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1. 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.

Author

Castillo C, Norcini M, Baquero-Buitrago J, Levacic D, Medina R, Montoya-Gacharna JV, Blanck TJ, Dubois M, and Recio-Pinto E

Subjects
Animals, Calcium Signaling drug effects, Calcium Signaling physiology, Cells, Cultured, Cytoplasm drug effects, Cytoplasm enzymology, Drug Synergism, Ganglia, Spinal drug effects, Protein Kinase C drug effects, Rats, Rats, Sprague-Dawley, Sensory Receptor Cells drug effects, Sensory Receptor Cells enzymology, Substance P antagonists & inhibitors, Substance P metabolism, Cytoplasm metabolism, Ganglia, Spinal cytology, Ganglia, Spinal metabolism, N-Methylaspartate pharmacology, Protein Kinase C physiology, Sensory Receptor Cells metabolism, Substance P physiology, Up-Regulation physiology
Abstract

The involvement of substance P (SP) in neuronal sensitization through the activation of the neurokinin-1-receptor (NK1r) in postsynaptic dorsal horn neurons has been well established. In contrast, the role of SP and NK1r in primary sensory dorsal root ganglion (DRG) neurons, in particular in the soma, is not well understood. In this study, we evaluated whether SP modulated the NMDA-evoked transient increase in cytoplasmic Ca2+ ([Ca2+]cyt) in the soma of dissociated adult DRG neurons. Cultures were treated with nerve growth factor (NGF), prostaglandin E2 (PGE2) or both NGF+PGE2. Treatment with NGF+PGE2 increased the percentage of N-methyl-D-aspartate (NMDA) responsive neurons. There was no correlation between the percentage of NMDA responsive neurons and the level of expression of the NR1 and NR2B subunits of the NMDA receptor or of the NK1r. Pretreatment with SP did not alter the percentage of NMDA responsive neurons; while it potentiated the NMDA-evoked [Ca2+]cyt transient by increasing its magnitude and by prolonging the period during which small- and some medium-sized neurons remained NMDA responsive. The SP-mediated potentiation was blocked by the SP-antagonist ([D-Pro4, D-Trp7,9]-SP (4-11)) and by the protein kinase C (PKC) blocker bisindolylmaleimide I (BIM); and correlated with the phosphorylation of PKCε. The Nk1r agonist [Sar9, Met(O2)11]-SP (SarMet-SP) also potentiated the NMDA-evoked [Ca2+]cyt transient. Exposure to SP or SarMet-SP produced a rapid increase in the labeling of phosphorylated-PKCε. In none of the conditions we detected phosphorylation of the NR2B subunit at Ser-1303. Phosphorylation of the NR2B subunit at Tyr1472 was enhanced to a similar extent in cells exposed to NMDA, SP or NMDA+SP, and that enhancement was blocked by BIM. Our findings suggest that NGF and PGE2 may contribute to the injury-evoked sensitization of DRG neurons in part by enhancing their NMDA-evoked [Ca2+]cyt transient in all sized DRG neurons; and that SP may further contribute to the DRG sensitization by enhancing and prolonging the NMDA-evoked increase in [Ca2+]cyt in small- and medium-sized DRG neurons., (Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.)

Published
2011
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2. 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

Author

Jose V. Montoya-Gacharna, D. Levacic, M. Dubois, C. Castillo, Thomas J. J. Blanck, J. Baquero-Buitrago, Monica Norcini, Esperanza Recio-Pinto, and R. Medina

Subjects
Bisindolylmaleimide, medicine.medical_specialty, Cytoplasm, N-Methylaspartate, Sensory Receptor Cells, Neuropeptide, Biology, Substance P, Rats, Sprague-Dawley, chemistry.chemical_compound, Dorsal root ganglion, Internal medicine, Ganglia, Spinal, medicine, Animals, Calcium Signaling, Protein kinase C, Cells, Cultured, Protein Kinase C, General Neuroscience, Long-term potentiation, Drug Synergism, Sensory neuron, Rats, Up-Regulation, Nerve growth factor, medicine.anatomical_structure, Endocrinology, nervous system, chemistry, NMDA receptor, Neuroscience
Abstract

The involvement of substance P (SP) in neuronal sensitization through the activation of the neurokinin-1-receptor (NK1r) in postsynaptic dorsal horn neurons has been well established. In contrast, the role of SP and NK1r in primary sensory dorsal root ganglion (DRG) neurons, in particular in the soma, is not well understood. In this study, we evaluated whether SP modulated the NMDA-evoked transient increase in cytoplasmic Ca 2+ ([Ca 2+ ] cyt ) in the soma of dissociated adult DRG neurons. Cultures were treated with nerve growth factor (NGF), prostaglandin E 2 (PGE 2 ) or both NGF+PGE 2 . Treatment with NGF+PGE 2 increased the percentage of N-methyl- d -aspartate (NMDA) responsive neurons. There was no correlation between the percentage of NMDA responsive neurons and the level of expression of the NR1 and NR2B subunits of the NMDA receptor or of the NK1r. Pretreatment with SP did not alter the percentage of NMDA responsive neurons; while it potentiated the NMDA-evoked [Ca 2+ ] cyt transient by increasing its magnitude and by prolonging the period during which small- and some medium-sized neurons remained NMDA responsive. The SP-mediated potentiation was blocked by the SP-antagonist ([D-Pro 4 , D-Trp 7,9 ]-SP (4–11)) and by the protein kinase C (PKC) blocker bisindolylmaleimide I (BIM); and correlated with the phosphorylation of PKCe. The Nk1r agonist [Sar 9 , Met(O 2 ) 11 ]-SP (SarMet-SP) also potentiated the NMDA-evoked [Ca 2+ ] cyt transient. Exposure to SP or SarMet-SP produced a rapid increase in the labeling of phosphorylated-PKCe. In none of the conditions we detected phosphorylation of the NR2B subunit at Ser-1303. Phosphorylation of the NR2B subunit at Tyr1472 was enhanced to a similar extent in cells exposed to NMDA, SP or NMDA+SP, and that enhancement was blocked by BIM. Our findings suggest that NGF and PGE 2 may contribute to the injury-evoked sensitization of DRG neurons in part by enhancing their NMDA-evoked [Ca 2+ ] cyt transient in all sized DRG neurons; and that SP may further contribute to the DRG sensitization by enhancing and prolonging the NMDA-evoked increase in [Ca 2+ ] cyt in small- and medium-sized DRG neurons.

Published
2010

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