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Proton-induced currents in substantia gelatinosa neurons of the rat trigeminal subnucleus caudalis
Cho, J.H.,Choi, I.S.,Nakamura, M.,Lee, S.H.,Lee, M.G.,Jang, I.S. North-Holland ; Elsevier Science Ltd 2015 european journal of pharmacology Vol.762 No.-
Acid-sensing ion channels (ASICs) are widely expressed in both the peripheral and central nervous system, and contribute to the modulation of central nociceptive transmission under both physiological and pathophysiological conditions. In this study, we characterized the proton-induced membrane currents in acutely isolated rat substantia gelatinosa (SG) neurons of the trigeminal subnucleus caudalis using the whole cell patch-clamp technique. Exposure to acidic conditions (pH<6.5) induced the inward currents in a pH-dependent manner. Amiloride, a general ASIC antagonist, significantly blocked the proton-induced currents in a non-competitive manner. The pH 6.0-induced membrane current (I<SUB>pH6.0</SUB>) was greatly attenuated in the Na<SUP>+</SUP>-free external solution, and the reversal potential of the proton-induced currents was similar to the theoretical Na<SUP>+</SUP> equilibrium potential. The I<SUB>pH6.0</SUB> was reciprocally potentiated by a lower extracellular Ca<SUP>2+</SUP> concentration. The modulation of I<SUB>pH6.0</SUB> by divalent cations and other modulators suggests that the proton-induced currents are mediated by multiple types of ASIC subunits, including ASIC1a and ASIC2a. Multi-cell RT-PCR analysis revealed that SG neurons express these subunits. Exposure to a pH 6.0 solution directly depolarized the membrane potential, and generated a burst of action potentials in a current-clamp mode. This acidic pH-induced depolarization was significantly blocked by amiloride. The present results suggest that ASICs expressed on SG neurons play important roles in the regulation of nociceptive transmission from the orofacial tissues.
Physiological Factors Depressing Feed Intake and Saliva Secretion in Goats Fed on Dry Forage
Sunagawa, K.,Ooshiro, T.,Nakamura, N.,Ishii, Y.,Nagamine, I.,Shinjo, A Asian Australasian Association of Animal Productio 2007 Animal Bioscience Vol.20 No.1
Ruminants eating dry forage secrete large volumes of saliva which results in decreased plasma volume (hypovolemia) and the loss of $NaHCO_3$ from the blood. The present research investigated whether or not hypovolemia and the loss of $NaHCO_3$ from the blood in goats brought about by dry forage feeding actually depresses feed intake and saliva secretion, respectively. The present experiment consisted of three treatments (NI, ASI, MI). In the control treatment (NI), a solution was not infused. In the ASI treatment, i.v. infusion of artificial parotid saliva was initiated 1 h before feeding and continued for the entire 2 h feeding period. In the MI treatment, iso-osmotic mannitol solution was infused. The NI treatment showed that hematocrit and plasma total protein concentration were increased due to decreased circulating plasma volume brought about by feeding. In the ASI treatment, the fluid and $NaHCO_3$ that were lost from the blood because of a feeding-induced acceleration of saliva secretion was replenished with an intravenous infusion of artificial parotid saliva. This replenishment lessened the levels of suppression on both feeding and parotid saliva secretion. When only the lost fluid was replenished with an intravenous infusion of iso-osmotic mannitol solution in the MI treatment, the degree of feeding suppression was lessened but the level of saliva secretion suppression was not affected. These results indicate that the marked suppression of feed intake during the initial stages of dry forage feeding was caused by a feeding-induced hypovolemia while the suppression of saliva secretion was brought about by the loss of $NaHCO_3$ from the blood due to increased saliva secretion during the initial stages of feeding.
Coincidence measurement of the nonmesonic weak decay of <sup>12</sup><sub><i>Λ</i></sub>C
Kim, M.J.,Ajimura, S.,Aoki, K.,Banu, A.,Bhang, H.,Fukuda, T.,Hashimoto, O.,Hwang, J.I.,Kameoka, S.,Kang, B.H.,Kim, E.H.,Kim, J.H.,Maruta, T.,Miura, Y.,Miyake, Y.,Nagae, T.,Nakamura, M.,Nakamura, S.N. Elsevier 2006 Physics letters: B Vol.641 No.1
<P><B>Abstract</B></P><P>We have measured the angular correlation of the pair nucleons <I>np</I> and <I>nn</I> emitted from the nonmesonic weak decay (NMWD) of <SUP>12</SUP><SUB><I>Λ</I></SUB>C produced via the (<SUP>π+</SUP>,<SUP>K+</SUP>) reaction in coincidence measurement. The Λp→np and Λn→nn modes were clearly identified by measuring the back-to-back correlation of the emitted nucleon pairs which is the characteristic of two-body kinematics. From the measured nucleon pair numbers <SUB>Nnn</SUB> and <SUB>Nnp</SUB>, the ratio <SUB>Γn</SUB>/<SUB>Γp</SUB> of the partial decay widths <SUB>Γn</SUB>(Λn→nn) and <SUB>Γp</SUB>(Λp→np) of <SUP>12</SUP><SUB><I>Λ</I></SUB>C was extracted to be 0.51±0.13(stat)±0.05(syst); this result is almost free from the ambiguity due to the nuclear final state interaction and 3-body decay process, which were inherent in the previous results. The obtained <SUB>Γn</SUB>/<SUB>Γp</SUB> ratio of <SUP>12</SUP><SUB><I>Λ</I></SUB>C (<I>p</I>-shell) is close to that of <SUP>5</SUP><SUB><I>Λ</I></SUB>He (<I>s</I>-shell). The results are consistent with those of recent theoretical calculations.</P>
Nakamura, M.,Jang, I.S. Pergamon Press 2016 NEUROPHARMACOLOGY - Vol.105 No.-
Non-steroidal anti-inflammatory drugs (NSAIDs) are well-known inhibitors of cyclooxygenases (COXs) and are widely used for the treatment of inflammatory pain; however several NSAIDs display COX-independent analgesic action including the inhibition of voltage-gated Na<SUP>+</SUP> channels expressed in primary afferent neurons. In the present study, we examined whether NSAIDs modulate tetrodotoxin-resistant (TTX-R) Na<SUP>+</SUP> channels and if this modulation depends on the extracellular pH. The TTX-R Na<SUP>+</SUP> currents were recorded from small-sized trigeminal ganglion neurons by using a whole-cell patch clamp technique. Among eight NSAIDs tested in this study, several drugs, including aspirin and ibuprofen, did not affect TTX-R Na<SUP>+</SUP> channels either at pH 7.4 or at pH 6.0. However, we found that indomethacin, and, to a lesser extent, ibuprofen and naproxen potently inhibited the peak amplitude of TTX-R Na<SUP>+</SUP> currents at pH 6.0. The indomethacin-induced inhibition of TTX-R Na<SUP>+</SUP> channels was more potent at depolarized membrane potentials. Indomethacin significantly shifted both the voltage-activation and voltage-inactivation relationships to depolarizing potentials at pH 6.0. Indomethacin accelerated the development of inactivation and retarded the recovery from inactivation of TTX-R Na<SUP>+</SUP> channels at pH 6.0. Given that indomethacin and several other NSAIDs could further suppress local nociceptive signals by inhibiting TTX-R Na<SUP>+</SUP> channels at an acidic pH in addition to the classical COX inhibition, these drugs could be particularly useful for the treatment of inflammatory pain.
Nakamura, M.,Choi, K.H.,Choi, S.K.,Do, C.S.,Jun, J.H.,Kwon, H.K.,Lee, S.M.,Moon, R.J.,Yi, K.J.,Jang, I.S. North-Holland ; Elsevier Science Ltd 2010 european journal of pharmacology Vol.635 No.1
Neurons within the periaqueductal gray (PAG) have been implicated in the central regulation of pain signals by affecting the descending inhibitory pathway. Here we report on the functional role of presynaptic kainate receptors within the PAG. Using a conventional whole-cell patch clamp technique, we recorded GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) from mechanically isolated rat PAG neurons in the presence of 300nM tetrodotoxin and 20@?M dl-2-amino-5-phosphonovaleric acid under voltage-clamp conditions. Kainic acid at a 10@?M concentration significantly increased the frequency of GABAergic mIPSCs without affecting their amplitude, suggesting that kainic acid acts presynaptically to enhance spontaneous GABA release. The kainic acid-induced increase in mIPSC frequency was completely blocked by CNQX, a selective AMPA/kainate receptor antagonist. While neither AMPA nor NMDA affected GABAergic mIPSC frequency, ATPA, a selective agonist of GluR5-containing kainate receptors, increased GABAergic mIPSC frequency in a concentration-dependent manner. The kainic acid-induced increase in mIPSC frequency was completely suppressed either in the presence of 100@?M Cd<SUP>2+</SUP>, a general voltage-dependent Ca<SUP>2+</SUP> channel (VDCC) blocker, or in the Na<SUP>+</SUP>-free external solution. These results suggest that presynaptic kainate receptors have a low permeability to Ca<SUP>2+</SUP>, and that their activation elicits a presynaptic depolarization large enough to activate presynaptic VDCCs. Presynaptic kainate receptors on GABAergic nerve terminals appear to modulate GABAergic transmission, and in doing so may play an important role in the regulation of PAG neuron excitability.
Nakamura, M.,Jang, I.S. North-Holland ; Elsevier Science Ltd 2010 european journal of pharmacology Vol.640 No.1
The periaqueductal gray (PAG) is a major component of the descending pain inhibitory pathway, which is related to central analgesia. In the present study, we have investigated the possible roles of presynaptic nicotinic acetylcholine receptors in GABAergic transmission onto PAG neurons. In acutely isolated rat PAG neurons, GABAergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded by use of a whole-cell patch clamp technique. Acetylcholine (30μM) transiently increased both the frequency and amplitude of GABAergic mIPSCs. However, acetylcholine did not affect the GABA-induced membrane currents. This facilitatory action of acetylcholine disappeared in the presence of mecamylamine, a nonselective nicotinic receptor antagonist, and mimicked by nicotine, a nicotinic receptor agonist. The nicotine-induced increase in mIPSC frequency was completely blocked by dihydro-β-erythroidine, a selective β2-containing nicotinic receptor antagonist, but not methyllycaconitine or α-bungarotoxin, selective α7 nicotinic receptor antagonists. The results suggest that acetylcholine or nicotine acts presynaptic β2-containing nicotinic receptors, presumably α4β2 nicotinic receptors, to enhance spontaneous GABA release onto PAG neurons. The nicotine-induced increase in mIPSC frequency was completely occluded in the presence of Cd<SUP>2+</SUP>, a general voltage-dependent Ca<SUP>2+</SUP> channels blocker, and in the absence of extracellular Ca<SUP>2+</SUP> or Na<SUP>+</SUP>. The results suggest that presynaptic nicotinic receptors are less permeable to Ca<SUP>2+</SUP>, and that the activation of these receptors depolarizes GABAergic nerve terminals. In conclusion, presynaptic nicotinic receptors would temporally regulate the excitability of PAG neurons being not overexcited and eventually contribute to the cholinergic modulation of output from the PAG.