Glutamate stimulation of acetylcholine release from myenteric plexus is mediated by endogenous nitric oxide

Milusheva, E.; Kuneva, V.; Itzev, Dimitar E.; Kortezova, N; Sperlágh, Beáta; Mizhorkova, Z.

doi:10.1016/j.brainresbull.2005.05.011

Cited by 13 publications

(8 citation statements)

References 28 publications

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“…This assumption is supported by the data of Milusheva et al. 43 showing increased nicotinamide adenine dinucleotide phosphate (NADPH)‐diaphorase staining and stimulation of acetylcholine release after glutamate application. It is also concordant with the finding of Bartho and Lefebvre 44 showing a stimulatory effect of NO on ileal cholinergic neurons.…”

Section: Discussionmentioning

confidence: 57%

“…9,42 As the pharmacological profile of enteric NMDA receptors is similar to central NMDA receptors, it seems reasonable to suggest that activation of myenteric NMDA receptors followed by massive calcium influx through the NMDA receptor-ion complex, may stimulate NO synthesis which in turn would enhance acetylcholine efflux. This assumption is supported by the data of Milusheva et al 43 showing increased nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase staining and stimulation of acetylcholine release after glutamate application. It is also concordant with the finding of Bartho and Lefebvre 44 showing a stimulatory effect of NO on ileal cholinergic neurons.…”

Section: Discussionmentioning

confidence: 60%

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Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kaszaki

Palásthy

Erczes

et al. 2007

Neurogastroenterology Motil

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Kynurenic acid (KynA), an endogenous antagonist of N-methyl-d-aspartate (NMDA) glutamate receptors, protects the central nervous system in excitotoxic neurological diseases. We hypothesized that the inhibition of enteric glutamate receptors by KynA may influence dysmotility in the gastrointestinal tract. Group 1 of healthy dogs served as the sham-operated control, in group 2, the animals were treated with KynA, while in groups 3 and 4 mechanical colon obstruction was maintained for 7 h. Group 4 was treated with KynA at the onset of ileus. Hemodynamics and motility changes were monitored, and the activities of xanthine oxidoreductase (XOR) and myeloperoxidase (MPO) were determined from tissue samples. Colon obstruction induced a hyperdynamic circulatory reaction, significantly elevated the motility index and increased the mucosal leucocyte accumulation and the XOR activity. The KynA treatment augmented the tone of the colon, permanently decreased the motility index of the giant colonic contractions and reduced the increases in XOR and MPO activities. These effects were concomitant with the in vitro inhibition of XOR activity. In conclusion, KynA antagonizes the obstruction-induced motility responses and XOR activation in the colon. Inhibition of enteric NMDA receptors may provide an option to influence intestinal hypermotility and inflammatory changes.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 60%

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kaszaki

Palásthy

Erczes

et al. 2007

Neurogastroenterology Motil

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“…14,15 Moreover, release of acetylcholine caused by NMDA, or by glutamate acting through NMDA receptors, was inhibited by tetrodotoxin, implying that activation of NMDA receptors excites enteric neurons. 14,16 Consistent with this, NMDA agonists depolarized enteric neurons of the guinea-pig ileum. 17 In contrast, a detailed investigation of the actions of glutamate receptor agonists on guinea-pig enteric neurons found no evidence of excitation mediated through NMDA receptors.…”

Section: Introductionmentioning

confidence: 55%

“…Glutamate release was detected when enteric neurons were stimulated electrically or by a nicotinic agonist 14,15 . Moreover, release of acetylcholine caused by NMDA, or by glutamate acting through NMDA receptors, was inhibited by tetrodotoxin, implying that activation of NMDA receptors excites enteric neurons 14,16 . Consistent with this, NMDA agonists depolarized enteric neurons of the guinea‐pig ileum 17 .…”

Section: Introductionmentioning

confidence: 59%

Effects of NMDA receptor antagonists on visceromotor reflexes and on intestinal motility, in vivo

Shafton¹,

Bogeski²,

Kitchener³

et al. 2007

Neurogastroenterology Motil

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Antagonists of NMDA receptors can inhibit both the transmission of pain signals from the intestine and enteric reflexes. However, it is unknown whether doses of the NMDA antagonist, ketamine, that are used in anaesthetic mixtures suppress motility reflexes and visceromotor responses (VMRs). In fact, whether intestinal motility is affected by NMDA receptor blockers in vivo has been little investigated. We studied the effects of ketamine and memantine, administered intravenously or intrathecally. Rats were maintained under alpha-chloralose plus xylazine or pentobarbitone anaesthesia; VMR and jejunal motility were measured. Under alpha-chloralose/xylazine anaesthesia, i.v. ketamine inhibited VMRs at 6 mg kg h(-1), but not at 3 mg kg h(-1). It did not inhibit propulsive reflexes in the jejunum at 10 mg kg h(-1), but reduced them by 30% at 20 mg kg h(-1). Under alpha-chloralose/pentobarbitone anaesthesia, i.v. ketamine reduced propulsive reflexes at 40 mg kg h(-1) and VMR at 10 mg kg h(-1). Memantine inhibited VMRs at 20 mg kg h(-1) and propulsion at 2 mg kg h(-1). Ketamine and memantine, intrathecally, prevented VMRs, but not jejunal propulsion. We conclude that peripherally administered ketamine reduces both VMR and motility reflexes, but not at doses used in anaesthetic mixes (1.8-2.4 mg kg h(-1)). Effects on motility reflexes are likely to be due to non-NMDA receptor actions, possibly on nicotinic receptors.

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“…This autoregulation may be driven by local nitric oxide production [11]. What drives the autoregulation is at the present time speculative but may be intrinsically related to the excitatory amino acids because nitric oxide is associated with excitatory amino acids as will be discussed later [12]. Another aspect of diabetic retinopathy that is poorly recognized and occurs because of autoregulation is a compensatory increase in the flow through the remaining vessels [10].…”

Section: Introductionmentioning

confidence: 99%

A Role for Excitatory Amino Acids in Diabetic Eye Disease

Pulido

Erie³

et al. 2007

Journal of Diabetes Research

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Diabetic retinopathy is a leading cause of vision loss. The primary clinical hallmarks are vascular changes that appear to contribute to the loss of sight. In a number of neurodegenerative disorders there is an appreciation that increased levels of excitatory amino acids are excitotoxic. The primary amino acid responsible appears to be the neurotransmitter glutamate. This review examines the nature of glutamatergic signaling at the retina and the growing evidence from clinical and animal model studies that glutamate may be playing similar excitotoxic roles at the diabetic retina.

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Glutamate stimulation of acetylcholine release from myenteric plexus is mediated by endogenous nitric oxide

Cited by 13 publications

References 28 publications

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Effects of NMDA receptor antagonists on visceromotor reflexes and on intestinal motility, in vivo

A Role for Excitatory Amino Acids in Diabetic Eye Disease

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