title: Hindbrain glucoprivation effects on gastric vagal reflex circuits and gastric motility in the rat are suppressed by the astrocyte inhibitor fluorocitrate.
abstract: Fasting and hypoglycemia elicit powerful gastrointestinal contractions. Whereas the relationship between utilizable nutrient and gastric motility is well recognized, the explanation of this phenomenon has remained incomplete. A relatively recent controversial report suggested that astrocytes in the dorsal hindbrain may be the principal detectors of glucoprivic stimuli. Our own studies also show that a subset of astrocytes in the solitary nucleus (NST) is activated by low glucose. It is very likely that information about glucopenia may directly impact gastric control because the hindbrain is also the location of the vago-vagal reflex circuitry regulating gastric motility. Our in vivo single unit neurophysiological recordings in intact rats show fourth ventricular application of 2-deoxyglucose (2-DG) inhibits NST neurons and activates dorsal motor nucleus (DMN) neurons involved in the gastric accommodation reflex. Additionally, as shown in earlier studies, either systemic insulin or central 2-DG causes an increase in gastric motility. These effects on motility were blocked by fourth ventricle pretreatment with the astrocyte inactivator fluorocitrate. Fluorocitrate administered alone has no effect on gastric-NST or -DMN neuron responsiveness, or on gastric motility. These results suggest that glucoprivation-induced increases in gastric motility are dependent on intact hindbrain astrocytes.
authors.affiliation: Laboratory for Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808 gerlinda.hermann@pbrc.edu.
authors.forename: Gerlinda E
authors.identifier: http://orcid.org/0000-0003-0405-2820
authors.initials: GE
authors.lastname: Hermann
authors.affiliation: Laboratory for Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808.
authors.forename: Edouard
authors.initials: E
authors.lastname: Viard
authors.affiliation: Laboratory for Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808.
authors.forename: Richard C
authors.initials: RC
authors.lastname: Rogers
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000704:Analysis of Variance; D000818:Animals; D002951:Citrates / Q000494:pharmacology*; D003847:Deoxyglucose / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005769:Gastrointestinal Motility / Q000187:drug effects*; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D012018:Reflex / Q000187:drug effects* / Q000502:physiology; D012249:Rhombencephalon / Q000166:cytology*; D014630:Vagus Nerve / Q000187:drug effects* / Q000502:physiology
chemical_list: D002951:Citrates; D004791:Enzyme Inhibitors; D007328:Insulin; C007744:fluorocitrate; D003847:Deoxyglucose; D005947:Glucose
keywords: astrocytes; dorsal motor nucleus; fluorocitrate; solitary nucleus; vago-vagal reflex
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