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Joseph H. Szurszewski - One of the best experts on this subject based on the ideXlab platform.

  • hydrogen sulfide selectively potentiates central preGanglionic fast nicotinic synaptic input in mouse Superior Mesenteric Ganglion
    The Journal of Neuroscience, 2013
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Hydrogen sulfide (H2S) plays important roles in the enteric system in the wall of the gastrointestinal tract. There have been no studies on whether H2S is endogenously generated in peripheral sympathetic ganglia and, if so, its effect on synaptic transmission. In this study, we examined the effect of H2S on cholinergic excitatory fast synaptic transmission in the mouse Superior Mesenteric Ganglion (SMG). Our study revealed that NaHS and endogenously generated H2S selectively potentiated cholinergic fast EPSPs (F-EPSPs) evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. The H2S-producing enzyme cystathionine-γ-lyase (CSE) was expressed in both neurons and glial cells. The CSE blocker PAG (dl-propargylglycine) significantly reduced the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. Inhibiting the breakdown of endogenously generated H2S with stigmatellin potentiated the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. Splanchnic F-EPSPs but not colonic F-EPSPs were reduced in CSE knock-out (KO) mice. Functional studies showed that NaHS enhanced the inhibitory effect of splanchnic nerve stimulation on colonic motility. Colonic motility in CSE-KO mice was significantly higher than colonic motility in wild-type mice. We conclude that endogenously generated H2S acted selectively on presynaptic terminals of splanchnic nerves to modulate fast cholinergic synaptic input and that this effect of H2S modulates CNS control of gastrointestinal motility. Our results show for the first time that the facilitatory effect of endogenous H2S in the mouse SMG is pathway specific.

  • 489 endogenous h2s produced in prevertebral sympathetic ganglia predominantly by cse in neurons and glia cells modulates central cholinergic synaptic input
    Gastroenterology, 2012
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Hydrogen sulfide(H2S), mainly produced endogenously by two enzymes, cystathionine γlyase(CSE) and cystathionine β-synthase(CBS), is a messenger molecule in the central nervous system, in the GI tract and in sympathetic prevertebral ganglia. Our previous study found, in mouse Superior Mesenteric Ganglion(SMG), that exogenous H2S acts selectively on splanchnic nerve terminals to potentiate fast excitatory post synaptic potentials (F-EPSPs). In this study, we investigated the distribution of CSE and CBS and the role of endogenously produced H2S on central sympathetic input. Methods: The SMG, splanchnic nerve trunks and colonic nerve trunk were dissected from adult SJL/J mice. Immunostaining was performed with antibodies for CSE and CBS and for vesicular acetylcholine transporter(VAChT) to identify cholinergic nerve terminals. Microelectrodes were used for intracellular recordings. Results: CSE immunoreactivity(IR) was found in neurons and glia cells and did not co-localize with VAChT-IR. CBS-IR was found only in glia cells. To determine whether the F-EPSPs could be potentiated by endogenously released H2S, we tested the effect of inhibiting H2S breakdown with stigmatellin, a specific sulfide quinone reductase inhibitor, on F-EPSPs. Stigmatellin(1μM) significantly(P<0.05) increased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(21.0±4.8mV and 441±107ms●mV with stigmatellin vs. 18.4±5.3mV and 338±108ms●mV before stigmatellin, n=4) but had no significant effect on F-EPSPs evoked by colonic nerve stimulation. In contrast, the CSE inhibitor, dl-propargylglycine(PAG, 1mM), significantly(P<0.05) decreased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(23.7±3.9mV and 824±288ms●mV with PAG vs. 27.0±4.1mV and 1230±414ms●mV before PAG, n=6), but had no effect on F-EPSPs evoked by colonic nerve stimulation. Surprisingly, the CBS inhibitor, aminooxyacetic acid(AOAA, 0.5mM), increased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(23.6±12.1mV and 651±455ms●mV with AOAA vs. 20.2±10.9mV and 438±318ms●mV before AOAA, n=4, P<0.05) and increased the amplitude and the area of F-EPSPs evoked by colonic nerve stimulation(36.2±8.2mV and 1609±468ms●mV with AOAA vs. 28.9±8.1mV and 1084±402ms●mV before AOAA, n=6, P<0.05). Bicuculline(20μM), a specific GABA-A receptor inhibitor, blocked the potentiating effect of AOAA suggesting that the AOAA induced potentiation of F-EPSPs was due to the inhibition of GABA transaminase-induced accumulation of GABA. Conclusion: We conclude that endogenously produced H2S in the mouse SMG modulates fast cholinergic synaptic input in a pathwayspecific manner. H2S modulates fast cholinergic synaptic input from central splanchnic nerve terminals but has no affect on input from peripheral cholinergic input. (Funded by NIH DK17238)

  • P21 Endogenous H2S produced by CSE selectively facilitates acetylcholine release from synaptic terminals of central origin in mouse Superior Mesenteric Ganglion
    Nitric Oxide, 2012
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Abdominal sympathetic prevertebral ganglia in mammals play a major physiological role in regulating motility, absorption and secretion in the gastrointestinal tract and its accessory organs. Hydrogen sulfide (H2S) has emerged as an important messenger molecule in the central nervous system and enteric nervous system. We designed experiments to test the hypotheses that prevertebral ganglia have the enzymatic machinery to generate H2S, that H2S is continuously generated and released in the prevertebral ganglia and that H2S modulates fast cholinergic nicotinic excitatory synaptic input (F-EPSP). Methods The Superior Mesenteric Ganglion (SMG) and attached splanchnic and colonic nerve trunks were dissected from adult SJL/J mice. The use of mouse tissue was approved by the Institutional Animal Care and Use Committee. Sharp glass microelectrodes were used for intracellular recordings and bi-polar stimulating electrodes were used to evoke F-EPSPs. Immunostaining was performed with antibodies for cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) and with vesicular acetylcholine transporter to identify preGanglionic cholinergic terminals. Since the amount of tissue in mouse prevertebral ganglia was less than the amount required for the assay method (gas chromatography), we used guinea pig prevertebral ganglia to measure endogenous H2S generation. Results Immunoreactivity of CSE was found in neurons and glia cells. There was no colocalization of CSE with immunoreactivity of vesicular acetylcholine transporter. Immunoreactivity of CBS was only found in some glia cells. There was no colocalization between immunoreactivity of CBS and immunoreactivity of vesicular acetylcholine transporter. Endogenous H2S was generated and released from homogenized guinea pig sympathetic prevertebral ganglia at a rate of 2.52 ± 0.52 pmol/min/mg tissue weight, suggesting that H2S is generated in intact prevertebral ganglia. To determine whether the F-EPSPs are potentiated by endogenously released H2S in mouse SMG, we tested the effect of inhibiting H2S break-down using stigmatellin, a specific sulfide quinone reductase inhibitor. Stigmatellin (1 μM) significantly (p  dl -propargylglycine (PAG) (1 μM) on F-EPSPs evoked by splanchnic and colonic nerve stimulation in the presence of PAG. The amplitude and area of F-EPSPs evoked by splanchnic nerve stimulation were significantly (p   0.05) effect on F-EPSPs evoked by colonic nerve stimulation (30.2 ± 6.1 mV and 808 ± 235 ms · mV with PAG vs. 26.9 ± 7.6 mV and 855 ± 241 ms · mV before PAG; n = 5). Conclusions H2S is enzymatically generated and released in the mouse prevertebral ganglia where it potentiates fast cholinergic synaptic input in a pathway specific manner.

Yukihiko Yasui - One of the best experts on this subject based on the ideXlab platform.

  • Origins of nerve fibers containing nitric oxide synthase in the rat celiac-Superior Mesenteric Ganglion
    Cell and Tissue Research, 1995
    Co-Authors: Tokio Domoto, Makoto Teramoto, Keiichiro Tanigawa, Katsuhiro Tamura, Yukihiko Yasui
    Abstract:

    The origin of nitric oxide synthase-containing nerve fibers in rat celiac-Superior Mesenteric Ganglion was examined using retrograde tracing techniques combined with the immunofluorescence method. Fluoro-Gold was injected into the celiac-Superior Mesenteric Ganglion. Neuronal cell bodies retrogradely labeled with Fluoro-Gold in the thoracic spinal cord, the dorsal root ganglia at the thoracic level, the nodose Ganglion, and the intestine from the duodenum to the proximal colon were examined for nitric oxide synthase immunoreactivity. About 60% of sympathetic preGanglionic neurons in the intermediolateral nucleus projecting to the celiac-Superior Mesenteric Ganglion were immunoreactive for nitric oxide synthase, as were approximately 27% of nodose Ganglion neurons and about 65% of dorsal root Ganglion neurons projecting to the cceliac-Superior Mesenteric Ganglion. Neurons projecting to the celiac-Superior Mesenteric Ganglion were found in the myenteric plexus of the small and large intestine. In the proximal colon, about 23% of such neurons were immunoreactive for nitric oxide synthase. However, in the small intestine, no immunoreactivity was found in these neurons.

O. Häppölä - One of the best experts on this subject based on the ideXlab platform.

  • 5 hydroxytryptamine immunoreactive nerve fibers in the rat and porcine prevertebral sympathetic ganglia effect of precursor loading and relation to catecholaminergic neurons
    Neuroscience Letters, 1995
    Co-Authors: T Karhulaa, M Lakomy, Mariusz Majewski, Seppo Soinila, J Kaleczyk, O. Häppölä
    Abstract:

    Localization of 5-hydroxytryptamine immunoreactivity was studied in the rat coeliac-Superior Mesenteric Ganglion complex and in the porcine Superior and inferior Mesenteric ganglia by the indirect immunofluorescence technique. In normal rats, only 5-hydroxytryptamine immunoreactive SIF cells were seen in the coeliac-Superior Mesenteric Ganglion complex. In the rats, pretreated with a 5-hydroxytryptamine precursor, L-tryptophan, and with a monoamine oxidase inhibitor, nialamide, a large number of 5-hydroxytryptamine-immunoreactive nerve fiber terminals were detected. In normal porcine Superior and inferior Mesenteric ganglia, intense 5-hydroxytryptamine immunoreactivity was found in numerous nerve fibers which were located around tyrosine hydroxylase-immunoreactive principal neurons. The origin and function of these fibers are discussed.

  • neuropeptides in the porcine coeliac Superior Mesenteric Ganglion
    Folia Histochemica Et Cytobiologica, 1993
    Co-Authors: M Lakomy, O. Häppölä, Mariusz Majewski, K Wasowicz
    Abstract:

    The occurrence and distribution of tyrosine hydroxylase, neuropeptide Y, somatostatin, Met5-enkephalin-Arg6-Gly7-Leu8, vasoactive intestinal polypeptide, substance P, calcitonin gene-related peptide, bombesin gastrin releasing peptide and galanin were immunohistochemically studied in the perikarya and nerve fibres of the porcine coeliac-Superior Mesenteric Ganglion of untreated juvenile pigs. Subpopulations of neurons containing immunoreactivities to tyrosine hydroxylase, neuropeptide Y, Met5-enkephalin-Arg6-Gly7-Leu8, somatostatin, vasoactive intestinal polypeptide and galanin were disclosed in the studied Ganglion, whereas principal Ganglionic cells were non-immunoreactive for other investigated peptides. Double-immunofluorescence and analysis of consecutive sections revealed a partial colocalization of tyrosine hydroxylase and neuropeptide Y, Met5-enkephalin-Arg6-Gly7-Leu8 and somatostatin, whereas immunoreactivity to vasoactive intestinal polypeptide and/or to neuropeptide Y was found in non-noradrenergic neurons in this Ganglion. All of neuropeptides studied were found in nerve fibres in this Ganglion. The results of this study were compared with those of previous studies performed on other species.

Lei Sha - One of the best experts on this subject based on the ideXlab platform.

  • hydrogen sulfide selectively potentiates central preGanglionic fast nicotinic synaptic input in mouse Superior Mesenteric Ganglion
    The Journal of Neuroscience, 2013
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Hydrogen sulfide (H2S) plays important roles in the enteric system in the wall of the gastrointestinal tract. There have been no studies on whether H2S is endogenously generated in peripheral sympathetic ganglia and, if so, its effect on synaptic transmission. In this study, we examined the effect of H2S on cholinergic excitatory fast synaptic transmission in the mouse Superior Mesenteric Ganglion (SMG). Our study revealed that NaHS and endogenously generated H2S selectively potentiated cholinergic fast EPSPs (F-EPSPs) evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. The H2S-producing enzyme cystathionine-γ-lyase (CSE) was expressed in both neurons and glial cells. The CSE blocker PAG (dl-propargylglycine) significantly reduced the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. Inhibiting the breakdown of endogenously generated H2S with stigmatellin potentiated the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation. Splanchnic F-EPSPs but not colonic F-EPSPs were reduced in CSE knock-out (KO) mice. Functional studies showed that NaHS enhanced the inhibitory effect of splanchnic nerve stimulation on colonic motility. Colonic motility in CSE-KO mice was significantly higher than colonic motility in wild-type mice. We conclude that endogenously generated H2S acted selectively on presynaptic terminals of splanchnic nerves to modulate fast cholinergic synaptic input and that this effect of H2S modulates CNS control of gastrointestinal motility. Our results show for the first time that the facilitatory effect of endogenous H2S in the mouse SMG is pathway specific.

  • 489 endogenous h2s produced in prevertebral sympathetic ganglia predominantly by cse in neurons and glia cells modulates central cholinergic synaptic input
    Gastroenterology, 2012
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Hydrogen sulfide(H2S), mainly produced endogenously by two enzymes, cystathionine γlyase(CSE) and cystathionine β-synthase(CBS), is a messenger molecule in the central nervous system, in the GI tract and in sympathetic prevertebral ganglia. Our previous study found, in mouse Superior Mesenteric Ganglion(SMG), that exogenous H2S acts selectively on splanchnic nerve terminals to potentiate fast excitatory post synaptic potentials (F-EPSPs). In this study, we investigated the distribution of CSE and CBS and the role of endogenously produced H2S on central sympathetic input. Methods: The SMG, splanchnic nerve trunks and colonic nerve trunk were dissected from adult SJL/J mice. Immunostaining was performed with antibodies for CSE and CBS and for vesicular acetylcholine transporter(VAChT) to identify cholinergic nerve terminals. Microelectrodes were used for intracellular recordings. Results: CSE immunoreactivity(IR) was found in neurons and glia cells and did not co-localize with VAChT-IR. CBS-IR was found only in glia cells. To determine whether the F-EPSPs could be potentiated by endogenously released H2S, we tested the effect of inhibiting H2S breakdown with stigmatellin, a specific sulfide quinone reductase inhibitor, on F-EPSPs. Stigmatellin(1μM) significantly(P<0.05) increased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(21.0±4.8mV and 441±107ms●mV with stigmatellin vs. 18.4±5.3mV and 338±108ms●mV before stigmatellin, n=4) but had no significant effect on F-EPSPs evoked by colonic nerve stimulation. In contrast, the CSE inhibitor, dl-propargylglycine(PAG, 1mM), significantly(P<0.05) decreased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(23.7±3.9mV and 824±288ms●mV with PAG vs. 27.0±4.1mV and 1230±414ms●mV before PAG, n=6), but had no effect on F-EPSPs evoked by colonic nerve stimulation. Surprisingly, the CBS inhibitor, aminooxyacetic acid(AOAA, 0.5mM), increased the amplitude and the area of F-EPSPs evoked by splanchnic nerve stimulation(23.6±12.1mV and 651±455ms●mV with AOAA vs. 20.2±10.9mV and 438±318ms●mV before AOAA, n=4, P<0.05) and increased the amplitude and the area of F-EPSPs evoked by colonic nerve stimulation(36.2±8.2mV and 1609±468ms●mV with AOAA vs. 28.9±8.1mV and 1084±402ms●mV before AOAA, n=6, P<0.05). Bicuculline(20μM), a specific GABA-A receptor inhibitor, blocked the potentiating effect of AOAA suggesting that the AOAA induced potentiation of F-EPSPs was due to the inhibition of GABA transaminase-induced accumulation of GABA. Conclusion: We conclude that endogenously produced H2S in the mouse SMG modulates fast cholinergic synaptic input in a pathwayspecific manner. H2S modulates fast cholinergic synaptic input from central splanchnic nerve terminals but has no affect on input from peripheral cholinergic input. (Funded by NIH DK17238)

  • P21 Endogenous H2S produced by CSE selectively facilitates acetylcholine release from synaptic terminals of central origin in mouse Superior Mesenteric Ganglion
    Nitric Oxide, 2012
    Co-Authors: Lei Sha, David R. Linden, Gianrico Farrugia, Joseph H. Szurszewski
    Abstract:

    Abdominal sympathetic prevertebral ganglia in mammals play a major physiological role in regulating motility, absorption and secretion in the gastrointestinal tract and its accessory organs. Hydrogen sulfide (H2S) has emerged as an important messenger molecule in the central nervous system and enteric nervous system. We designed experiments to test the hypotheses that prevertebral ganglia have the enzymatic machinery to generate H2S, that H2S is continuously generated and released in the prevertebral ganglia and that H2S modulates fast cholinergic nicotinic excitatory synaptic input (F-EPSP). Methods The Superior Mesenteric Ganglion (SMG) and attached splanchnic and colonic nerve trunks were dissected from adult SJL/J mice. The use of mouse tissue was approved by the Institutional Animal Care and Use Committee. Sharp glass microelectrodes were used for intracellular recordings and bi-polar stimulating electrodes were used to evoke F-EPSPs. Immunostaining was performed with antibodies for cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) and with vesicular acetylcholine transporter to identify preGanglionic cholinergic terminals. Since the amount of tissue in mouse prevertebral ganglia was less than the amount required for the assay method (gas chromatography), we used guinea pig prevertebral ganglia to measure endogenous H2S generation. Results Immunoreactivity of CSE was found in neurons and glia cells. There was no colocalization of CSE with immunoreactivity of vesicular acetylcholine transporter. Immunoreactivity of CBS was only found in some glia cells. There was no colocalization between immunoreactivity of CBS and immunoreactivity of vesicular acetylcholine transporter. Endogenous H2S was generated and released from homogenized guinea pig sympathetic prevertebral ganglia at a rate of 2.52 ± 0.52 pmol/min/mg tissue weight, suggesting that H2S is generated in intact prevertebral ganglia. To determine whether the F-EPSPs are potentiated by endogenously released H2S in mouse SMG, we tested the effect of inhibiting H2S break-down using stigmatellin, a specific sulfide quinone reductase inhibitor. Stigmatellin (1 μM) significantly (p  dl -propargylglycine (PAG) (1 μM) on F-EPSPs evoked by splanchnic and colonic nerve stimulation in the presence of PAG. The amplitude and area of F-EPSPs evoked by splanchnic nerve stimulation were significantly (p   0.05) effect on F-EPSPs evoked by colonic nerve stimulation (30.2 ± 6.1 mV and 808 ± 235 ms · mV with PAG vs. 26.9 ± 7.6 mV and 855 ± 241 ms · mV before PAG; n = 5). Conclusions H2S is enzymatically generated and released in the mouse prevertebral ganglia where it potentiates fast cholinergic synaptic input in a pathway specific manner.

Tokio Domoto - One of the best experts on this subject based on the ideXlab platform.

  • Origins of nerve fibers containing nitric oxide synthase in the rat celiac-Superior Mesenteric Ganglion
    Cell and Tissue Research, 1995
    Co-Authors: Tokio Domoto, Makoto Teramoto, Keiichiro Tanigawa, Katsuhiro Tamura, Yukihiko Yasui
    Abstract:

    The origin of nitric oxide synthase-containing nerve fibers in rat celiac-Superior Mesenteric Ganglion was examined using retrograde tracing techniques combined with the immunofluorescence method. Fluoro-Gold was injected into the celiac-Superior Mesenteric Ganglion. Neuronal cell bodies retrogradely labeled with Fluoro-Gold in the thoracic spinal cord, the dorsal root ganglia at the thoracic level, the nodose Ganglion, and the intestine from the duodenum to the proximal colon were examined for nitric oxide synthase immunoreactivity. About 60% of sympathetic preGanglionic neurons in the intermediolateral nucleus projecting to the celiac-Superior Mesenteric Ganglion were immunoreactive for nitric oxide synthase, as were approximately 27% of nodose Ganglion neurons and about 65% of dorsal root Ganglion neurons projecting to the cceliac-Superior Mesenteric Ganglion. Neurons projecting to the celiac-Superior Mesenteric Ganglion were found in the myenteric plexus of the small and large intestine. In the proximal colon, about 23% of such neurons were immunoreactive for nitric oxide synthase. However, in the small intestine, no immunoreactivity was found in these neurons.