scholarly journals TRP Channels Involved in Spontaneous L-Glutamate Release Enhancement in the Adult Rat Spinal Substantia Gelatinosa

Cells ◽  
2014 ◽  
Vol 3 (2) ◽  
pp. 331-362 ◽  
Author(s):  
Eiichi Kumamoto ◽  
Tsugumi Fujita ◽  
Chang-Yu Jiang
2007 ◽  
Vol 58 ◽  
pp. S180
Author(s):  
Masafumi Kosugi ◽  
Terumasa Nakatsuka ◽  
Tsugumi Fujita ◽  
Takahiro Aoyama ◽  
Eiichi Kumamoto

2013 ◽  
Vol 110 (3) ◽  
pp. 658-671 ◽  
Author(s):  
Hai-Yuan Yue ◽  
Chang-Yu Jiang ◽  
Tsugumi Fujita ◽  
Eiichi Kumamoto

Transient receptor potential (TRP) channels are thought to play a role in regulating nociceptive transmission to spinal substantia gelatinosa (SG) neurons. It remains to be unveiled whether the TRP channels in the central nervous system are different in property from those involved in receiving nociceptive stimuli in the peripheral nervous system. We examined the effect of the vanilloid compound zingerone, which activates TRPV1 channels in the cell body of a primary afferent neuron, on glutamatergic excitatory transmission in the SG neurons of adult rat spinal cord slices by using the whole cell patch-clamp technique. Bath-applied zingerone reversibly and concentration-dependently increased spontaneous excitatory postsynaptic current (EPSC) frequency. This effect was accompanied by an inward current at −70 mV that was resistant to glutamate receptor antagonists. These zingerone effects were repeated and persisted in Na+-channel blocker tetrodotoxin-, La3+-, or IP3-induced Ca2+-release inhibitor 2-aminoethoxydiphenyl borate-containing or Ca2+-free Krebs solution. Zingerone activity was resistant to the selective TRPV1 antagonist capsazepine but sensitive to the nonselective TRP antagonist ruthenium red, the TRPA1 antagonist HC-030031, and the Ca2+-induced Ca2+-release inhibitor dantrolene. TRPA1 agonist allyl isothiocyanate but not capsaicin inhibited the facilitatory effect of zingerone. On the other hand, zingerone reduced monosynaptically evoked EPSC amplitudes, as did TRPA1 agonists. Like allyl isothiocyanate, zingerone enhanced GABAergic spontaneous inhibitory transmission in a manner sensitive to tetrodotoxin. We conclude that zingerone presynaptically facilitates spontaneous excitatory transmission, probably through Ca2+-induced Ca2+-release mechanisms, and produces a membrane depolarization in SG neurons by activating TRPA1 but not TRPV1 channels.


2003 ◽  
Vol 89 (1) ◽  
pp. 257-264 ◽  
Author(s):  
Noriaki Matsumoto ◽  
Eiichi Kumamoto ◽  
Hidemasa Furue ◽  
Megumu Yoshimura

An ischemia-induced change in glutamatergic transmission was investigated in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by use of the whole cell patch-clamp technique; the ischemia was simulated by superfusing an oxygen- and glucose-free medium (ISM). Following ISM superfusion, 21 of 37 SG neurons tested produced an outward current (23 ± 4 pA at a holding potential of −70 mV), which was followed by a slow and subsequent rapid inward current; the remaining neurons had only inward currents. During such a change in holding currents, spontaneous excitatory postsynaptic currents (EPSCs) were remarkably decreased in a frequency with time (half-decay time of the frequency: about 65 s). The frequency of spontaneous EPSCs was reduced to 28 ± 13% ( n = 37) of the control level during the generation of the slow inward current (about 4 min after the beginning of ISM superfusion) without a change in the amplitude of spontaneous EPSCs. When ISM was superfused together with either bicuculline (10 μM) or CGP35348 (20 μM; GABAA and GABAB receptor antagonists, respectively), spontaneous EPSC frequency reduced by ISM recovered to the control level and then the frequency markedly increased [by 325 ± 120% ( n = 22) and 326 ± 91% ( n = 17), respectively, 4 min after ISM superfusion]; this alteration in the frequency was not accompanied by a change in spontaneous EPSC amplitude. Superfusing TTX (1 μM)-containing ISM resulted in a similar recovery of spontaneous EPSC frequency and following increase (by 328 ± 26%, n = 12) in the frequency; strychnine (1 μM) did not affect ISM-induced changes in spontaneous EPSC frequency ( n = 5). It is concluded that the ischemic simulation inhibits excitatory transmission to SG neurons, whose action is in part mediated by the activation of presynaptic GABAAand GABAB receptors, probably due to GABA released from interneurons as a result of an ischemia-induced increase in neuronal activities. This action might protect SG neurons from an excessive excitation mediated by l-glutamate during ischemia.


2015 ◽  
Vol 606 ◽  
pp. 94-99 ◽  
Author(s):  
Zhi-Hao Xu ◽  
Chong Wang ◽  
Tsugumi Fujita ◽  
Chang-Yu Jiang ◽  
Eiichi Kumamoto

2010 ◽  
Vol 68 ◽  
pp. e337
Author(s):  
Lian-Hua Piao ◽  
Tsugumi Fujita ◽  
Hai-Yuan Yue ◽  
Chang-Yu Jiang ◽  
Masanari Inoue ◽  
...  

2019 ◽  
Vol 20 (3) ◽  
pp. 526 ◽  
Author(s):  
Mohammad Hossain ◽  
Marina Bakri ◽  
Farhana Yahya ◽  
Hiroshi Ando ◽  
Shumpei Unno ◽  
...  

Dental pain is a common health problem that negatively impacts the activities of daily living. Dentine hypersensitivity and pulpitis-associated pain are among the most common types of dental pain. Patients with these conditions feel pain upon exposure of the affected tooth to various external stimuli. However, the molecular mechanisms underlying dental pain, especially the transduction of external stimuli to electrical signals in the nerve, remain unclear. Numerous ion channels and receptors localized in the dental primary afferent neurons (DPAs) and odontoblasts have been implicated in the transduction of dental pain, and functional expression of various polymodal transient receptor potential (TRP) channels has been detected in DPAs and odontoblasts. External stimuli-induced dentinal tubular fluid movement can activate TRP channels on DPAs and odontoblasts. The odontoblasts can in turn activate the DPAs by paracrine signaling through ATP and glutamate release. In pulpitis, inflammatory mediators may sensitize the DPAs. They could also induce post-translational modifications of TRP channels, increase trafficking of these channels to nerve terminals, and increase the sensitivity of these channels to stimuli. Additionally, in caries-induced pulpitis, bacterial products can directly activate TRP channels on DPAs. In this review, we provide an overview of the TRP channels expressed in the various tooth structures, and we discuss their involvement in the development of dental pain.


2019 ◽  
Vol 15 ◽  
pp. 174480691882424 ◽  
Author(s):  
Akiko Koga ◽  
Tsugumi Fujita ◽  
Lian-Hua Piao ◽  
Terumasa Nakatsuka ◽  
Eiichi Kumamoto

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