The role of substance P in epilepsy and seizure  disorders

Wang, Xue Feng; Ge, Tongtong; Fan, Jie; Yang, Wei; Cui, Ran

doi:10.18632/oncotarget.20606

Cited by 16 publications

(9 citation statements)

References 90 publications

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“…The PNS and CNS neurons as well as resident satellite glia, microglia, and astrocytes can also produce inflammatory mediators, including pro-inflammatory cytokines and chemokines, neuropeptides and reactive oxygen species. The release of neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) by activated primary sensory neurons has been shown to have paracrine effects on immune cells and can increase the inflammation and subsequently amplify the itch sensation [122,123]. The same localized immune activation can be mimicked after viral infection of PNS neurons.…”

Section: The Immune Mechanisms Of Prv-induced Neuropathic Itchmentioning

confidence: 99%

The Neuropathic Itch Caused by Pseudorabies Virus

Laval

Enquist

2020

Pathogens

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Pseudorabies virus (PRV) is an alphaherpesvirus related to varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV1). PRV is the causative agent of Aujeskzy’s disease in swine. PRV infects mucosal epithelium and the peripheral nervous system (PNS) of its host where it can establish a quiescent, latent infection. While the natural host of PRV is the swine, a broad spectrum of mammals, including rodents, cats, dogs, and cattle can be infected. Since the nineteenth century, PRV infection is known to cause a severe acute neuropathy, the so called “mad itch” in non-natural hosts, but surprisingly not in swine. In the past, most scientific efforts have been directed to eradicating PRV from pig farms by the use of effective marker vaccines, but little attention has been given to the processes leading to the mad itch. The main objective of this review is to provide state-of-the-art information on the mechanisms governing PRV-induced neuropathic itch in non-natural hosts. We highlight similarities and key differences in the pathogenesis of PRV infections between non-natural hosts and pigs that might explain their distinctive clinical outcomes. Current knowledge on the neurobiology and possible explanations for the unstoppable itch experienced by PRV-infected animals is also reviewed. We summarize recent findings concerning PRV-induced neuroinflammatory responses in mice and address the relevance of this animal model to study other alphaherpesvirus-induced neuropathies, such as those observed for VZV infection.

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Section: The Immune Mechanisms Of Prv-induced Neuropathic Itchmentioning

confidence: 99%

The Neuropathic Itch Caused by Pseudorabies Virus

Laval

Enquist

2020

Pathogens

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“…SP participates in the development of an inflammatory response in the brain after such injury including activation of microglia and release of proinflammatory cytokines 19 , 20 . The increase in neuronal excitability caused by SP raises the issue whether SP has a proconvulsant action 21 .…”

Section: Introductionmentioning

confidence: 99%

The potential of substance P to initiate and perpetuate cortical spreading depression (CSD) in rat in vivo

Richter

Eitner

Leuchtweis

et al. 2018

Sci Rep

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The tachykinin substance P (SP) increases neuronal excitability, participates in homeostatic control, but induces brain oedema after stroke or trauma. We asked whether SP is able to induce cortical spreading depression (CSD) which often aggravates stroke-induced pathology. In anesthetized rats we applied SP (10−5, 10−6, 10−7, or 10−8 mol/L) to a restricted cortical area and recorded CSDs there and in remote non-treated areas using microelectrodes. SP was either applied in artificial cerebrospinal fluid (ACSF), or in aqua to perform a preconditioning. Plasma extravasation in cortical grey matter was assessed with Evans Blue. Only SP dissolved in aqua induced self-regenerating CSDs. SP dissolved in ACSF did not ignite CSDs even when excitability was increased by acetate-preconditioning. Aqua alone elicited as few CSDs as the lowest concentration of SP. Local pretreatment with 250 nmol/L of a neurokinin 1 receptor antagonist prevented the SP-induced plasma extravasation, the initiation of CSDs by 10−5 mol/L SP diluted in aqua, and the initiation of CSDs by aqua alone, but did not suppress KCl-induced CSD. Thus neurokinin 1 receptor antagonists may be used to explore the involvement of SP in CSDs in clinical studies.

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“…For example, the gastrin-releasing peptide (GRP) modulates VIP and somatostatin interneuron activity to maintain excitatory and inhibitory (E/I) balances underlying the formation of memories in the neocortex [ 107 ]. Alternatively, NPY, corticotropin-releasing factor (CRF), and dynorphin regulate inhibitory GABAergic activity to maintain the balance of neural networks in the amygdala [ 108 , 109 , 110 , 111 ], and substance P prolongs the potentiation of glutamatergic NMDA receptors, enhancing neuronal excitability, in a number of brain regions including the SCN, striatum, and nucleus tractus solitaries [ 112 ]. The pivotal role of neuropeptides in regulating the balance of excitatory/inhibitory activity is further evidenced by their ability to attenuate the severity of seizures during large reductions in inhibitory activity, or epileptogenesis [ 113 ].…”

Section: Function Of Neuropeptides In the Neurological Systemmentioning

confidence: 99%

Potentials of Neuropeptides as Therapeutic Agents for Neurological Diseases

Yeo

Cunliffe

et al. 2022

Biomedicines

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Despite recent leaps in modern medicine, progress in the treatment of neurological diseases remains slow. The near impermeable blood-brain barrier (BBB) that prevents the entry of therapeutics into the brain, and the complexity of neurological processes, limits the specificity of potential therapeutics. Moreover, a lack of etiological understanding and the irreversible nature of neurological conditions have resulted in low tolerability and high failure rates towards existing small molecule-based treatments. Neuropeptides, which are small proteinaceous molecules produced by the body, either in the nervous system or the peripheral organs, modulate neurological function. Although peptide-based therapeutics originated from the treatment of metabolic diseases in the 1920s, the adoption and development of peptide drugs for neurological conditions are relatively recent. In this review, we examine the natural roles of neuropeptides in the modulation of neurological function and the development of neurological disorders. Furthermore, we highlight the potential of these proteinaceous molecules in filling gaps in current therapeutics.

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The role of substance P in epilepsy and seizure disorders

Cited by 16 publications

References 90 publications

The Neuropathic Itch Caused by Pseudorabies Virus

The Neuropathic Itch Caused by Pseudorabies Virus

The potential of substance P to initiate and perpetuate cortical spreading depression (CSD) in rat in vivo

Potentials of Neuropeptides as Therapeutic Agents for Neurological Diseases

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