Supraspinal regulation of spinal reflex discharge into cardiac sympathetic nerves

Coote, John H.; Sato, Akio

doi:10.1016/0006-8993(78)90906-x

Cited by 33 publications

(4 citation statements)

References 30 publications

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“…8). It has been shown that the spinal response in the somato-cardiac sympathetic reflex is tonically inhibited from the brain in CNS-intact cats [17] and in rats [5,18]. It is well known that an innocuous passive movement of the knee joint does not result in any changes in heart rate [2,19], but that a noxious passive movement of the knee joint results in increased cardiac sympathetic nerve activity [1] and heart rate [2] in anesthetized, CNS-intact cats.…”

Section: Discussionmentioning

confidence: 99%

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Nakayama¹,

Suzuki²,

Ito³

2006

J. Physiol. Sci

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Somatic afferent regulation of heart rate by noxious knee joint stimulation has been proven in anesthetized cats to be a reflex response whose reflex center is in the brain and whose efferent arc is a cardiac sympathetic nerve. In the present study we examined whether articular stimulation could influence heart rate by this efferent sympathetic pathway in spinalized rats. In central nervous system (CNS)-intact rats, noxious articular movement of either the knee or elbow joint resulted in an increase in cardiac sympathetic nerve activity and heart rate. However, although in acutely spinalized rats a noxious movement of the elbow joint resulted in a significant increase in cardiac sympathetic nerve activity and heart rate, a noxious movement of the knee joint had no such effect and resulted in only a marginal increase in heart rate. Because this marginal increase was abolished by adrenalectomy suggests that it was due to the release of adrenal catecholamines. In conclusion, the spinal cord appears to be capable of mediating, by way of cardiac sympathetic nerves, the propriospinally induced reflex increase in heart rate that follows noxious stimulation of the elbow joint, but not the knee joint.

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Section: Discussionmentioning

confidence: 99%

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Nakayama¹,

Suzuki²,

Ito³

2006

J. Physiol. Sci

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“…M. TYCE AND T. L. YAKSH spinal processing of nociceptive information (Duggan, 1978;, autonomic (Sato, 1973;Smits, Van Essen & Struyker-Boudrer, 1978;Coote & Sato, 1978;Cabot, Wild & Cohen, 1979) and motor function (Sastry & Sinclair, 1977). Thus, the ionophoretic administration of noradrenaline and serotonin has been shown to exert inhibitory influences on the discharge of dorsal horn neurones (Belcher, Ryall & Schaffner, 1978;Headley, Duggan & Griersmith, 1978).…”

Section: Introductionmentioning

confidence: 99%

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Tyce¹,

Yaksh²

1981

The Journal of Physiology

156

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SUMMARY1. Superfusates taken from spinal cords of cats anaesthetized with chloralose and urethane were assayed for endogenous serotonin and noradrenaline by high-pressure liquid chromatography with electrochemical detection.2. Stimulating the dorsolateral funiculus, caudal to a spinal transaction, enhanced in a frequency-dependent manner the levels of monoamines in the spinal superfusate.3. Tyramine added to the superfusate enhanced the release of noradrenaline and serotonin. 4. In cats with intact neuraxes, stimulation of the sciatic nerve at high, but not low intensities produced a 2-to 3-fold increase in the levels of monoamines in the spinal superfusate. This evoked monoamine efflux was attenuated by cold block of the cervical spinal cord.5. Stimulation of the infraorbital branch of the trigeminal nerve evoked the release of noradrenaline and serotonin from the lumbar cord in animals with intact neuraxes. Cold block of the cervical cord blocked trigeminal-evoked release of lumbar serotonin and noradrenaline.6. That the monoamine efflux was not due to elevations in blood pressure was indicated by the failure of vasoxyl, an a-agonist producing hypertension, to evoke any changes in spinal monoamine levels. 7. The monoamine release was not dependent upon either an opiate-sensitive link or upon the activation of the sympathetic ganglia, because systemic administration of naloxone (an opiate antagonist) and chlorisondamine (a ganglionic blocking agent) failed to antagonize the evoked release of amines.8. These results suggest the existence of a spinopetal monoamine system which is activated by peripheral stimuli. The modulatory influence associated with increasing monoamine tone in the spinal cord clearly indicated that somatic stimuli may activate a descending monoamine pathway which serves to modulate the magnitude of the ascending sensory message.

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“…If the brainstem plays a major role in generating tonic excitatory drive to sympathetic preganglionic neurons, it is reasonable to ask whether it plays a similar role in inhibiting these neurons. Many workers have demonstrated supraspinal inhibition of reflex responses of sympathetic neurons (Coote and Sato, 1978;Coote, 1988;Muller, et al, 1988), and there is evidence that some baroreceptor inhibition may be mediated at spinal levels by descending pathways from supraspinal systems (McCall, et al, 1977;Coote, et al, 1981). Few data support the notion of tonic supraspinal inhibition of sympathetic activity other than Alexander's (1946) observation that sympathetic activity that had been reduced by a lesion that removed the influence of the rostral medulla was slightly increased by subsequent cervical spinal transection.…”

Section: What Is the Evidence For Tonic Supraspinal Inhibition Of Symmentioning

confidence: 99%

Medullo‐Spinal Modulation of Sympathetic Output and Spinal Afferent Input

Schramm

Poree

1991

Cardiovasc electrophysiol

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Associated Inhibition of Sympathetic and Afferent Activities. In intact animals, it is important that most "tonic" sympathetic activity be regulated by brainstem systems that have access to "central commands" from higher centers and to highly specific cranial nerve afferents. The importance of this supraspinal regulation is manifested by severe derangements of sympathetic regulation after spinal cord injury. A major component of these derangements is an exaggerated responsiveness of sympathetic neurons to visceral and somatic afferent activity. Although much is known about medullo-spinal systems that excite sympathetic preganglionic neurons, little is known about those systems that, in intact animals, isolate preganglionic neurons from spinal afferent input. This brief review will consider the evidence that either identical or cospatial medullary systems regulate the output of sympathetic preganglionic neurons and afferent input to the spinal cord. Further, evidence from this laboratory is presented, which indicates that a recently described system in the rostral cervical spinal cord, perhaps in concert with medullary systems, may play an important role in regulating the excitation of sympathetic preganglionic neurons by spinal afferents. (J Cardiovasc Electrophysiol, Vol. 2, Supplement, pp. S18-S25, April 1991) renal sympathetic activity, autonomic hyperreflexia, sensory modulation, cervical spinal cord, rostral ventrolateral medulla

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Supraspinal regulation of spinal reflex discharge into cardiac sympathetic nerves

Cited by 33 publications

References 30 publications

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

The Articulo-Cardiac Sympathetic Reflex in Spinalized, Anesthetized Rats

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Medullo‐Spinal Modulation of Sympathetic Output and Spinal Afferent Input

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