The Experts below are selected from a list of 7053 Experts worldwide ranked by ideXlab platform
Ilsung Jang - One of the best experts on this subject based on the ideXlab platform.
-
Effects of nitrous oxide on Glycinergic transmission in rat spinal neurons.
Brain research bulletin, 2020Co-Authors: Michiko Nakamura, Ilsung Jang, Toshitaka Yamaga, Naoki Kotani, Norio AkaikeAbstract:We investigated the effects of nitrous oxide (N2O) on Glycinergic inhibitory whole-cell and synaptic responses using a "synapse bouton preparation," dissociated mechanically from rat spinal sacral dorsal commissural nucleus (SDCN) neurons. This technique can evaluate pure single- or multi-synaptic responses from native functional nerve endings and enable us to accurately quantify how N2O influences pre- and postsynaptic transmission. We found that 70 % N2O enhanced exogenous glycine-induced whole-cell currents (IGly) at glycine concentrations lower than 3 × 10-5 M, but did not affect IGly at glycine concentrations higher than 10-4 M. N2O did not affect the amplitude and 1/e decay-time of both spontaneous and miniature Glycinergic inhibitory postsynaptic currents recorded in the absence and presence of tetrodotoxin (sIPSCs and mIPSCs, respectively). The decrease in frequency induced by N2O was observed in sIPSCs but not in mIPSCs, which was recorded in the presence of both tetrodotoxin and Cd2+, which block voltage-gated Na+ and Ca2+ channels, respectively. N2O also decreased the amplitude and increased the failure rate and paired-pulse ratio of action potential-evoked Glycinergic inhibitory postsynaptic currents. N2O slightly decreased the Ba2+ currents mediated by voltage-gated Ca2+ channels in SDCN neurons. We found that N2O suppresses Glycinergic responses at synaptic levels with presynaptic effect having much more predominant role. The difference between Glycinergic whole-cell and synaptic responses suggests that extrasynaptic responses seriously modulate whole-cell currents. Our results strongly suggest that these responses may thus in part explain analgesic effects of N2O via marked glutamatergic inhibition by Glycinergic responses in the spinal cord.
-
pregnenolone sulfate modulates Glycinergic transmission in rat medullary dorsal horn neurons
European Journal of Pharmacology, 2013Co-Authors: Jungsu Hong, Jinhwa Cho, Insun Choi, Maangee Lee, Ilsung JangAbstract:Abstract The neurosteroid pregnenolone sulfate (PS), a representative excitatory neuromodulator, has a variety of neuropharmacological actions, such as memory enhancement and convulsant effects. In this study, the effects of PS on Glycinergic transmission, such as Glycinergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs), were investigated in acutely isolated medullary dorsal horn neurons by use of a conventional whole-cell patch-clamp technique. PS significantly increased the frequency but decreased the amplitude of Glycinergic mIPSCs in a concentration-dependent manner. PS also accelerated the decay time constant of Glycinergic mIPSCs. The PS-induced decrease in mIPSC amplitude was due to the direct postsynaptic inhibition of glycine receptors because PS inhibited the glycine-induced Cl − currents in a noncompetitive manner. The PS-induced increase in mIPSC frequency was not due to the activation of α7 nicotinic acetylcholine, NMDA, σ1 receptors and voltage-dependent Ca 2+ channels, which are known to be molecular targets of PS. On the other hand, the PS-induced increase in mIPSC frequency was completely attenuated either in the Ca 2+ -free external solution or in the presence of transient receptor potential (TRP) channel blockers, suggesting that PS elicits an increase in Ca 2+ concentration within Glycinergic nerve terminals via the activation of putative TRP channels. The PS-mediated modulation of Glycinergic synaptic transmission, such as the enhancement of presynaptic glycine release and direct inhibition of postsynaptic glycine receptors, might have a broad impact on the excitability of medullary dorsal horn neurons and therefore affect the processing of nociceptive transmission from orofacial tissues.
-
TRPA1-like channels enhance Glycinergic transmission in medullary dorsal horn neurons.
Journal of neurochemistry, 2012Co-Authors: Jinhwa Cho, Insun Choi, Moon-young Jeong, Heon-jin Lee, Ilsung JangAbstract:The effect of icilin, a potent agonist of transient receptor potential ankyrin 1 (TRPA1) and TRPM8, on Glycinergic transmission was examined in mechanically isolated rat medullary dorsal horn neurons by use of the conventional whole-cell patch-clamp technique. Icilin increased the frequency of Glycinergic spontaneous miniature inhibitory post-synaptic currents (mIPSCs) in a dose-dependent manner. Either allyl isothiocyanate(AITC) or cinnamaldehyde, other TRPA1 agonists, also increased mIPSC frequency, but the extent of facilitation induced by AITC or cinnamaldehyde was less than that induced by icilin. However, menthol, a TRPM8 agonist, had no facilitatory effect on Glycinergic mIPSCs. The icilin-induced increase in mIPSC frequency was significantly inhibited by either HC030031, a selective TRPA1 antagonist, or ruthenium red, a non-selective transient receptor potential channel blocker. Icilin failed to increase Glycinergic mIPSC frequency in the absence of extracellular Ca(2+), suggesting that the icilin-induced increase in mIPSC frequency is mediated by the Ca(2+) influx from the extracellular space. In contrast, icilin still increased mIPSC frequency either in the Na(+) -free external solution or in the presence of Cd(2+), a general voltage-dependent Ca(2+) channel blocker. The present results suggest that icilin acts on pre-synaptic TRPA1-like ion channels, which are permeable to Ca(2+), to enhance Glycinergic transmission onto medullary dorsal horn neurons. The TRPA1-like channel-mediated enhancement of Glycinergic transmission in medullary dorsal horn neurons would contribute to the regulation of pain information from the peripheral tissues.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca(2+) channels in the rat trigeminal subnucleus caudalis.
European journal of pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K(+) channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca(2+) influx passing through presynaptic N-type and P/Q-type Ca(2+) channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca(2+) channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca(2+) channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca(2+) channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca2+ channels in the rat trigeminal subnucleus caudalis
European Journal of Pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:Abstract We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K + channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca 2+ influx passing through presynaptic N-type and P/Q-type Ca 2+ channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca 2+ channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca 2+ channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca 2+ channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
Insun Choi - One of the best experts on this subject based on the ideXlab platform.
-
pregnenolone sulfate modulates Glycinergic transmission in rat medullary dorsal horn neurons
European Journal of Pharmacology, 2013Co-Authors: Jungsu Hong, Jinhwa Cho, Insun Choi, Maangee Lee, Ilsung JangAbstract:Abstract The neurosteroid pregnenolone sulfate (PS), a representative excitatory neuromodulator, has a variety of neuropharmacological actions, such as memory enhancement and convulsant effects. In this study, the effects of PS on Glycinergic transmission, such as Glycinergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs), were investigated in acutely isolated medullary dorsal horn neurons by use of a conventional whole-cell patch-clamp technique. PS significantly increased the frequency but decreased the amplitude of Glycinergic mIPSCs in a concentration-dependent manner. PS also accelerated the decay time constant of Glycinergic mIPSCs. The PS-induced decrease in mIPSC amplitude was due to the direct postsynaptic inhibition of glycine receptors because PS inhibited the glycine-induced Cl − currents in a noncompetitive manner. The PS-induced increase in mIPSC frequency was not due to the activation of α7 nicotinic acetylcholine, NMDA, σ1 receptors and voltage-dependent Ca 2+ channels, which are known to be molecular targets of PS. On the other hand, the PS-induced increase in mIPSC frequency was completely attenuated either in the Ca 2+ -free external solution or in the presence of transient receptor potential (TRP) channel blockers, suggesting that PS elicits an increase in Ca 2+ concentration within Glycinergic nerve terminals via the activation of putative TRP channels. The PS-mediated modulation of Glycinergic synaptic transmission, such as the enhancement of presynaptic glycine release and direct inhibition of postsynaptic glycine receptors, might have a broad impact on the excitability of medullary dorsal horn neurons and therefore affect the processing of nociceptive transmission from orofacial tissues.
-
TRPA1-like channels enhance Glycinergic transmission in medullary dorsal horn neurons.
Journal of neurochemistry, 2012Co-Authors: Jinhwa Cho, Insun Choi, Moon-young Jeong, Heon-jin Lee, Ilsung JangAbstract:The effect of icilin, a potent agonist of transient receptor potential ankyrin 1 (TRPA1) and TRPM8, on Glycinergic transmission was examined in mechanically isolated rat medullary dorsal horn neurons by use of the conventional whole-cell patch-clamp technique. Icilin increased the frequency of Glycinergic spontaneous miniature inhibitory post-synaptic currents (mIPSCs) in a dose-dependent manner. Either allyl isothiocyanate(AITC) or cinnamaldehyde, other TRPA1 agonists, also increased mIPSC frequency, but the extent of facilitation induced by AITC or cinnamaldehyde was less than that induced by icilin. However, menthol, a TRPM8 agonist, had no facilitatory effect on Glycinergic mIPSCs. The icilin-induced increase in mIPSC frequency was significantly inhibited by either HC030031, a selective TRPA1 antagonist, or ruthenium red, a non-selective transient receptor potential channel blocker. Icilin failed to increase Glycinergic mIPSC frequency in the absence of extracellular Ca(2+), suggesting that the icilin-induced increase in mIPSC frequency is mediated by the Ca(2+) influx from the extracellular space. In contrast, icilin still increased mIPSC frequency either in the Na(+) -free external solution or in the presence of Cd(2+), a general voltage-dependent Ca(2+) channel blocker. The present results suggest that icilin acts on pre-synaptic TRPA1-like ion channels, which are permeable to Ca(2+), to enhance Glycinergic transmission onto medullary dorsal horn neurons. The TRPA1-like channel-mediated enhancement of Glycinergic transmission in medullary dorsal horn neurons would contribute to the regulation of pain information from the peripheral tissues.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca(2+) channels in the rat trigeminal subnucleus caudalis.
European journal of pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K(+) channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca(2+) influx passing through presynaptic N-type and P/Q-type Ca(2+) channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca(2+) channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca(2+) channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca(2+) channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca2+ channels in the rat trigeminal subnucleus caudalis
European Journal of Pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:Abstract We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K + channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca 2+ influx passing through presynaptic N-type and P/Q-type Ca 2+ channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca 2+ channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca 2+ channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca 2+ channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
-
Cyclic AMP-mediated long-term facilitation of Glycinergic transmission in developing spinal dorsal horn neurons.
Journal of neurochemistry, 2009Co-Authors: Insun Choi, Jinhwa Cho, Jun Kim, Byung Ju Choi, Michiko Nakamura, Hye-mi Park, Sang-jung Kim, Jong-ju Lee, Ilsung JangAbstract:cAMP is known to regulate neurotransmitter release via protein kinase A (PKA)-dependent and/or PKA-independent signal transduction pathways at a variety of central synapses. Here we report the cAMP-mediated long-lasting enhancement of Glycinergic transmission in developing rat spinal substantia gelatinosa neurons. Forskolin, an adenylyl cyclase activator, elicited a long-lasting increase in the amplitude of nerve-evoked Glycinergic inhibitory postsynaptic currents (IPSCs), accompanied by a long-lasting decrease in the paired-pulse ratio in immature substantia gelatinosa neurons, and this forskolin-induced increase in Glycinergic IPSCs decreased with postnatal development. Forskolin also decreased the failure rate of Glycinergic IPSCs evoked by minimal stimulation, and increased the frequency of Glycinergic miniature IPSCs. All of these data suggest that forskolin induces the long-lasting enhancement of Glycinergic transmission by increasing in the presynaptic release probability. This pre-synaptic action of forskolin was mediated by hyperpolarization and cyclic nucleotide-activated cation channels and an increase in intraterminal Ca2+ concentration but independent of PKA. The present results suggest that cAMP-dependent signal transduction pathways represent a dynamic mechanism by which Glycinergic IPSCs could potentially be modulated during postnatal development.
Karl Kandler - One of the best experts on this subject based on the ideXlab platform.
-
Inhibitory synapses in the developing auditory system are glutamatergic
Nature Neuroscience, 2005Co-Authors: Deda C Gillespie, Gunsoo Kim, Karl KandlerAbstract:Activity-dependent synapse refinement is crucial for the formation of precise excitatory and inhibitory neuronal circuits. Whereas the mechanisms that guide refinement of excitatory circuits are becoming increasingly clear, the mechanisms guiding inhibitory circuits have remained obscure. In the lateral superior olive (LSO), a nucleus in the mammalian sound localization system that receives inhibitory input from the medial nucleus of the trapezoid body (MNTB), specific elimination and strengthening of synapses that are both GABAergic and Glycinergic (GABA/Glycinergic synapses) is essential for the formation of a precise tonotopic map. We provide evidence that immature GABA/Glycinergic synapses in the rat LSO also release the excitatory neurotransmitter glutamate, which activates postsynaptic NMDA receptors (NMDARs). Immunohistochemical studies demonstrate synaptic colocalization of the vesicular glutamate transporter 3 with the vesicular GABA transporter, indicating that GABA, glycine and glutamate are released from single MNTB terminals. Glutamatergic transmission at MNTB-LSO synapses is most prominent during the period of synapse elimination. Synapse-specific activation of NMDARs by glutamate release at GABAergic and Glycinergic synapses could be important in activity-dependent refinement of inhibitory circuits.
-
elimination and strengthening of Glycinergic gabaergic connections during tonotopic map formation
Nature Neuroscience, 2003Co-Authors: Gunsoo Kim, Karl KandlerAbstract:Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation
-
Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation.
Nature neuroscience, 2003Co-Authors: Gunsoo Kim, Karl KandlerAbstract:Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation
-
Excitatory action of an immature Glycinergic/GABAergic sound localization pathway.
Physiology & behavior, 2002Co-Authors: Karl Kandler, Paul H M Kullmann, F Aura Ene, Gunsoo KimAbstract:Most mammals determine the azimuthal direction of incoming sound using auditory cues arising from differences in interaural sound intensity. The first station in the ascending auditory pathway, which processes interaural intensity differences, is the lateral superior olive (LSO), a binaural nucleus in the auditory brainstem. LSO neurons encode interaural intensity differences by integrating excitatory input from the ipsilateral cochlea and inhibitory input from the contralateral cochlea. Both inputs converge on single neurons in a highly organized, frequency-specific manner. The correct development of the precise arrangement of these inputs and their physiological properties depends on neuronal activity. Previous studies have shown that inhibitory, Glycinergic/GABAergic inputs to the LSO are transiently depolarizing, and it has been hypothesized that this depolarizing action enables developing inhibitory inputs to act as excitatory inputs. In support of this hypothesis, we recently demonstrated that depolarizing Glycinergic/GABAergic inputs can increase the intracellular calcium concentration in immature LSO neurons and elicit action potentials. These results provide support for the notion that the influence of Glycinergic/GABAergic synaptic activity on development of the LSO involves calcium-dependent signaling mechanisms.
Jinhwa Cho - One of the best experts on this subject based on the ideXlab platform.
-
pregnenolone sulfate modulates Glycinergic transmission in rat medullary dorsal horn neurons
European Journal of Pharmacology, 2013Co-Authors: Jungsu Hong, Jinhwa Cho, Insun Choi, Maangee Lee, Ilsung JangAbstract:Abstract The neurosteroid pregnenolone sulfate (PS), a representative excitatory neuromodulator, has a variety of neuropharmacological actions, such as memory enhancement and convulsant effects. In this study, the effects of PS on Glycinergic transmission, such as Glycinergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs), were investigated in acutely isolated medullary dorsal horn neurons by use of a conventional whole-cell patch-clamp technique. PS significantly increased the frequency but decreased the amplitude of Glycinergic mIPSCs in a concentration-dependent manner. PS also accelerated the decay time constant of Glycinergic mIPSCs. The PS-induced decrease in mIPSC amplitude was due to the direct postsynaptic inhibition of glycine receptors because PS inhibited the glycine-induced Cl − currents in a noncompetitive manner. The PS-induced increase in mIPSC frequency was not due to the activation of α7 nicotinic acetylcholine, NMDA, σ1 receptors and voltage-dependent Ca 2+ channels, which are known to be molecular targets of PS. On the other hand, the PS-induced increase in mIPSC frequency was completely attenuated either in the Ca 2+ -free external solution or in the presence of transient receptor potential (TRP) channel blockers, suggesting that PS elicits an increase in Ca 2+ concentration within Glycinergic nerve terminals via the activation of putative TRP channels. The PS-mediated modulation of Glycinergic synaptic transmission, such as the enhancement of presynaptic glycine release and direct inhibition of postsynaptic glycine receptors, might have a broad impact on the excitability of medullary dorsal horn neurons and therefore affect the processing of nociceptive transmission from orofacial tissues.
-
TRPA1-like channels enhance Glycinergic transmission in medullary dorsal horn neurons.
Journal of neurochemistry, 2012Co-Authors: Jinhwa Cho, Insun Choi, Moon-young Jeong, Heon-jin Lee, Ilsung JangAbstract:The effect of icilin, a potent agonist of transient receptor potential ankyrin 1 (TRPA1) and TRPM8, on Glycinergic transmission was examined in mechanically isolated rat medullary dorsal horn neurons by use of the conventional whole-cell patch-clamp technique. Icilin increased the frequency of Glycinergic spontaneous miniature inhibitory post-synaptic currents (mIPSCs) in a dose-dependent manner. Either allyl isothiocyanate(AITC) or cinnamaldehyde, other TRPA1 agonists, also increased mIPSC frequency, but the extent of facilitation induced by AITC or cinnamaldehyde was less than that induced by icilin. However, menthol, a TRPM8 agonist, had no facilitatory effect on Glycinergic mIPSCs. The icilin-induced increase in mIPSC frequency was significantly inhibited by either HC030031, a selective TRPA1 antagonist, or ruthenium red, a non-selective transient receptor potential channel blocker. Icilin failed to increase Glycinergic mIPSC frequency in the absence of extracellular Ca(2+), suggesting that the icilin-induced increase in mIPSC frequency is mediated by the Ca(2+) influx from the extracellular space. In contrast, icilin still increased mIPSC frequency either in the Na(+) -free external solution or in the presence of Cd(2+), a general voltage-dependent Ca(2+) channel blocker. The present results suggest that icilin acts on pre-synaptic TRPA1-like ion channels, which are permeable to Ca(2+), to enhance Glycinergic transmission onto medullary dorsal horn neurons. The TRPA1-like channel-mediated enhancement of Glycinergic transmission in medullary dorsal horn neurons would contribute to the regulation of pain information from the peripheral tissues.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca(2+) channels in the rat trigeminal subnucleus caudalis.
European journal of pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K(+) channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca(2+) influx passing through presynaptic N-type and P/Q-type Ca(2+) channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca(2+) channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca(2+) channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca(2+) channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
-
Tyramine reduces Glycinergic transmission by inhibiting presynaptic Ca2+ channels in the rat trigeminal subnucleus caudalis
European Journal of Pharmacology, 2011Co-Authors: Insun Choi, Jinhwa Cho, Maangee Lee, Ilsung JangAbstract:Abstract We have recently reported that tyramine acts on putative presynaptic trace amine receptors to inhibit Glycinergic transmission in substantia gelatinosa (SG) neurons of the rat trigeminal subnucleus caudalis. However, it is still unknown how tyramine elicits presynaptic inhibition of glycine release. In the present study, therefore, we investigated cellular mechanisms underlying the tyramine-induced inhibition of Glycinergic transmission in SG neurons using a conventional whole-cell patch clamp technique. Tyramine (100 μM) reversibly and repetitively decreased the amplitude of action potential-dependent Glycinergic inhibitory postsynaptic currents (IPSCs), and increased the paired-pulse ratio. Pharmacological data suggest that the tyramine-induced decrease in Glycinergic IPSCs was not mediated by the modulation of adenylyl cyclase, protein kinase A and C, or G-protein coupled inwardly rectifying K + channels. On the other hand, Glycinergic IPSCs were mainly mediated by the Ca 2+ influx passing through presynaptic N-type and P/Q-type Ca 2+ channels. The tyramine-induced decrease in Glycinergic IPSCs was completely blocked by ω-conotoxin GVIA, an N-type Ca 2+ channel blocker, but not ω-agatoxin IVA, a P/Q-type Ca 2+ channel blocker. The results suggest that tyramine acts presynaptically to decrease action potential-dependent glycine release onto SG neurons via the selective inhibition of presynaptic N-type Ca 2+ channels. This tyramine-induced inhibition of Glycinergic transmission in SG neurons might affect the process of orofacial nociceptive signals.
-
Cyclic AMP-mediated long-term facilitation of Glycinergic transmission in developing spinal dorsal horn neurons.
Journal of neurochemistry, 2009Co-Authors: Insun Choi, Jinhwa Cho, Jun Kim, Byung Ju Choi, Michiko Nakamura, Hye-mi Park, Sang-jung Kim, Jong-ju Lee, Ilsung JangAbstract:cAMP is known to regulate neurotransmitter release via protein kinase A (PKA)-dependent and/or PKA-independent signal transduction pathways at a variety of central synapses. Here we report the cAMP-mediated long-lasting enhancement of Glycinergic transmission in developing rat spinal substantia gelatinosa neurons. Forskolin, an adenylyl cyclase activator, elicited a long-lasting increase in the amplitude of nerve-evoked Glycinergic inhibitory postsynaptic currents (IPSCs), accompanied by a long-lasting decrease in the paired-pulse ratio in immature substantia gelatinosa neurons, and this forskolin-induced increase in Glycinergic IPSCs decreased with postnatal development. Forskolin also decreased the failure rate of Glycinergic IPSCs evoked by minimal stimulation, and increased the frequency of Glycinergic miniature IPSCs. All of these data suggest that forskolin induces the long-lasting enhancement of Glycinergic transmission by increasing in the presynaptic release probability. This pre-synaptic action of forskolin was mediated by hyperpolarization and cyclic nucleotide-activated cation channels and an increase in intraterminal Ca2+ concentration but independent of PKA. The present results suggest that cAMP-dependent signal transduction pathways represent a dynamic mechanism by which Glycinergic IPSCs could potentially be modulated during postnatal development.
Gunsoo Kim - One of the best experts on this subject based on the ideXlab platform.
-
Inhibitory synapses in the developing auditory system are glutamatergic
Nature Neuroscience, 2005Co-Authors: Deda C Gillespie, Gunsoo Kim, Karl KandlerAbstract:Activity-dependent synapse refinement is crucial for the formation of precise excitatory and inhibitory neuronal circuits. Whereas the mechanisms that guide refinement of excitatory circuits are becoming increasingly clear, the mechanisms guiding inhibitory circuits have remained obscure. In the lateral superior olive (LSO), a nucleus in the mammalian sound localization system that receives inhibitory input from the medial nucleus of the trapezoid body (MNTB), specific elimination and strengthening of synapses that are both GABAergic and Glycinergic (GABA/Glycinergic synapses) is essential for the formation of a precise tonotopic map. We provide evidence that immature GABA/Glycinergic synapses in the rat LSO also release the excitatory neurotransmitter glutamate, which activates postsynaptic NMDA receptors (NMDARs). Immunohistochemical studies demonstrate synaptic colocalization of the vesicular glutamate transporter 3 with the vesicular GABA transporter, indicating that GABA, glycine and glutamate are released from single MNTB terminals. Glutamatergic transmission at MNTB-LSO synapses is most prominent during the period of synapse elimination. Synapse-specific activation of NMDARs by glutamate release at GABAergic and Glycinergic synapses could be important in activity-dependent refinement of inhibitory circuits.
-
elimination and strengthening of Glycinergic gabaergic connections during tonotopic map formation
Nature Neuroscience, 2003Co-Authors: Gunsoo Kim, Karl KandlerAbstract:Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation
-
Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation.
Nature neuroscience, 2003Co-Authors: Gunsoo Kim, Karl KandlerAbstract:Elimination and strengthening of Glycinergic/GABAergic connections during tonotopic map formation
-
Excitatory action of an immature Glycinergic/GABAergic sound localization pathway.
Physiology & behavior, 2002Co-Authors: Karl Kandler, Paul H M Kullmann, F Aura Ene, Gunsoo KimAbstract:Most mammals determine the azimuthal direction of incoming sound using auditory cues arising from differences in interaural sound intensity. The first station in the ascending auditory pathway, which processes interaural intensity differences, is the lateral superior olive (LSO), a binaural nucleus in the auditory brainstem. LSO neurons encode interaural intensity differences by integrating excitatory input from the ipsilateral cochlea and inhibitory input from the contralateral cochlea. Both inputs converge on single neurons in a highly organized, frequency-specific manner. The correct development of the precise arrangement of these inputs and their physiological properties depends on neuronal activity. Previous studies have shown that inhibitory, Glycinergic/GABAergic inputs to the LSO are transiently depolarizing, and it has been hypothesized that this depolarizing action enables developing inhibitory inputs to act as excitatory inputs. In support of this hypothesis, we recently demonstrated that depolarizing Glycinergic/GABAergic inputs can increase the intracellular calcium concentration in immature LSO neurons and elicit action potentials. These results provide support for the notion that the influence of Glycinergic/GABAergic synaptic activity on development of the LSO involves calcium-dependent signaling mechanisms.
