ArticleNeurogastroenterology and motility2009
Modulation of inhibitory neurotransmission in brainstem vagal circuits by NPY and PYY is controlled by cAMP levels.
Article in Neurogastroenterology and motility, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Central control of gastrointestinal functions in health and disease.Physiological reviews · 2026Review
- Article
- Stress-induced neuroplasticity in the gastric response to brainstem oxytocin in male rats.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Protein Kinase C-Dependent Effects of Neurosteroids on Synaptic GABAFrontiers in physiology · 2021Article
- Sex-steroid-dependent plasticity of brain-stem autonomic circuits.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Review
- Necrotizing enterocolitis: It's not all in the gut.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- GABAJournal of neurophysiology · 2019Article
- NPY2 receptor activation in the dorsal vagal complex increases food intake and attenuates CCK-induced satiation in male rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- Central control of gastrointestinal motility.Current opinion in endocrinology, diabetes, and obesity · 2019Review
- Vagally mediated gastric effects of brain stem αAmerican journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Vagal neurocircuitry and its influence on gastric motility.Nature reviews. Gastroenterology & hepatology · 2016Review
- Inhibitory neurotransmission regulates vagal efferent activity and gastric motility.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Peptide YY signaling in the lateral parabrachial nucleus increases food intake through the Y1 receptor.American journal of physiology. Endocrinology and metabolism · 2015Article
- Developmental specification of metabolic circuitry.Frontiers in neuroendocrinology · 2015Review
- Characterization of synapses in the rat subnucleus centralis of the nucleus tractus solitarius.Journal of neurophysiology · 2015Article
- Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity.The Journal of physiology · 2015Article
- Plasticity in the brainstem vagal circuits controlling gastric motor function triggered by corticotropin releasing factor.The Journal of physiology · 2014Article
- Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Comprehensive Physiology · 2014Review
- cAMP-dependent insulin modulation of synaptic inhibition in neurons of the dorsal motor nucleus of the vagus is altered in diabetic mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Regulation of leptin receptor-expressing neurons in the brainstem by TRPV1.Physiological reports · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic polypeptides such as neuropeptide Y (NPY) and peptide YY (PYY) exert profound, vagally mediated effects on gastrointestinal (GI) motility. Vagal efferent outflow to the GI tract is determined principally by tonic GABAergic synaptic inputs onto dorsal motor nucleus of the vagus (DMV) neurons, yet neither peptide modulates GABAergic transmission. We showed recently that opioid peptides appear similarly ineffective because of the low resting cAMP levels. Using whole cell recordings from identified DMV neurons, we aimed to correlate the influence of brainstem cAMP levels with the ability of pancreatic polypeptides to modulate GABAergic synaptic transmission. Neither NPY, PYY, nor the Y1 or Y2 receptor selective agonists [Leu,Pro]NPY or NPY(3-36) respectively, inhibited evoked inhibitory postsynaptic current (eIPSC) amplitude unless cAMP levels were elevated by forskolin or 8-bromo-cAMP, by exposure to adenylate cyclase-coupled modulators such as cholecystokinin octapeptide (sulfated) (CCK-8s) or thyrotropin releasing hormone (TRH), or by vagal deafferentation. The inhibition of eIPSC amplitude by [Leu,Pro]NPY or NPY(3-36) was stable for approximately 30 min following the initial increase in cAMP levels. Thereafter, the inhibition declined gradually until the agonists were again ineffective after 60 min. Analysis of spontaneous and miniature currents revealed that such inhibitory effects were due to actions at presynaptic Y1 and Y2 receptors. These results suggest that, similar to opioid peptides, the effects of pancreatic polypeptides on GABAergic transmission depend upon the levels of cAMP within gastric inhibitory vagal circuits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.