ArticleNeuroscience2015
Molecular and functional changes in glucokinase expression in the brainstem dorsal vagal complex in a murine model of type 1 diabetes.
Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- FGF19 in the Hindbrain Lowers Blood Glucose and Alters Excitability of Vagal Motor Neurons in Hyperglycemic Mice.Endocrinology · 2021Article
- Fibroblast Growth Factor 19 Increases the Excitability of Pre-Motor Glutamatergic Dorsal Vagal Complex Neurons From Hyperglycemic Mice.Frontiers in endocrinology · 2021Article
- Protein Kinase C-Dependent Effects of Neurosteroids on Synaptic GABAFrontiers in physiology · 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
- A voltage-dependent depolarization induced by low external glucose in neurons of the nucleus of the tractus solitarius: interaction with KThe Journal of physiology · 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
- Improved glucose homeostasis in male obese Zucker rats coincides with enhanced baroreflexes and activation of the nucleus tractus solitarius.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- High glucose increases action potential firing of catecholamine neurons in the nucleus of the solitary tract by increasing spontaneous glutamate inputs.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Adenovirus-mediated suppression of hypothalamic glucokinase affects feeding behavior.Scientific reports · 2017Article
- Glutamatergic drive facilitates synaptic inhibition of dorsal vagal motor neurons after experimentally induced diabetes in mice.Journal of neurophysiology · 2016Article
- Insights into the role of neuronal glucokinase.American journal of physiology. Endocrinology and metabolism · 2016Review
- Differential effects of rapamycin treatment on tonic and phasic GABAergic inhibition in dentate granule cells after focal brain injury in mice.Experimental neurology · 2016Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Glucose concentration changes in the nucleus tractus solitarius (NTS) affect visceral function and metabolism by influencing central vagal circuits, especially inhibitory, GABAergic NTS neurons. Acutely elevated glucose can alter NTS neuron activity, and prolonged hyperglycemia and hypoinsulemia in animal models of type 1 diabetes results in plasticity of neural responses in the NTS. NTS neurons contributing to metabolic regulation therefore act as central glucose sensors and are functionally altered in type 1 diabetes. Glucokinase (GCK) mediates cellular utilization of glucose, linking increased glucose concentration to excitability changes mediated by ATP-sensitive K(+) channels (KATP). Using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot, and in vitro electrophysiology, we tested the hypothesis that changes in GCK expression in the NTS accompany the development of diabetes symptoms in the streptozotocin (STZ)-treated mouse model of type 1 diabetes. After several days of hyperglycemia in STZ-treated mice, RNA expression of GCK, but not Kir6.2 or SUR1, was decreased versus controls in the dorsal vagal complex. Electrophysiological recordings in vitro indicated that neural responses to acute hyperglycemia, and synaptic responsiveness to blockade of GCK with glucosamine, were attenuated in GABAergic NTS neurons from STZ-treated mice, consistent with reduced molecular and functional expression of GCK in the vagal complex of hyperglycemic, STZ-treated mice. Altered autonomic responses to glucose in type 1 diabetes may therefore involve reduced functional GCK expression in the dorsal vagal complex.
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