scholarly journals Prostaglandin E 2 inhibits calcium current in two sub‐populations of acutely isolated mouse trigeminal sensory neurons

2002 ◽  
Vol 539 (2) ◽  
pp. 433-444 ◽  
Author(s):  
Stephanie L. Borgland ◽  
Mark Connor ◽  
Renae M. Ryan ◽  
Helen J. Ball ◽  
MacDonald J. Christie
Keyword(s):  
Sensory Neurons ◽  
Calcium Current ◽  
Prostaglandin E

scholarly journals 5-HT Inhibits Calcium Current and Synaptic Transmission from Sensory Neurons in Lamprey

1997 ◽  
Vol 17 (5) ◽  
pp. 1786-1794 ◽  
Author(s):  
Abdeljabbar El Manira ◽  
Weiqi Zhang ◽  
Erik Svensson ◽  
Nathalie Bussières
Keyword(s):  
Synaptic Transmission ◽  
Sensory Neurons ◽  
Calcium Current

scholarly journals Cell-Specific Alterations of T-Type Calcium Current in Painful Diabetic Neuropathy Enhance Excitability of Sensory Neurons

2007 ◽  
Vol 27 (12) ◽  
pp. 3305-3316 ◽  
Author(s):  
M. M. Jagodic ◽  
S. Pathirathna ◽  
M. T. Nelson ◽  
S. Mancuso ◽  
P. M. Joksovic ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Sensory Neurons ◽  
Calcium Current ◽  
Painful Diabetic Neuropathy

scholarly journals Sphingosine 1-phosphate receptor 2 antagonist JTE-013 increases the excitability of sensory neurons independently of the receptor

2012 ◽  
Vol 108 (5) ◽  
pp. 1473-1483 ◽  
Author(s):  
Chao Li ◽  
Xian Xuan Chi ◽  
Wenrui Xie ◽  
J. A. Strong ◽  
J.-M. Zhang ◽  
...  
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
Neuronal Excitability ◽  
Small Diameter ◽  
G Protein Coupled Receptors ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Sphingosine 1 Phosphate ◽  
G Protein Coupled

Previously we demonstrated that sphingosine 1-phosphate receptor 1 (S1PR1) played a prominent, but not exclusive, role in enhancing the excitability of small-diameter sensory neurons, suggesting that other S1PRs can modulate neuronal excitability. To examine the potential role of S1PR2 in regulating neuronal excitability we used the established selective antagonist of S1PR2, JTE-013. Here we report that exposure to JTE-013 alone produced a significant increase in excitability in a time- and concentration-dependent manner in 70–80% of recorded neurons. Internal perfusion of sensory neurons with guanosine 5′- O-(2-thiodiphosphate) (GDP-β-S) via the recording pipette inhibited the sensitization produced by JTE-013 as well as prostaglandin E2. Pretreatment with pertussis toxin or the selective S1PR1 antagonist W146 blocked the sensitization produced by JTE-013. These results indicate that JTE-013 might act as an agonist at other G protein-coupled receptors. In neurons that were sensitized by JTE-013, single-cell RT-PCR studies demonstrated that these neurons did not express the mRNA for S1PR2. In behavioral studies, injection of JTE-013 into the rat's hindpaw produced a significant increase in the mechanical sensitivity in the ipsilateral, but not contralateral, paw. Injection of JTE-013 did not affect the withdrawal latency to thermal stimulation. Thus JTE-013 augments neuronal excitability independently of S1PR2 by unknown mechanisms that may involve activation of other G protein-coupled receptors such as S1PR1. Clearly, further studies are warranted to establish the causal nature of this increased sensitivity, and future studies of neuronal function using JTE-013 should be interpreted with caution.

Opioid modulation of calcium current in cultured sensory neurons: μ-modulation of baroreceptor input

1999 ◽  
Vol 277 (2) ◽  
pp. H705-H713 ◽  
Author(s):  
Mary Hamra ◽  
Robert S. McNeil ◽  
Martin Runciman ◽  
Diana L. Kunze
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
Mechanism Of Action ◽  
Pertussis Toxin ◽  
Calcium Current ◽  
Receptor Agonist ◽  
Age Groups ◽  
Opiate Receptor ◽  
Μ Opiate Receptor ◽  
Patch Technique

We used the whole cell open-patch or perforated-patch technique to characterize μ-opioid modulation of Ca2+ current ( I Ca) in nodose sensory neurons and in a specific subpopulation of nodose cells, aortic baroreceptor neurons. The μ-opiate receptor agonist Tyr-d-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) inhibited I Ca in 95% of neonatal [postnatal day (P)1–P3] nodose neurons. To the contrary, only 64% of juvenile cells (P20–P35) and 61% of adult cells (P60–P110) responded to DAGO. DAGO-mediated inhibition of I Ca was naloxone sensitive, irreversible in the presence of guanosine 5′- O-(3-thiotriphosphate), absent with guanosine 5′- O-(2-thiodiphosphate), and eliminated with pertussis toxin; DAGO’s inhibition of I Ca was G protein mediated. Incubation of neurons with ω-conotoxin GVIA eliminated the effect of DAGO in neonatal but not in juvenile cells. In the latter, DAGO reduced 37% of the current remaining in the presence of ω-conotoxin. In the subset of nodose neurons, aortic baroafferents, the effect of DAGO was concentration dependent, with an IC50 of 1.82 × 10−8 M. DAGO slowed activation of I Ca, but activation curves constructed from tail currents were the same with and without DAGO (100 nM). In summary, μ-opiate modulation of I Ca in nodose neurons was demonstrated in three age groups, including specifically labeled baroafferents. The demonstration of a mechanism of action of μ-opioids on baroreceptor afferents provides a basis for the attenuation of the baroreflex that occurs at the level of the nucleus tractus solitarii.

scholarly journals In vivo characterization of distinct modality-specific subsets of somatosensory neurons using GCaMP

2016 ◽  
Vol 2 (11) ◽  
pp. e1600990 ◽  
Author(s):  
Edward C. Emery ◽  
Ana P. Luiz ◽  
Shafaq Sikandar ◽  
Rán Magnúsdóttir ◽  
Xinzhong Dong ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Transgenic Mice ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Rational Approach ◽  
Prostaglandin E ◽  
Nociceptive Neurons ◽  
Ganglion Neurons

Mechanistic insights into pain pathways are essential for a rational approach to treating this vast and increasing clinical problem. Sensory neurons that respond to tissue damage (nociceptors) may evoke pain sensations and are typically classified on the basis of action potential velocity. Electrophysiological studies have suggested that most of the C-fiber nociceptors are polymodal, responding to a variety of insults. In contrast, gene deletion studies in the sensory neurons of transgenic mice have frequently resulted in modality-specific deficits. We have used an in vivo imaging approach using the genetically encoded fluorescent calcium indicator GCaMP to study the activity of dorsal root ganglion sensory neurons in live animals challenged with painful stimuli. Using this approach, we can visualize spatially distinct neuronal responses and find that >85% of responsive dorsal root ganglion neurons are modality-specific, responding to either noxious mechanical, cold, or heat stimuli. These observations are mirrored in behavioral studies of transgenic mice. For example, deleting sodium channel Nav1.8 silences mechanical- but not heat-sensing sensory neurons, consistent with behavioral deficits. In contrast, primary cultures of axotomized sensory neurons show high levels of polymodality. After intraplantar treatment with prostaglandin E2, neurons in vivo respond more intensely to noxious thermal and mechanical stimuli, and additional neurons (silent nociceptors) are unmasked. Together, these studies define polymodality as an infrequent feature of nociceptive neurons in normal animals.

IA current compared to low threshold calcium current in cranial sensory neurons

1985 ◽  
Vol 62 (2) ◽  
pp. 249-254 ◽  
Author(s):  
J.-L. Bossu ◽  
J.-L. Dupont ◽  
A. Feltz
Keyword(s):  
Sensory Neurons ◽  
Calcium Current ◽  
Low Threshold ◽  
Ia Current

ENANTIOSELECTIVE BLOCKADE OF T-TYPE CALCIUM CURRENT IN RAT SENSORY NEURONS BY A NOVEL ANESTHETIC STEROID (+)-ACN

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 156A
Author(s):  
S. M. Todorovic ◽  
D. F. Covey ◽  
C. J. Lingle
Keyword(s):  
Sensory Neurons ◽  
Calcium Current
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