Tonic descending inhibition of the spinal somato-sympathetic reflex from the lower brain stem

Dembowsky, Klaus; Czachurski, J.; Amendt, Klaus; Seller, H.

doi:10.1016/0165-1838(80)90043-0

Cited by 56 publications

(21 citation statements)

References 61 publications

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“…This episodic hypertension can result in debilitating headaches, seizures, strokes, and even death. After severe SCI, the loss of supraspinal inhibitory influences (Dembowsky et al, 1980) permits unchecked activity of spinal reflexes to produce autonomic dysreflexia. These exaggerated reflexes begin within weeks of SCI and are caused by any stimulation of the skin, muscle, or organs (Mathias and Frankel, 1992).…”

Section: Discussionmentioning

confidence: 99%

Transient Blockade of the CD11d/CD18 Integrin Reduces Secondary Damage after Spinal Cord Injury, Improving Sensory, Autonomic, and Motor Function

Gris¹,

Marsh²,

Oatway³

et al. 2004

J. Neurosci.

303

270

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The early inflammatory response to spinal cord injury (SCI) causes significant secondary damage. Strategies that nonselectively suppress inflammation have not improved outcomes after SCI, perhaps because inflammation has both adverse and beneficial effects after SCI. We have shown that the selective, time-limited action of a monoclonal antibody (mAb) to the CD11d subunit of the CD11d/CD18 integrin, delivered intravenously during the first 48 hr after SCI in rats, markedly decreases the infiltration of neutrophils and delays the entry of hematogenous monocyte-macrophages into the injured cord. We hypothesized that this targeted strategy would lead to neuroprotection and improved neurological outcomes. In this study the development of chronic pain was detected in rats by assessing mechanical allodynia on the trunk and hindpaws 2 weeks to 3 months after a clinically relevant clip-compression SCI at the twelfth thoracic segment. The anti-CD11d mAb treatment reduced this pain by half. Motor performance also improved as rats were able to plantar-place their hindpaws and use them for weight support instead of sweeping movements only. Improved cardiovascular outcome was shown after SCI at the fourth thoracic segment by significant decreases in autonomic dysreflexia. Locomotor performance was also improved. These functional changes correlated with significantly greater amounts and increased organization of myelin and neurofilament near the lesion. The improved neurological recovery after the specific reduction of early inflammation after SCI demonstrates that this selective strategy increases tissue at the injury site and improves its functional capacity. This early neuroprotective treatment would be an ideal foundation for building later cell-based therapies.

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Section: Discussionmentioning

confidence: 99%

Transient Blockade of the CD11d/CD18 Integrin Reduces Secondary Damage after Spinal Cord Injury, Improving Sensory, Autonomic, and Motor Function

Gris¹,

Marsh²,

Oatway³

et al. 2004

J. Neurosci.

303

270

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“…Sympathetic activation generated by SSR originates from both spinal and supraspinal levels (4, 45). In anesthetized animals, the shortlatency spinal SSR is rarely observed due to tonic suppression by descending supraspinal inputs from several sources, including the RVLM and A5 and A6 regions (10,11,19,55). With an intact neuraxis, the SSR is generated wholly by supraspinal inputs dependent on RVLM circuitry (38).…”

mentioning

confidence: 99%

Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Burke

Neale

Korim

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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To determine the organization of presympathetic vasomotor drive by phenotypic populations of rostral ventrolateral medulla (RVLM) neurons, we examined the somatosympathetic reflex (SSR) evoked in four sympathetic nerves together with selective lesions of RVLM presympathetic neurons. Urethane-anesthetized (1.3 g/kg ip), paralyzed, vagotomized and artificially ventilated Sprague-Dawley rats (n = 41) were used. First, we determined the afferent inputs activated by sciatic nerve (SN) stimulation at graded stimulus intensities (50 sweeps at 0.5-1 Hz, 1-80 V). Second, we recorded sympathetic nerve responses (cervical, renal, splanchnic, and lumbar) to intensities of SN stimulation that activated A-fiber afferents (low) or both A- and C-fiber afferents (high). Third, with low-intensity SN stimulation, we examined the cervical SSR following RVLM microinjection of somatostatin, and we determined the splanchnic SSR in rats in which presympathetic C1 neurons were lesioned following intraspinal injections of anti-dopamine-β-hydroxylase-saporin (anti-DβH-SAP). Low-intensity SN stimulation activated A-fiber afferents and evoked biphasic responses in the renal, splanchnic, and lumbar nerves and a single peak in the cervical nerve. Depletion of presympathetic C1 neurons (59 ± 4% tyrosine hydroxylase immunoreactivity profiles lesioned) eliminated peak 2 of the splanchnic SSR and attenuated peak 1, suggesting that only RVLM neurons with fast axonal conduction were spared. RVLM injections of somatostatin abolished the single early peak of cervical SSR confirming that RVLM neurons with fast axonal conduction were inhibited by somatostatin. It is concluded that unmyelinated RVLM presympathetic neurons, presumed to be all C1, innervate splanchnic, renal, and lumbar but not cervical sympathetic outflows, whereas myelinated C1 and non-C1 RVLM neurons innervate all sympathetic outflows examined. These findings suggest that multiple levels of neural control of vasomotor tone exist; myelinated populations may set baseline tone, while unmyelinated neurons may be recruited to provide actions at specific vascular beds in response to distinct stressors.

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“…These axons are responsible for tonic inhibition of the spinal component of the somato-sympathetic reflex (Dembowsky, Czachurski, Amendt & Seller, 1980) and may also be the path of inhibition of purely visceral reflexes (Muller, Dembowsky, Czachurski & Seller, 1988). Electrical stimulation of the dorsolateral funiculus causes a reduction in blood pressure and in sympathetic nerve activity after, but not before, spinal cord transection (Coote & Macleod, 1974;Schramm & Chornoboy, 1982;Schramm & Livingstone, 1987).…”

Section: Discussionmentioning

confidence: 99%

Evidence for descending tonic inhibition specifically affecting sympathetic pathways to the kidney in rats.

Hayes¹,

Yardley²,

Weaver³

1991

The Journal of Physiology

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SUMMARY1. The present study investigated the possibility that pre-and postganglionic neurones innervating the kidney and spleen in rats are affected by descending inhibitory as well as descending excitatory influences. This hypothesis was tested by comparing the effects of cervical spinal cord transection to the effects of blockade of tonic activity of excitatory neurones in the rostral ventrolateral medulla (RVLM).2. Electrical discharge of multifibre postganglionic renal and splenic and preganglionic greater splanchnic nerves and 13th thoracic (T13) white rami was recorded in artificially respired, urethane-anaesthetized rats. In one group of rats, descending supraspinal pathways were interrupted by cervical spinal cord transection. In another group, tonic activity of rostral ventrolateral medulla (RVLM) neurones was blocked by bilateral microinjections of the inhibitory amino acid glycine. The effects of spinal cord transection were compared to effects of this bilateral RVLM blockade and to effects of unilateral RVLM blockade described in a previous study.3. Spinal cord transection caused decreases in preganglionic greater splanchnic and postganglionic splenic nerves which were of the same magnitude as those caused by bilateral blockade of the RVLM.4. In contrast, discharge of renal nerves was decreased more by bilateral RVLM blockade than by cervical spinal cord transection. Similarly, even unilateral RVLM blockade caused greater decreases in discharge of T13 white rami than were caused by spinal cord transection.5. These findings suggest that renal nerves and their preganglionic inputs (T13 white rami) are controlled in part by tonic sympathoinhibitory influences which can be unmasked by blockade of the RVLM. These sympathoinhibitory influences do not appear to affect the activity of splanchnic and splenic nerves.

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Tonic descending inhibition of the spinal somato-sympathetic reflex from the lower brain stem

Cited by 56 publications

References 61 publications

Transient Blockade of the CD11d/CD18 Integrin Reduces Secondary Damage after Spinal Cord Injury, Improving Sensory, Autonomic, and Motor Function

Transient Blockade of the CD11d/CD18 Integrin Reduces Secondary Damage after Spinal Cord Injury, Improving Sensory, Autonomic, and Motor Function

Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Evidence for descending tonic inhibition specifically affecting sympathetic pathways to the kidney in rats.

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