Interaction of NO and VIP in Gastrointestinal Smooth Muscle Relaxation

Geldre, Lieve A Van; Lefebvre, Romain

doi:10.2174/1381612043383890

Cited by 89 publications

(77 citation statements)

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“…Results of the present study concerning the co-localisation of CART with VIP and nNOS, are in agreement with previous studies, where such co--localisation has been described in human descending colon [19], as well as in the GI tract of pig [17,34,36] rat [8] and sheep [1]. They also suggest that CART may play the role of co-transmitter or neuromodulator and can induce VIP and/or NO release at the presynaptic level [35]. Similar situation may affect the correlation between CART and GAL.…”

Section: Discussionsupporting

confidence: 93%

Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum

et al. 2015

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The enteric nervous system consists of about one hundred million of neurons. In big mammals (including humans) intestinal enteric neuronal cells are grouped into three types of intramural ganglia located within myenteric, as well as outer and inner submucosal plexuses, which are connected by numerous nerve fibres. Both nerve fibres and cell bodies located in the gastrointestinal tract utilise a broad spectrum of active substances. One of them is cocaine-and amphetamine-regulated transcript peptide (CART). The goal of the current study was to determinate the distribution and degree of co-localisation of CART with substances taking part in intestinal motor activity by double labelling immunofluorescence technique. During the study CART-, neuronal isoform of nitric oxide synthase (nNOS)-, vasoactive intestinal peptide (VIP)-and/or galanin (GAL) -like immunoreactive (LI)

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Section: Discussionsupporting

confidence: 93%

Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum

et al. 2015

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“…Indeed, strikingly, 90% of the alpha-synuclein-positive neurons in the forestomach were NOS-positive. In myenteric neurons, VIP is found in nitrergic neurons (Ekblad et al, 1994;Van Geldre and Lefebvre, 2004). Consistent with this established coexpression of NOS and VIP, we also observed, in a limited series, that 70% of the alphasynuclein-positive neurons in the forestomach were co-reactive for VIP, and that 16% of the alpha-synuclein neurons in the remainder of the stomach were co-reactive for VIP [unpublished observations; n = 3; i.e., 1 rat (10 months old) from present series as well as 2 older F344 rats from a separate series; double labeling for VIP (rabbit polyclonal antiserum; Antibody Core no.…”

Section: Alpha-synuclein-positive Pathways Innervating the Gutmentioning

confidence: 99%

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

et al. 2008

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The protein alpha-synuclein is implicated in the development of Parkinson's disease. The molecule forms Lewy body aggregates that are hallmarks of the disease, has been associated with the spread of neuropathology from the peripheral to the central nervous system, and appears to be involved with the autonomic disorders responsible for the gastrointestinal (GI) symptoms of individuals afflicted with Parkinson's. To characterize the normative expression of alpha-synuclein in the innervation of the GI tract, we examined both the postganglionic neurons and the preganglionic projections by which the disease is postulated to retrogradely invade the CNS. Specifically, in Fischer 344 and Sprague Dawley rats, immunohistochemistry in conjunction with injections of the tracer DextranTexas Red was used to determine, respectively, the expression of alpha-synuclein in the myenteric plexus and in the vagal terminals. Alpha-synuclein is expressed in a subpopulation of myenteric neurons, with the proportion of positive somata increasing from the stomach (~3%) through duodenum (proximal, ~6%; distal, ~13%) to jejunum (~22%). Alpha-synuclein is co-expressed with the nitrergic enzyme NOS or the cholinergic markers calbindin and calretinin in regionally specific patterns: ~90% of forestomach neurons positive for alpha-synuclein express NOS, whereas ~92% of corpus-antrum neurons positive for alpha-synuclein express cholinergic markers. Vagal afferent endings in the myenteric plexus and the GI smooth muscle do not express alpha-synuclein, whereas, virtually all vagal preganglionic projections to the gut express alpha-synuclein, both in axons and in terminal varicosites in apposition with myenteric neurons. Vagotomy eliminates most, but not all, alpha-synuclein-positive neurites in the plexus. Some vagal preganglionic efferents expressing alphasynuclein form varicose terminal rings around myenteric plexus neurons that are also positive for the protein, thus providing a candidate alpha-synuclein-expressing pathway for the retrograde transport of putative Parkinson's pathogens or toxins from the ENS to the CNS.

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“…In the rat, relaxation of the stomach, ileum, and colon was mediated by NO, VIP, and peptide histidine isoleucine (PHI) (11); ATP and NO (12,13); and VIP, PACAP, and NO (14), respectively. Furthermore, there are reports indicating interactions between inhibitory mediators (15,16). Recently, differences were reported in the inhibitory mediators and the mechanisms of action between circular and longitudinal muscle layers in the mouse ileum (17).…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide and Carbon Monoxide Act as Inhibitory Neurotransmitters in the Longitudinal Muscle of C57BL/6J Mouse Distal Colon

et al. 2010

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Abstract. The present study was designed to identify the inhibitory neurotransmitters mediating nonadrenergic noncholinergic relaxation in the longitudinal muscle of C57/BL mouse distal colon. Relaxation induced by electrical field stimulation (EFS) was recorded isotonically in the presence of atropine and guanethidine. Cyclic guanosine-3′,5′-monophosphate (cyclic GMP) content was measured by radioimmunoassay. EFS-induced relaxation was inhibited by nitro-L -arginine ( L -NNA) and Sn (IV) protoporphyrin dichloride IX (SnPP-IX), a nitric oxide (NO) and carbon monoxide (CO) synthase inhibitor, respectively. A combination of both inhibitors produced an additive effect. ODQ, a soluble guanylate cyclase inhibitor, inhibited EFS-induced relaxation. NOR-1, a NO donor, and carbon monoxide-releasing molecule-2 (CORM-2), a CO donor, treatment relaxed the distal colon and increased cyclic GMP content. The effects of NOR-1 and CORM-2 were inhibited by ODQ. KT5823, a cyclic GMP-dependent protein kinase inhibitor, inhibited EFS-induced relaxation. EFS-induced relaxation in the presence of KT5823 was further inhibited by L -NNA, but not by SnPP-IX. In addition, KT5823 inhibited CORM-2-induced relaxation, but not NOR-1-induced relaxation. H89, a cyclic AMP-dependent protein kinase inhibitor, inhibited EFS-induced relaxation, and EFS-induced relaxation in the presence of H89 was further inhibited by L -NNA. These results suggested that NO and CO function as inhibitory neurotransmitters in the longitudinal muscle of C57BL mouse distal colon.

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Interaction of NO and VIP in Gastrointestinal Smooth Muscle Relaxation

Cited by 89 publications

References 0 publications

Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum

Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

Nitric Oxide and Carbon Monoxide Act as Inhibitory Neurotransmitters in the Longitudinal Muscle of C57BL/6J Mouse Distal Colon

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