Substance P in traumatic brain injury

Donkin, James; Turner, Renée J.; Hassan, Islam; Vink, Robert

doi:10.1016/s0079-6123(06)61007-8

Cited by 66 publications

(59 citation statements)

References 123 publications

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“…37,126 When administered after TBI, substance P antagonists reduce blood-brain barrier permeability, reduce edema, decrease axonal injury, enhance neuronal survival, and improve both motor and cognitive outcome. 127 As with bradykinin, there is significant interest in developing nonpeptide antagonists of substance P for use in treating TBI.…”

Section: Kinin Antagonistsmentioning

confidence: 99%

Multifunctional Drugs for Head Injury

2009

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Summary: Traumatic brain injury (TBI) remains one of the leading causes of mortality and morbidity worldwide in individuals under the age of 45 years, and, despite extensive efforts to develop neuroprotective therapies, there has been no successful outcome in any trial of neuroprotection to date. In addition to recognizing that many TBI clinical trials have not been optimally designed to detect potential efficacy, the failures can be attributed largely to the fact that most of the therapies investigated have been targeted toward an individual injury factor. The contemporary view of TBI is that of a very heterogenous type of injury, one that varies widely in etiology, clinical presentation, severity, and pathophysiology. The mechanisms involved in neuronal cell death after TBI involve an interaction of acute and delayed anatomic, molecular, biochemical, and physiological events that are both complex and multifaceted. Accordingly, neuropharmacotherapies need to be targeted at the multiple injury factors that contribute to the secondary injury cascade, and, in so doing, maximize the likelihood of a successful outcome. This review focuses on a number of such multifunctional compounds that have shown considerable success in experimental studies and that show maximum promise for success in clinical trials.

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Section: Kinin Antagonistsmentioning

confidence: 99%

Multifunctional Drugs for Head Injury

2009

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“…This time period is a critical window for interrupting secondary injury mechanisms (Kawamata and Katayama, 2007). Cerebral edema formation is due in part to neurogenic inflammatory mechanisms in which the release of substance P, a potent long-lasting vasoactive tachykinin, is believed to be the predominant mediator (Donkin et al, 2007(Donkin et al, , 2009. Substance P antagonists are currently proposed as a therapeutic approach for TBI (Vink and van den Heuvel, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies have shown that activated sensory fibers release substance P perivascularly, which then subsequently binds to local glial and neuronal cells (Black, 2002;Donkin et al, 2009;Marriott and Bost, 1998;Severini et al, 2002). Substance P is a potent vasogenic neuropeptide from the tachykinin family that is released as a result of mechanical, chemical, and electrical stimulation of sensory neuron C-fibers (Black, 2002;Donkin et al, 2007;Severini et al, 2002). Cerebral and meningeal blood vessels receive a dense supply of sensory afferents that release substance P when stimulated, whereby changes in blood flow and intracranial pressure promote its release.…”

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confidence: 99%

“…For instance, there is a significant amount of data implicating substance P as a primary mediator of gliosis. The importance of substance P in regulating gliosis in the injured CNS by mediating microglial and astrocyte activation and the release of proinflammatory mediators such as cytokines, prostaglandins, thromboxane B 2 , and superoxide ions, cannot be overlooked (Black, 2002;Donkin et al, 2007;Palma et al, 1997). Substance P receptors are found on non-neuronal cells, including astrocytes, lymphocytes, leukocytes, macrophages, and mast cells.…”

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confidence: 99%

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Acute Effects of a Selective Cannabinoid-2 Receptor Agonist on Neuroinflammation in a Model of Traumatic Brain Injury

Elliott

Tuma

Amenta

et al. 2011

Journal of Neurotrauma

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“…NGF was shown to increase the synthesis of the tachykinin substance P (SP) in airway sensory nerves (20)(21)(22). SP is released by primary afferent C-fibers (23,24), mediating both the airway hyperresponsiveness (25) and neurogenic inflammation (26,27) associated with exposure to O 3 .…”

mentioning

confidence: 99%

Role of Nerve Growth Factor in Ozone-Induced Neural Responses in Early Postnatal Airway Development

Hunter¹,

Carrell-Jacks²,

Batchelor³

et al. 2011

Am J Respir Cell Mol Biol

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Airway neural plasticity contributes to the process of airway remodeling in response to airway irritants. However, the mechanisms of neural remodeling in the airways during the early postnatal period, when responses to airway irritation may be most sensitive, have not been characterized. This study used a rat model to examine a possible mechanism of ozone (O 3 )-induced neural hyperresponsiveness during a critical period of developmental, postnatal day (PD) 6, that may be mediated by the neurotrophin nerve growth factor (NGF), resulting in an enhanced release of inflammatory neuropeptide substance P (SP) from airway nerves. Rat pups between PD6-PD28 were killed 24 hours after exposure to O 3 (2 ppm, 3 hours) or filtered air (FA), to establish a timeline of NGF synthesis, or else they were exposed to O 3 or NGF on PD6 or PD21 and re-exposed to O 3 on PD28, and killed on PD29. Measurement endpoints included NGF mRNA in tracheal epithelial cells, NGF protein in bronchoalveolar lavage fluid, airway SP-nerve fiber density (NFD), and SP-positive airway neurons in vagal ganglia. Acute exposure to O 3 increased NGF in bronchoalveolar lavage fluid on PD10 and PD15, and mRNA expression in epithelial cells on PD6, compared with FA controls. NGF protein and mRNA expression in the O 3 -PD6/O 3 -PD28 groups were significantly higher than in the O 3 -PD21/O 3 -PD28 and O 3 -PD6/FA-PD28 groups. NGF-PD6/O 3 -PD28 increased the SP innervation of airway smooth muscle and SP-positive sensory neurons, compared with the NGF-PD21/O 3 -PD28 or NGF-PD6/FA-PD28 groups. NGF enhanced sensory innervation, which may mediate acute responses or prolong sensitivity to O 3 during early life. The model may be relevant in O 3 responses during early childhood.

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Substance P in traumatic brain injury

Cited by 66 publications

References 123 publications

Multifunctional Drugs for Head Injury

Multifunctional Drugs for Head Injury

Acute Effects of a Selective Cannabinoid-2 Receptor Agonist on Neuroinflammation in a Model of Traumatic Brain Injury

Role of Nerve Growth Factor in Ozone-Induced Neural Responses in Early Postnatal Airway Development

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