ArticleJournal of neurophysiology2016
Glutamatergic drive facilitates synaptic inhibition of dorsal vagal motor neurons after experimentally induced diabetes in mice.
Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- The sympathoregulatory region of the mouse rostral brainstem relies on both GABA and glycine to generate inhibitory currents.The Journal of physiology · 2026Article
- GABAiScience · 2025Article
- Systemic Glucose Regulation by a Hindbrain Inhibitory Circuit in a Mouse Model of Type 1 Diabetes.Neuroendocrinology · 2024Article
- Article
- The elusive cephalic phase insulin response: triggers, mechanisms, and functions.Physiological reviews · 2023Review
- GABAergic leptin receptor-expressing neurons in the dorsomedial hypothalamus project to brown adipose tissue-related neurons in the paraventricular nucleus of mice.Autonomic neuroscience : basic & clinical · 2023Article
- Glutamatergic plasticity within neurocircuits of the dorsal vagal complex and the regulation of gastric functions.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- FGF19 in the Hindbrain Lowers Blood Glucose and Alters Excitability of Vagal Motor Neurons in Hyperglycemic Mice.Endocrinology · 2021Article
- Musings on the wanderer: What's new in our understanding of vago-vagal reflexes? VI. Central vagal circuits that control glucose metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Protein Kinase C-Dependent Effects of Neurosteroids on Synaptic GABAFrontiers in physiology · 2021Article
- Fibroblast Growth Factor 19 Increases the Excitability of Pre-Motor Glutamatergic Dorsal Vagal Complex Neurons From Hyperglycemic Mice.Frontiers in endocrinology · 2021Article
- GABAJournal of neurophysiology · 2019Article
- A hindbrain inhibitory microcircuit mediates vagally-coordinated glucose regulation.Scientific reports · 2019Article
- Altered A-type potassium channel function in the nucleus tractus solitarii in acquired temporal lobe epilepsy.Journal of neurophysiology · 2019Article
- Glycinergic neurotransmission in the rostral ventrolateral medulla controls the time course of baroreflex-mediated sympathoinhibition.The Journal of physiology · 2019Article
- Functional and molecular plasticity of γ and α1 GABAJournal of neurophysiology · 2017Article
- Gut-Brain Axis in Regulation of Blood Pressure.Frontiers in physiology · 2017Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
The role of central regulatory circuits in modulating diabetes-associated glucose dysregulation has only recently been under rigorous investigation. One brain region of interest is the dorsal motor nucleus of the vagus (DMV), which contains preganglionic parasympathetic motor neurons that regulate subdiaphragmatic visceral function. Previous research has demonstrated that glutamatergic and GABAergic neurotransmission are independently remodeled after chronic hyperglycemia/hypoinsulinemia. However, glutamatergic circuitry within the dorsal brain stem impinges on GABAergic regulation of the DMV. The present study investigated the role of glutamatergic neurotransmission in synaptic GABAergic control of DMV neurons after streptozotocin (STZ)-induced hyperglycemia/hypoinsulinemia by using electrophysiological recordings in vitro. The frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) was elevated in DMV neurons from STZ-treated mice. The effect was abolished in the presence of the ionotropic glutamate receptor blocker kynurenic acid or the sodium channel blocker tetrodotoxin, suggesting that after STZ-induced hyperglycemia/hypoinsulinemia, increased glutamatergic receptor activity occurs at a soma-dendritic location on local GABA neurons projecting to the DMV. Although sIPSCs in DMV neurons normally demonstrated considerable amplitude variability, this variability was significantly increased after STZ-induced hyperglycemia/hypoinsulinemia. The elevated amplitude variability was not related to changes in quantal release, but rather correlated with significantly elevated frequency of sIPSCs in these mice. Taken together, these findings suggest that GABAergic regulation of central vagal circuitry responsible for the regulation of energy homeostasis undergoes complex functional reorganization after several days of hyperglycemia/hypoinsulinemia, including both glutamate-dependent and -independent forms of plasticity.
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