmyelinated fibers which give rise to the elevation of slowest conduction in the compound action potential of the dorsal root. A similar component is absent in the ventral root action potential. Antidromic stimulation of the axons causes small potentials in the cell body, indicating that the antidromic spikes are blocked distantly to the soma, probably in the axon branches. The failure of antidromic invasion is correlated with differences in excitability of the axons and the neurite from which they arise. As recorded in the cell body, the postsynaptic potentials associated with stimulation of afferent fibers in the dorsal roots or cranial nerves are too small to discharge the soma spike. The indirect spike has two components, the first of which is due to the synaptically initiated activity of the neurite and which invades the cell body. The second component is then produced when the soma is fired. The neurite impulse arises at some distance from the cell body and propagates centrifugally as well as centripetally. An indirect stimulus frequently produces repetitive spikes which are observed to occur synchronously in all the cells examined at one time. Each discharge gives rise to a large efferent volley in each of the dorsal roots and cranial nerves examined. The synchronized responses of all the SMC to indirect stimulation occur with slightly different latencies. They are due to a combination of excitation by synaptic bombardment from the afferent pathways and by excitatory interconnections among the SMC. Direct stimulation of a cell may also excite all the others. This spread of activity is facilitated by repetitive direct excitation of the cell as well as by indirect stimulation.

Reflex responses of laryngeal and pharyngeal submucosal glands in dogs

1991 ◽  
Vol 71 (5) ◽  
pp. 1669-1673 ◽  
Author(s):  
M. A. Haxhiu ◽  
N. S. Cherniack ◽  
K. P. Strohl
Keyword(s):  
Intravenous Administration ◽  
Mechanical Stimulation ◽  
Gland Secretion ◽  
Submucosal Gland ◽  
C Fiber ◽  
Cervical Vagotomy ◽  
Bilateral Vagotomy ◽  
Alpha Chloralose ◽  
Irritant Receptors ◽  
Stimulation Of

In dogs tracheal secretion is enhanced reflexly and by locally acting mediators such as substance P (SP). To evaluate the role of these mechanisms on submucosal gland secretion in the larynx (L) and pharynx (Ph), we compared the effects of mechanical stimulation of intrapulmonary irritant receptors and stimulation of pulmonary C-fiber receptors by capsaicin (20 micrograms/kg iv) with the response produced by intravenous SP. In six alpha-chloralose-anesthetized, paralyzed, and artificially ventilated dogs, submucosal gland secretion was monitored by analyzing the areas covered by hillocks of liquid and calculating the volume of secreted liquid (microliter) in the L and Ph. Mechanical stimulation of the carina increased both the number of hillocks and the volume of secreted liquid in the L. Excitation of pulmonary C-fiber receptors also increased the number of hillocks, and total volume of secreted liquid was elevated from 1.9 +/- 0.5 to 8.3 +/- 1.4 microliters (P less than 0.01). These responses were significantly reduced by prior cervical vagotomy and intravenous administration of atropine. Neither stimulation of irritant receptors nor stimulation of pulmonary C-fiber receptors caused discernible effects on Ph submucosal gland secretion. However, intravenous SP increased the number of Ph hillocks and elevated the volume of secreted Ph liquid from 1.0 +/- 0.6 to 10.2 +/- 1 microliters (P less than 0.01); similar responses to intravenous SP were observed in the L. Prior intravenous administration of atropine methylnitrate or bilateral vagotomy did not alter Ph or L secretory responses to intravenous SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Intraesophageal chemicals enhance responsiveness of upper thoracic spinal neurons to mechanical stimulation of esophagus in rats

2008 ◽  
Vol 294 (3) ◽  
pp. G708-G716 ◽  
Author(s):  
Chao Qin ◽  
Jay P. Farber ◽  
Robert D. Foreman
Keyword(s):  
Mechanical Stimulus ◽  
Male Rats ◽  
High Threshold ◽  
Noncardiac Chest Pain ◽  
Thoracic Esophagus ◽  
Spinal Neurons ◽  
Thoracic Spinal ◽  
Study Results ◽  
Excitatory Responses ◽  
Esophageal Hypersensitivity

Esophageal hypersensitivity is one of the most common causes of noncardiac chest pain in patients. In this study, we investigated whether exposure of the esophagus to acid and other chemical irritants affected activity of thoracic spinal neurons responding to esophageal distension (ED) in rats. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital sodium-anesthetized, -paralyzed, and -ventilated male rats. ED (0.2 or 0.4 ml, 20 s) was produced by water inflation of a latex balloon placed orally into the middle thoracic region of the esophagus. The chemicals were administered via a tube that was passed through the stomach and placed in the thoracic esophagus. To irritate the esophagus, 0.2 ml of HCl (0.01 N), bradykinin (10 μg/ml), or capsaicin (10 μg/ml) were injected for 1–2 min. Only neurons excited by ED were included in this study. Results showed that intraesophageal instillation of HCl, bradykinin, and capsaicin increased activity in 3/20 (15%), 7/25 (28%), and 9/20 (45%) neurons but enhanced excitatory responses to ED in 9/17 (53%), 8/15 (53%), and 7/11 (64%) of the remaining spinal neurons, respectively. Furthermore, intraesophageal chemicals were more likely to enhance the responsiveness of low-threshold neurons than high-threshold neurons to the esophageal mechanical stimulus. Normal saline (pH 7.4, 0.2 ml) or vehicle instilled in the esophagus did not significantly affect activity or ED responses of neurons. We conclude that enhanced responses of thoracic spinal neurons to ED by the chemically challenged esophagus may provide a possible pathophysiological basis for visceral hypersensitivity in patients with gastroesophageal reflux and/or esophagitis.

Chemical activation of C1-C2 spinal neurons modulates intercostal and phrenic nerve activity in rats

2004 ◽  
Vol 286 (6) ◽  
pp. R1069-R1076 ◽  
Author(s):  
Fang Lu ◽  
Chao Qin ◽  
Robert D. Foreman ◽  
Jay P. Farber
Keyword(s):  
Phrenic Nerve ◽  
Chemical Activation ◽  
Dorsal Surface ◽  
Male Rats ◽  
Tonic Activity ◽  
Spinal Neurons ◽  
Thoracic Spinal ◽  
Upper Cervical ◽  
N 93 ◽  
Propriospinal Neurons

Chemical activation of upper cervical spinal neurons modulates activity of thoracic respiratory interneurons in rats. The aim of the present study was to examine the effects of chemical activation of C1-C2 spinal neurons on thoracic spinal respiratory motor outflows. Electroneurograms of left phrenic ( n = 23) and intercostal nerves (ICNs, n = 93) between T3 and T8 spinal segments were recorded from 36 decerebrated, vagotomized, paralyzed, and ventilated male rats. To activate upper cervical spinal neurons, glutamate pledgets (1 M, 1 min) were placed on the dorsal surface of the C1-C2 spinal cord. Glutamate on C1-C2 increased ICN tonic activity in 56/59 (95%) ICNs. The average maximal tonic activity of ICN was increased by 174% ( n = 59). After spinal transection at rostral C1, glutamate on C1-C2 still increased ICN tonic activity in 33/35 ICNs. However, the effects of C1-C2 glutamate on ICN phasic activity were highly variable, with observations of augmentation or suppression of both inspiratory and expiratory discharge. C1-C2 glutamate augmented the average amplitude of phrenic burst by 20%, whereas the increases in amplitude of ICN inspiratory activity, when they occurred, averaged 120%. The burst rate of phrenic nerve discharge was decreased from 34.2 ± 1.6 to 26.3 ± 2.0 (mean ± SE) breaths/min during C1-C2 glutamate. These data suggested that upper cervical propriospinal neurons might play a role in descending modulation of thoracic respiratory and nonrespiratory motor activity.

Induction of c-fos expression in spinal neurons by nociceptive and nonnociceptive stimulation of LUT

1993 ◽  
Vol 265 (2) ◽  
pp. R326-R333 ◽  
Author(s):  
L. A. Birder ◽  
W. C. de Groat
Keyword(s):  
Acetic Acid Solution ◽  
Spinal Neurons ◽  
Abdominal Incision ◽  
Afferent Pathways ◽  
Sacral Parasympathetic Nucleus ◽  
Chemical Irritation ◽  
Fos Expression ◽  
Number Of Cells ◽  
Stimulation Of ◽  
Lower Urinary

Expression of c-fos gene in spinal neurons was detected with an immunocytochemical technique to study the spinal processing of nociceptive and nonnociceptive input from the lower urinary tract (LUT) of the urethan-anesthetized rat. Two preparations were used to activate afferent pathways in the LUT: 1) the urinary bladder was exposed through an abdominal incision, and saline or 1% acetic acid solution was infused directly into the bladder lumen and expelled through the urethra; and 2) the bladder was catheterized through the urethra, and the urethral outlet was ligated to allow distension and reflex contractions to occur under isovolumetric conditions. The first preparation mimicked the physiological changes occurring during normal voiding, whereas the second preparation generated high (presumably nociceptive) pressures when the bladder contracted against a closed outlet. The results indicate that distension-induced voiding increased c-fos expression largely in the region of the sacral parasympathetic nucleus (52% of the total number of cells/L6 section) and the dorsal commissure (25% of the total number of cells), whereas nociceptive stimuli markedly increased the number of c-fos-positive cells in the dorsal commissure (3.5 x increase above the number induced by distension, representing 50% of the total number of cells/L6 section). Bladder contractions against a closed outlet elicited a distribution of c-fos-positive cells similar to that induced by chemical irritation. Drugs that suppressed bladder reflexes did not reduce c-fos induced by distension, indicating that voiding reflexes do not contribute to c-fos expression.

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