Interaction of descending spinal sympathetic pathways and afferent nerves

1978 ◽  
Vol 234 (3) ◽  
pp. H223-H229
Author(s):  
S. M. Barman ◽  
R. D. Wurster
Keyword(s):  
Nerve Fibers ◽  
Nerve Activity ◽  
Afferent Nerves ◽  
Afferent Nerve Fibers ◽  
Somatosympathetic Reflex ◽  
Reflex Activation ◽  
Dorsolateral Funiculus ◽  
Ventrolateral Funiculus ◽  
Stimulation Of ◽  
Excitatory Pathway

With the use of computer-aided techniques, the interaction of descending spinal sympathetic pathways and afferent nerve fibers (cervical dorsal roots and tibial nerve) in regulation of thoracic (T2) preganglionic nerve activity was investigated in anesthetized, vagotomized, and paralyzed cats. High-frequency activation of a sympathoinhibitory pathway (ventrolateral funiculus) depressed the evoked discharges in the T2 preganglionic nerve elicited by stimulation of a sympathoexcitatory pathway (dorsolateral funiculus) and the spinal component of the somatosympathetic reflex. Submaximal evoked responses were also inhibited through baroreceptor reflex activation (blood pressure elevations up to 225 mmHg). Facilitation of the spinal component of the somatosympathetic reflex occurred during stimulation of the excitatory pathway. Carotid occlusion (baroreceptor inactivation) facilitated the submaximal evoked discharges from stimulation of the descending excitatory pathway. These data support the contention that sympathetic nerve activity can be modified by the integration of excitatory and inhibitory impulses at the spinal level.

Excitation of cardiac sympathetic afferent nerves: effects on renal function

1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver
Keyword(s):  
Renal Function ◽  
Chemical Stimulation ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Stimulation Of

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.

Facilitatory role of efferent renal nerve activity on renal sensory receptors

1987 ◽  
Vol 253 (4) ◽  
pp. F767-F777 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith ◽  
G. F. DiBona
Keyword(s):  
Superior Vena ◽  
Isotonic Saline ◽  
Vena Cava ◽  
Urinary Sodium Excretion ◽  
Nerve Fibers ◽  
Facilitatory Effect ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Stimulation Of

The effects of decreasing and increasing efferent renal nerve activity (ERNA) on the renorenal reflex responses to stimulation of renal mechanoreceptors (MR) (increased ureteral pressure) or renal chemoreceptors (CR) (retrograde ureteropelvic perfusion with 0.9 M NaCl) were examined in anesthetized rats. During prevailing ERNA, renal MR stimulation increased ipsilateral afferent renal nerve activity (ARNA) from 6 to 41 counts/s (spike counter) (n = 37) and from 2 to 6 resets/min, (voltage integrator) (n = 23), contralateral urine flow rate from 5.3 to 7.4 microliters . min-1 . g-1 (n = 38) and urinary sodium excretion from 0.7 to 1.1 mumol . min-1 . g-1 (n = 38) (all P less than 0.01), without affecting mean arterial pressure or contralateral glomerular filtration rate. Similar results were obtained with renal CR stimulation. Decreasing ERNA 74+/- 4% by hexamethonium, 10% body weight isotonic saline volume expansion, or inflation of a balloon at the junction of right atria and superior vena cava abolished the increase in ipsilateral ARNA and the contralateral diuresis and natriuresis produced by stimulation of renal MR or CR. Increasing ERNA 254+/- 120% (peak response, n = 15, P less than 0.01) by placing the rat's tail in 53 degrees C water increased basal ARNA 249+/- 80% (n = 6, P less than 0.05) and enhanced the ipsilateral ARNA response 202+/- 78% (n = 9, P less than 0.01) to renal MR stimulation. These results indicate that ERNA exerts a facilitatory effect on renal MR and CR and their afferent renal nerve fibers in the renorenal reflexes.

Fos induction in rat brain neurons after stimulation of the hepatoportal Na-sensitive mechanism

1997 ◽  
Vol 272 (3) ◽  
pp. R913-R923 ◽  
Author(s):  
H. Morita ◽  
Y. Yamashita ◽  
Y. Nishida ◽  
M. Tokuda ◽  
O. Hatase ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Area Postrema ◽  
Vena Cava ◽  
Plasma Osmolality ◽  
Systemic Circulation ◽  
Afferent Nerve ◽  
Hypothalamic Nucleus ◽  
Nerve Activity ◽  
Afferent Nerves ◽  
Stimulation Of

Responses of hepatic afferent nerves to intraportal bolus injection of hypertonic solutions were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to an intraportal injection of 0.75 M NaCl or NaHCO3 but did not respond to a similar injection of 1.5 M mannitol, 0.75 M LiCl, or 0.15 M NaCl, implying that nerves in the hepatoportal area are sensitive to increases in Na concentrations and that this leads to stimulation of hepatic afferent nerve activity. To study central activation in response to stimulation of the hepatic Na-sensitive mechanism, c-fos induction was monitored. After electrical stimulation of hepatic afferent nerves, neurons containing Fos-like immunoreactivity (Fos-li) were found in the area postrema, nucleus of the solitary tract, paraventricular hypothalamic nucleus, and supraoptic nucleus at 90 min after stimulation. Induction of Fos-li was also studied after simultaneous infusion of 0.45 M NaCl into the portal vein and distilled water into the inferior vena cava in conscious rats so as to keep the total amount of solution introduced into the systemic circulation isotonic, thus avoiding changes in mean arterial pressure, plasma osmolality, and plasma NaCl concentrations. Fos-li-containing neurons were found in the same regions in which they were found after electrical stimulation. However, few, if any, Fos-li-containing cells were found if the rats were hepatically denervated or if they received an intraportal infusion of hypertonic LiCl or mannitol. These data provide evidence for involvement of the brain stem and forebrain structures in NaCl regulatory functions induced by stimulation of the hepatoportal Na-sensitive mechanism. However, stimulation of the hepatoportal osmosensitive mechanism does not activate these central structures.

Recovery of phrenic activity and ventilation after cervical spinal hemisection in rats

2006 ◽  
Vol 100 (3) ◽  
pp. 800-806 ◽  
Author(s):  
David D. Fuller ◽  
Francis J. Golder ◽  
E. B. Olson ◽  
Gordon S. Mitchell
Keyword(s):  
Electrical Stimulation ◽  
Action Potentials ◽  
Minute Ventilation ◽  
Nerve Activity ◽  
Time Points ◽  
Phrenic Motoneurons ◽  
Ventrolateral Funiculus ◽  
Barometric Plethysmography ◽  
Stimulation Of ◽  
Spinal Hemisection

We tested two hypotheses: 1) that the spontaneous enhancement of phrenic motor output below a C2 spinal hemisection (C2HS) is associated with plasticity in ventrolateral spinal inputs to phrenic motoneurons; and 2) that phrenic motor recovery in anesthetized rats after C2HS correlates with increased capacity to generate inspiratory volume during hypercapnia in unanesthetized rats. At 2 and 4 wk post-C2HS, ipsilateral phrenic nerve activity was recorded in anesthetized, paralyzed, vagotomized, and ventilated rats. Electrical stimulation of the ventrolateral funiculus contralateral to C2HS was used to activate crossed spinal synaptic pathway phrenic motoneurons. Inspiratory phrenic burst amplitudes ipsilateral to C2HS were larger in the 4- vs. 2-wk groups ( P < 0.05); however, no differences in spinally evoked compound phrenic action potentials could be detected. In unanesthetized rats, inspiratory volume and frequency were quantified using barometric plethysmography at inspired CO2 fractions between 0.0 and 0.07 (inspired O2 fraction 0.21, balance N2) before and 2, 3, and 5 wk post-C2HS. Inspiratory volume was diminished, and frequency enhanced, at 0.0 inspired CO2 fraction ( P < 0.05) 2-wk post-C2HS; further changes were not observed in the 3- and 5-wk groups. Inspiratory frequency during hypercapnia was unaffected by C2HS. Hypercapnic inspiratory volumes were similarly attenuated at all time points post-C2HS ( P < 0.05), thereby decreasing hypercapnic minute ventilation ( P < 0.05). Thus increases in ipsilateral phrenic activity during 4 wk post-C2HS have little impact on the capacity to generate inspiratory volume in unanesthetized rats. Enhanced crossed phrenic activity post-C2HS may reflect plasticity associated with spinal axons not activated by our ventrolateral spinal stimulation.

Depression of Nociceptive Sensory Activity in the Rat Spinal Cord Due to the Intrathecal Administration of Drugs: Effect of Diazepam

Neurosurgery ◽  
1984 ◽  
Vol 15 (6) ◽  
pp. 917-920 ◽  
Author(s):  
Ilmar Jurna
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Spinal Reflexes ◽  
Sensory Response ◽  
Motor Responses ◽  
Afferent Nerve Fibers ◽  
C Fiber ◽  
Stimulation Of

Abstract The intrathecal (i.t.) administration of morphine inhibits nociceptive motor responses and activity in ascending axons evoked by stimulation of nociceptive afferent nerve fibers (nociceptive sensory response) in the rat. The i.t. administration of cholecystokinin octapeptide and ceruletide inhibits nociceptive motor responses, but does not affect ascending nociceptive activity. This shows that drug-induced depression of nociceptive motor responses is not always associated with depression of the nociceptive sensory response of the spinal cord. The microiontophoretic application of substance P excites single dorsal horn neurons that respond to noxious stimulation, whereas the i.t. administration of substance P inhibits both nociceptive motor and sensory responses. Thus, the results obtained from the i.t. administration of a drug may differ from those obtained from its application to single spinal neurons. Diazepam inhibits spinal reflexes and may reduce pain sensation in humans. To assess whether a spinal action is involved in the pain-relieving effect of diazepam, experiments were carried out on spinalized rats in which activity evoked by the stimulation of nociceptive and nonnociceptive afferent nerve fibers of the sural nerve was recorded from single ascending axons below the site of spinal cord transection. Diazepam, 20 ųg i.t., reduced activity evoked by afferent A delta and C fiber stimulation and by stimulation of afferent A beta fibers. The depressant effect caused by diazepam, 2 mg/kg i.v., on C fiber-evoked ascending activity was reduced by the i.t. injection of the benzodiazepine antagonist, Ro 15-1788 (40 ųg), an imidazodiazepine. It is concluded that the depression by diazepam of C fiber-evoked ascending activity contributes to pain relief caused by the drug.

Characterization of midline medulla role in the trigeminal depressor response

1989 ◽  
Vol 256 (5) ◽  
pp. R1111-R1120 ◽  
Author(s):  
M. E. Clement ◽  
R. B. McCall
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Depressor Response ◽  
Reflex Activation ◽  
Stimulation Of

The purpose of the present investigation was to determine the role of the midline medulla in mediating the trigeminal depressor response. Previously we found that lesions of the midline medulla abolished the decrease in blood pressure resulting from electrical stimulation of the spinal trigeminal complex. Electrical stimulation (5 Hz) of the spinal trigeminal tract elicited a decrease in arterial blood pressure that was associated with an inhibition of sympathetic nerve activity recorded from the inferior cardiac nerve of anesthetized cats. The effect of single shocks applied to the trigeminal complex on sympathetic activity was determined using computer-averaging techniques. Single shock stimulation consistently elicited an excitation of sympathetic activity that was followed by an inhibition of sympathetic nerve discharge. The gamma-aminobutyric acid antagonist picrotoxin blocked the depressor response elicited by electrical stimulation of the midline medulla but not by stimulation of the spinal trigeminal complex. Extracellular recordings of the discharges of midline medullary neurons were made to determine the effects of trigeminal stimulation on sympathoinhibitory, sympathoexcitatory, and serotonin neurons. Sympathoinhibitory and sympathoexcitatory neurons were identified by the relationship between unitary discharges and sympathetic nerve activity and by their response to baroreceptor reflex activation. Serotonin (5-HT) neurons were identified using criteria previously developed in our laboratory. These included 1) a slow regular discharge rate, 2) sensitivity to the inhibitory action of the 5-HT1A agonist 8-OH 8-hydroxy-2-(di-n-propylamino)tetralin, 3) failure to respond to baroreceptor reflex activation, and 4) the discharges of the 5-HT neurons were not related to sympathetic activity. Stimulation of the spinal trigeminal complex typically inhibited the discharges of sympathoinhibitory neurons. In contrast, stimulation of the trigeminal complex consistently excited both sympathoexcitatory and 5-HT neurons. These results are discussed in relationship to the role of the midline medulla in mediating the trigeminal depressor response.

Sign in / Sign up

Export Citation Format

Share Document