Vagally mediated effects of brain stem dopamine on gastric tone and phasic contractions of the rat

Anselmi, Laura; Toti, Luca; Bove, Cecilia; Travagli, R. Alberto

doi:10.1152/ajpgi.00180.2017

Cited by 20 publications

(24 citation statements)

References 42 publications

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“…These data support further the monosynaptic nature and tonic excitatory influence on DMV neurons, vagal efferent outflow, and gastric motor functions of this pathway. Interestingly, while microinjection of dopamine in the DVC is gastroinhibitory via DA2-mediated actions 22 , here we show that the response to benztropine is mediated via DA1 receptors. These data suggest strongly that the nigro-vagal fibers target selective subpopulations of DMV neurons dedicated to modulation of specific neurocircuits; the observation is supported also by the differential responses on tone vs motility obtained with yohimbine pretreatment.…”

Section: Discussionmentioning

confidence: 50%

A Nigro−Vagal Pathway Controls Gastric Motility and Is Affected in a Rat Model of Parkinsonism

et al. 2017

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Background & Aims In most patients with Parkinson's disease, gastrointestinal (GI) dysfunctions, such as gastroparesis and constipation, are prodromal to the cardinal motor symptoms of the disease. Sporadic Parkinson's disease has been proposed to develop following ingestion of neurotoxicants that affect the brain–gut axis via the vagus nerve, and then travel to higher centers compromising the substantia nigra pars compacta (SNpc), and, later, the cerebral cortex. We aimed to identify the pathway that connects the brainstem vagal nuclei and the SNpc, and to determine whether this pathway is compromised in a rat model of Parkinsonism. Methods To study this neural pathway in rats, we placed tracers in the dorsal vagal complex (DVC) or SNpc; brainstem and midbrain were examined for tracer distribution and neuronal neurochemical phenotype. Rats were given injections of paraquat once weekly for 3 weeks to induce features of Parkinsonism, or vehicle (control). Gastric tone and motility were recorded following NMDA microinjection in the SNpc and/or optogenetic stimulation of nigro-vagal terminals in the DVC. Results Stimulation of the SNpc increased gastric tone and motility via activation of dopamine 1 receptors in the DVC. In the paraquat-induced model of Parkinsonism, this nigro-vagal pathway was compromised during the early stages of motor deficit development. Conclusions We identified and characterized a nigro-vagal monosynaptic pathway in rats that controls gastric tone and motility. This pathway might be involved in the prodromal gastric dysmotility observed in patients with early-stage Parkinson's disease.

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Section: Discussionmentioning

confidence: 50%

A Nigro−Vagal Pathway Controls Gastric Motility and Is Affected in a Rat Model of Parkinsonism

et al. 2017

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“…Moreover, DA2 receptor‐mediated effect is more prominent than the DA1 receptor‐mediated effects . Thus, stimulation of dopaminergic projections of substantia nigra pars compacta (SNpc) causes some gastric excitation due to stimulation of DA1 receptors on the DMV‐C‐e neurons .…”

Section: Gastric Excitatory Vagal Motor Circuit (Gevmc)mentioning

confidence: 99%

“…exert different effects on vagal circuits, based on the receptor type and the neural input. For example, dopamine may use either stimulatory effect via the dopamine 1 (DA1) receptors or inhibitory effect via the dopamine 2 (DA2) receptors on the DMV neurons of the GEVC.Moreover, DA2 receptor-mediated effect is more prominent than the DA1 receptor-mediated effects 77. Thus, stimulation of dopaminergic projections of substantia nigra pars compacta (SNpc) causes some gastric excitation due to stimulation of DA1 receptors on the DMV-C-e neurons 77.…”

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confidence: 99%

Advances in the physiology of gastric emptying

Goyal

Guo

Mashimo

2019

Neurogastroenterology Motil

222

154

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There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP‐1 inhibit gastric emptying via the GIVMC, and in the inter‐digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.

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“…Previous work has shown that elevated levels of brain stem dopamine lead to reduced food intake [21] and gastric relaxation [22]. Moreover, dopamine administration in the brain stem reduced gastric tone and motility which was abolished by vagotomy [18]. Studies linking alterations in vagal signaling to the development of Parkinson's disease [23,24] further support the assumption of afferent signaling between the gut and key dopaminergic brain regions along the vagal pathway.…”

Section: Discussionmentioning

confidence: 84%

“…Afferently, stimulation of the vagal sensory ganglion in mice was found to induce dopamine release in the substantia nigra [17]. Efferently, dopamine administration to the dorsal vagal complex in rats modulated the upper gastrointestinal tract by reducing gastric tone and motility via DA2 receptors in the dorsal motor nucleus of the vagus [18]. Thus, while vagal stimulation mostly targets afferent pathways, studies in rodents provide evidence for brain-mediated effects on downstream targets.…”

Section: Introductionmentioning

confidence: 99%