The N-methyl-D-aspartate-evoked cytoplasmic calcium increase in adult rat dorsal root ganglion neuronal somata was potentiated by substance P pretreatment in a protein kinase C-dependent manner

Castillo, Cecilia; Norcini, Monica; Baquero-Buitrago, J.; Levačić, Danijela; Medina, Rafael; Montoya-Gacharna, Jose V.; Blanck, Thomas J. J.; Dubois, Michel Y.; Recio-Pinto, Esperanza

doi:10.1016/j.neuroscience.2010.12.040

Cited by 18 publications

(18 citation statements)

References 67 publications

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“…Using an NK1R antagonist or capsaicin to destroy SP-ergic fibers can block NK1R internalization in the spinal dorsal horn when NMDA is injected into the cerebral ventricle [33], [34]. Through the activation of NK1Rs, SP potentiates currents through NMDA receptors [35] and the NMDA-evoked cytoplasmic Ca 2+ ([Ca 2+ ] cyt ) transient [36]. These data also suggest that C fibers remain activated during the secondary phase of visceral pain and may continually release SP in the DCN.…”

Section: Discussionmentioning

confidence: 91%

Acute Colitis Induces Neurokinin 1 Receptor Internalization in the Rat Lumbosacral Spinal Cord

Zhang

et al. 2013

PLoS ONE

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Substance P (SP) and its receptor, the neurokinin 1 receptor (NK1R), play important roles in transmitting and regulating somatosensory nociceptive information. However, their roles in visceral nociceptive transmission and regulation remain to be elucidated. In the previous study, moderate SP immunoreactive (SP-ir) terminals and NK1R-ir neurons were observed in the dorsal commissural nucleus (DCN) of the lumbosacral spinal cord. Thus we hypothesized that the SP-NK1R system is involved in visceral pain transmission and control within the DCN. The acute visceral pain behaviors, the colon histological changes and the temporal and spatial changes of NK1R-ir structures and Fos expression in the neurons of the DCN were observed in rats following lower colon instillation with 5% formalin. The formalin instillation induced significant acute colitis as revealed by the histological changes in the colon. NK1R internalization in the DCN was obvious at 8 min. It reached a peak (75.3%) at 30 min, began to decrease at 90 min (58.1%) and finally reached the minimum (19.7%) at 3 h after instillation. Meanwhile, formalin instillation induced a biphasic visceral pain response as well as a strong expression of Fos protein in the nuclei of neurons in the DCN. Finally, intrathecal treatment with the NK1R antagonist L732138 attenuated the NK1R internalization, Fos expression and visceral nociceptive responses. The present results suggest that the visceral nociceptive information arising from inflamed pelvic organs, such as the lower colon, might be mediated by the NK1R-ir neurons in the DCN of the lumbosacral spinal cord.

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Section: Discussionmentioning

confidence: 91%

Acute Colitis Induces Neurokinin 1 Receptor Internalization in the Rat Lumbosacral Spinal Cord

Zhang

et al. 2013

PLoS ONE

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“…Desensitization to SP-evoked current was exhibited in almost all SP-responsive DRG neurons in control rats, while desensitization diminished in a larger proportion (two thirds) of DRG neurons in rats with inflammation (40). In addition, pretreatment with SP potentiated the N-methyl-d-asparate (NMDA)-evoked cytosolic calcium transient response in DRG PANs, and this response was blocked by an NK1R-antagonist (41). The reports suggest that the SP-NK1R axis not only activates postsynaptic dorsal horn neurons but also contributes to DRG sensitization in DRG PANs; that is, they develop and maintain inflammatory pain.…”

Section: Tks and Inflammationmentioning

confidence: 96%

Tachykinin: recent developments and novel roles in health and disease

Onaga

2014

Biomolecular Concepts

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Over 80 years has passed since the discovery of substance P (SP), and a variety of peptides of the tachykinin (TK) family have been found and investigated. SP, neurokinin A (NKA), and neurokinin B (NKB) are representative peptides in mammalian species. SP and NKA are major excitatory neurotransmitters in the peripheral nervous system, while NKB is primarily involved in the central nervous system (CNS). Moreover, TK peptides play roles not only as neurotransmitters but also as local factors and are involved in almost all aspects of the regulation of physiological functions and pathophysiological processes. The role of SP as a mediator of pain processing and inflammation in peripheral tissues in coordination with transient receptor potential channels is well established, while novel aspects of TKs in relation to hematopoiesis, venous thromboembolism, tendinopathy, and taste perception have been clarified. In the CNS, the NKB signaling system in the hypothalamus has been shown to play a crucial role in the regulation of gonadotropin hormone secretion and the onset of puberty, and molecular biological studies have elucidated novel prophylaxic activities of TKs against neurogenic movement disorders based on their molecular structure. This review provides an overview of the novel aspects of TKs reported around the world in the last 5 years, with particular focus on nociception, inflammation, hemopoiesis, gonadotropin secretion, and CNS diseases.

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“…As expected when comparisons were done only between one of the SNI groups (Sural-SNI or Tibial-SNI) and Sham it resulted in a large number of genes that displayed changes in their expression in that SNI group; however, when comparisons were done by selecting the genes that their expression changed in one of the SNI groups but not in the Sham and in the other SNI group; the number of genes that changed was highly reduced. Some genes of interest that changed only in the dorsal root ganglia from Tibial-SNI (presumably genes that could be involved in limiting the level of sustained mechanical allodynia) include a reduction in Hcn2 which encodes a hyperpolarization activated cyclic nucleotide-gated K channel 2 that has been shown to contribute to spontaneous rhythmic activity in both heart and brain (Dibbens et al, 2010;Lin et al, 2009); an increase in Map3k10 a kinase that functions preferentially on the JNK signaling pathway, and that has been reported to be involved in nerve growth factor (NGF) induced neuronal apoptosis (NGF is increased following nerve injury) (see ref in (Castillo et al, 2011)). A decrease in Rbm9, a gene that encodes an RNA binding protein that is believe to be a key regulator of alternative exon splicing in the nervous system.…”

Section: Peripheral Nerve Injury Alters the Dorsal Root Ganglia Envirmentioning

confidence: 99%

An Approach to Identify Nerve Injury-Evoked Changes that Contribute to the Development or Protect Against the Development of Sustained Neuropathic Pain

Recio-Pinto¹,

Norcini²,

Blanck³

2012

Basic Principles of Peripheral Nerve Disorders

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The N-methyl-D-aspartate-evoked cytoplasmic calcium increase in adult rat dorsal root ganglion neuronal somata was potentiated by substance P pretreatment in a protein kinase C-dependent manner

Cited by 18 publications

References 67 publications

Acute Colitis Induces Neurokinin 1 Receptor Internalization in the Rat Lumbosacral Spinal Cord

Acute Colitis Induces Neurokinin 1 Receptor Internalization in the Rat Lumbosacral Spinal Cord

Tachykinin: recent developments and novel roles in health and disease

An Approach to Identify Nerve Injury-Evoked Changes that Contribute to the Development or Protect Against the Development of Sustained Neuropathic Pain

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