Localization and changes of substance P in spinal cord of paraplegic cats

Naftchi, N. E.; Abrahams, S.; Paul, Helene; Lowman, Edward W.; Scholosser, W.

doi:10.1016/0006-8993(78)90335-9

Cited by 47 publications

(12 citation statements)

References 16 publications

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“…It was reasoned that if functional restoration were to occur in the central nervous system (CNS), it was essential to reestablish the fluiddynamic state of the cell membranes. As already mentioned, a significant part of the architecture of descending (1,2,5) and ascending (6) pathways remains intact. We postulated that a specific agonist might provide the appropriate signal or stimulus to its own membrane receptors on the descending or ascending tracts and serve as a guide for nerve tracts to grow along their genetically regulated paths.…”

mentioning

confidence: 76%

“…In contrast to monoaminergic descending pathways, substance P (SP)-containing fibers in the spinal cord represent ascending spinal tracts; SP accumulates below the lesion level (6). Therefore, after chordotomy, the axons of descend- ing and ascending neurons from the cells of origin to the site of the lesion remain biologically and functionally viable.…”

mentioning

confidence: 99%

“…At my laboratory we have investigated membrane pathology in the traumatically injured spinal cords of cats, using physiological, biochemical (3,5), immunocytochemical (6), and light microscopic, scanning, and transmission electron microscopic (7) techniques. We have also examined the pathology from the standpoint of lipid-free radical damage to neuronal membranes (7).…”

mentioning

confidence: 99%

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Functional Restoration of the Traumatically Injured Spinal Cord in Cats by Clonidine

Naftchi

1982

Science

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The long-term, chronic, paralysis resulting from spinal cord injury in the cat has been reversed by the use of an alpha 2-adrenergic receptor agonist, clonidine. Administration of this drug resulted in "normalization" of sensory-motor and autonomic dysfunctions. Preliminary studies of the clonidine in humans with traumatically injured spinal cord indicate that autonomic dysreflexia can be controlled and spasticity minimized. The data suggest that biochemical and pharmacologic manipulation of receptors may ameliorate paralysis following traumatic injury to the spinal cord as well as to the brain and brainstem.

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mentioning

confidence: 76%

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confidence: 99%

mentioning

confidence: 99%

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Functional Restoration of the Traumatically Injured Spinal Cord in Cats by Clonidine

Naftchi

1982

Science

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“…Immunoreactivity for substance P (SP) as well as calcitonin gene-related peptide (CGRP) increases in nerve fibres in the dorsal horn and LL V-VII region at the thoracic and lumbar levels after spinal cord transection (Naftchi et al 1978;Cassam et al 1997;Krenz and Weaver 1998). An overabundance of SP and CGRP, either as the result of increased expression or neurite sprouting, may enhance the response of dorsal horn and LL V-VII neurones to noxious and innocuous stimulation (Biella et al 1991;Neugebauer et al 1996) and could contribute to increased excitatory neurotransmission and Fos expression.…”

Section: Discussionmentioning

confidence: 98%

Increased spinal expression of c-Fos following stimulation of the lower urinary tract in chronic spinal cord-injured rats

Callsen-Cencic

Mense

1999

Histochemistry and Cell Biology

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c-Fos expression was studied in the lumbar and sacral spinal cord regions involved in processing afferent input from the lower urinary tract and a comparison was made between spinal cord-injured (SCI) animals and control animals with intact neuraxes. Afferent pathways from the lower urinary tract were activated either by insertion of a catheter through the urethra into the urinary bladder or by catheterisation plus induction of reflex micturition contractions by intravesical saline infusion. Placement of a catheter alone elicited Fos expression in a similar number of neurones in SCI and control rats mainly in the medial dorsal horn (MDH) and dorsal commissure (DCM) in the segments L1-2 and L5-S1 with a maximum in L5. Additional saline infusion induced low-frequency, high-amplitude, rhythmic bladder contractions of long duration in the rats with intact spinal cords, whereas in SCI rats, bladder distension elicited reflex contractions at a higher frequency, smaller amplitude and shorter duration. However, the basal and mean bladder pressure, as well as the total contraction time relative to the whole recording time, was not significantly different. Distension-induced bladder contractions markedly increased Fos expression primarily in the spinal segments L5-S1 in the control rats, where the majority of bladder and urethral afferent fibres terminates. Fos-positive cells were located in the MDH, lateral dorsal horn (LDH), DCM and the lateral aspect of laminae V-VII. Compared to controls, Fos expression after spinal cord injury (SCI) occurred in a significantly greater number of neurones throughout the segments L3-S1 following induction of bladder reflexes. The greatest proportional increase in the number of Fos-positive cells occurred in L3-5 which normally receive only little afferent input from the urinary bladder. Cell numbers predominantly increased in the LDH and lateral lamina V-VII. The data are consistent with the concept of a neuroplastic reorganisation of spinal pathways after SCI. Unmasking of silent synapses or formation of new connections by afferent axonal sprouting caudal to the lesion, as evident from the increased numbers of cells expressing Fos after bladder distension, could be factors underlying the emergence of reflexogenic micturition in chronic SCI rats.

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“…Therefore, the modulation of SP following trauma to the spinal cord may occur throughout the entire CNS. There was also an increase in SP evident following T12 transection of the spinal cord in female cats [153]. In contrast, a weight drop model of trauma in rodents resulted in decreased SP at the site of injury [154].…”

Section: Traumatic Spinal Cord Injurymentioning

confidence: 99%

Blocking Neurogenic Inflammation for the Treatment of Acute Disorders of the Central Nervous System

Lewis

Turner

Vink

2013

International Journal of Inflammation

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Classical inflammation is a well-characterized secondary response to many acute disorders of the central nervous system. However, in recent years, the role of neurogenic inflammation in the pathogenesis of neurological diseases has gained increasing attention, with a particular focus on its effects on modulation of the blood-brain barrier BBB. The neuropeptide substance P has been shown to increase blood-brain barrier permeability following acute injury to the brain and is associated with marked cerebral edema. Its release has also been shown to modulate classical inflammation. Accordingly, blocking substance P NK1 receptors may provide a novel alternative treatment to ameliorate the deleterious effects of neurogenic inflammation in the central nervous system. The purpose of this paper is to provide an overview of the role of substance P and neurogenic inflammation in acute injury to the central nervous system following traumatic brain injury, spinal cord injury, stroke, and meningitis.

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Localization and changes of substance P in spinal cord of paraplegic cats

Cited by 47 publications

References 16 publications

Functional Restoration of the Traumatically Injured Spinal Cord in Cats by Clonidine

Functional Restoration of the Traumatically Injured Spinal Cord in Cats by Clonidine

Increased spinal expression of c-Fos following stimulation of the lower urinary tract in chronic spinal cord-injured rats

Blocking Neurogenic Inflammation for the Treatment of Acute Disorders of the Central Nervous System

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