Ionotropic Receptor Antagonist

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Jing Zhang Liu - One of the best experts on this subject based on the ideXlab platform.

  • microinjection of glutamate into dorsal motor nucleus of the vagus excites gallbladder motility through nmda Receptor nitric oxide cgmp pathway
    Neurogastroenterology and Motility, 2004
    Co-Authors: C. Y. Liu, Dong-ping Xie, Jing Zhang Liu
    Abstract:

    We have reported that both glutamate and nitric oxide (NO) participated in the regulation of gallbladder motility in dorsal motor nucleus of the vagus (DMV). The aim of this study is to investigate the type of Receptor in DMV that mediates the excitatory effect of glutamate on gallbladder motility and the correlation between the glutamate and NO. A frog bladder connected with a force transducer was inserted into the gallbladder to record the change of gallbladder pressure. Glutamate (65 mmol L(-1), 100 nL) microinjected into DMV significantly increased the strength of gallbladder phasic contraction. This effect was abolished by ketamine (180 mmol L(-1), 100 nL), the specific N-methyl-d-aspartic acid (NMDA) Receptor Antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (180 mmol L(-1), 100 nL), the non-NMDA Ionotropic Receptor Antagonist. N(G)-nitro-l-arginine-emthyl (l-NAME) (1 mol L(-1), 100 nL), the nitric oxide synthase (NOS) inhibitor, reversed the excitatory effect of glutamate on gallbladder motility. Microinjection of sodium nitroprusside (SNP), the NO donor, into DMV enhanced the gallbladder motility, and this effect was not modulated by ketamine. Microinjection of NMDA (5 mmol L(-1), 100 nL) increased the strength of gallbladder phasic contraction, and this effect was attenuated by methylene blue (100 mmol L(-1), 100 nL), the soluble guanylate cyclase inhibitor. These results suggest that glutamate regulate the gallbladder motility through the NMDA Receptor - NO - cGMP pathway in DMV.

C. Y. Liu - One of the best experts on this subject based on the ideXlab platform.

  • microinjection of glutamate into dorsal motor nucleus of the vagus excites gallbladder motility through nmda Receptor nitric oxide cgmp pathway
    Neurogastroenterology and Motility, 2004
    Co-Authors: C. Y. Liu, Dong-ping Xie, Jing Zhang Liu
    Abstract:

    We have reported that both glutamate and nitric oxide (NO) participated in the regulation of gallbladder motility in dorsal motor nucleus of the vagus (DMV). The aim of this study is to investigate the type of Receptor in DMV that mediates the excitatory effect of glutamate on gallbladder motility and the correlation between the glutamate and NO. A frog bladder connected with a force transducer was inserted into the gallbladder to record the change of gallbladder pressure. Glutamate (65 mmol L(-1), 100 nL) microinjected into DMV significantly increased the strength of gallbladder phasic contraction. This effect was abolished by ketamine (180 mmol L(-1), 100 nL), the specific N-methyl-d-aspartic acid (NMDA) Receptor Antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (180 mmol L(-1), 100 nL), the non-NMDA Ionotropic Receptor Antagonist. N(G)-nitro-l-arginine-emthyl (l-NAME) (1 mol L(-1), 100 nL), the nitric oxide synthase (NOS) inhibitor, reversed the excitatory effect of glutamate on gallbladder motility. Microinjection of sodium nitroprusside (SNP), the NO donor, into DMV enhanced the gallbladder motility, and this effect was not modulated by ketamine. Microinjection of NMDA (5 mmol L(-1), 100 nL) increased the strength of gallbladder phasic contraction, and this effect was attenuated by methylene blue (100 mmol L(-1), 100 nL), the soluble guanylate cyclase inhibitor. These results suggest that glutamate regulate the gallbladder motility through the NMDA Receptor - NO - cGMP pathway in DMV.

Dong-ping Xie - One of the best experts on this subject based on the ideXlab platform.

  • microinjection of glutamate into dorsal motor nucleus of the vagus excites gallbladder motility through nmda Receptor nitric oxide cgmp pathway
    Neurogastroenterology and Motility, 2004
    Co-Authors: C. Y. Liu, Dong-ping Xie, Jing Zhang Liu
    Abstract:

    We have reported that both glutamate and nitric oxide (NO) participated in the regulation of gallbladder motility in dorsal motor nucleus of the vagus (DMV). The aim of this study is to investigate the type of Receptor in DMV that mediates the excitatory effect of glutamate on gallbladder motility and the correlation between the glutamate and NO. A frog bladder connected with a force transducer was inserted into the gallbladder to record the change of gallbladder pressure. Glutamate (65 mmol L(-1), 100 nL) microinjected into DMV significantly increased the strength of gallbladder phasic contraction. This effect was abolished by ketamine (180 mmol L(-1), 100 nL), the specific N-methyl-d-aspartic acid (NMDA) Receptor Antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (180 mmol L(-1), 100 nL), the non-NMDA Ionotropic Receptor Antagonist. N(G)-nitro-l-arginine-emthyl (l-NAME) (1 mol L(-1), 100 nL), the nitric oxide synthase (NOS) inhibitor, reversed the excitatory effect of glutamate on gallbladder motility. Microinjection of sodium nitroprusside (SNP), the NO donor, into DMV enhanced the gallbladder motility, and this effect was not modulated by ketamine. Microinjection of NMDA (5 mmol L(-1), 100 nL) increased the strength of gallbladder phasic contraction, and this effect was attenuated by methylene blue (100 mmol L(-1), 100 nL), the soluble guanylate cyclase inhibitor. These results suggest that glutamate regulate the gallbladder motility through the NMDA Receptor - NO - cGMP pathway in DMV.

Xiyun Cui - One of the best experts on this subject based on the ideXlab platform.

  • effects and mechanisms of l glutamate microinjected into nucleus ambiguus on gastric motility in rats
    Chinese Medical Journal, 2010
    Co-Authors: Hongzhao Sun, Shuzhen Zhao, Xiyun Cui
    Abstract:

    Background L-glutamate (L-GLU) is a major neurotransmitter in the nucleus ambiguus (NA), which can modulate respiration, arterial pressure, heart rate, etc. This study investigated the effects and mechanisms of L-GLU microinjected into NA on gastric motility in rats. Methods A latex balloon connected with a pressure transducer was inserted into the pylorus through the forestomach for continuous recording of the gastric motility. The total amplitude, total duration, and motility index of gastric contraction waves within 5 minutes before microinjection and after microinjection were measured. Results L-GLU (5 nmol, 10 nmol and 20 nmol in 50 nl normal saline (PS) respectively) microinjected into the right NA significantly inhibited gastric motility, while microinjection of physiological saline at the same position and the same volume did not change the gastric motility. The inhibitory effect was blocked by D-2-amino-5-phophonovalerate (D-AP5, 5 nmol, in 50 nl PS), the specific N-methyl-D-aspartic acid (NMDA) Receptor Antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (5 nmol, in 50 nl PS), the non-NMDA Ionotropic Receptor Antagonist. Bilateral subdiaphragmatic vagotomy abolished the inhibitory effect by microinjection of L-GLU into NA. Conclusions Microinjection of L-GLU into NA inhibits the gastric motility through specific NMDA Receptor activity, not non-NMDA Receptor activity, and the efferent pathway is the vagal nerves.

Ralph E Davis - One of the best experts on this subject based on the ideXlab platform.

  • action of excitatory amino acids on hypodermis and the motornervous system of ascaris suum pharmacological evidence for a glutamate transporter
    Parasitology, 1998
    Co-Authors: Ralph E Davis
    Abstract:

    : Electrophysiological and pharmacological experiments suggest the presence of an electrogenic glutamate transporter in the motornervous system of the parasitic nematode Ascaris suum. This putative transporter occurs in hypodermis (a tissue in some respects analogous to glia) and in DE2 motorneurons, a dorsal excitatory motorneuron class which receives excitatory glutamatergic post-synaptic potentials. Glutamate application to hypodermis produced non-conductance mediated depolarizations that were smaller in amplitude and slower in rate of rise than DE2 responses where a glutamate-activated conductance occurs. The hypodermal response is sodium dependent and calcium independent. Excitatory amino acid Ionotropic Receptor agonists (kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid and N-methyl-D-aspartate) were ineffective in eliciting hypodermal responses. The Ionotropic Receptor Antagonist, 6,7-dinitroquinoline-2,3-dione, had no effect on hypodermal glutamate responses. The L- and D-form of glutamate, aspartate and homocysteate produced hypodermal and DE2 depolarizations consistent with the pharmacological profile for glutamate transporters in other systems. Glutamate transport inhibitors (L-trans-pyrrolidine-2,4-dicarboxylate and beta-hydroxyaspartate) elicited electrogenic depolarizations in hypodermis and DE2. These results suggest that the hypodermal glutamate response has an electrogenic transporter component, while the DE2 response has 2 components, one conductance-mediated and the other due to an electrogenic transporter.