Ventrolateral ventromedial hypothalamic nucleus GABA neuron adaptation to recurring Hypoglycemia correlates with up-regulated 5'-AMP-activated protein kinase activity.
AMPK
adrenergic receptor
glutamate decarboxylase
recurrent insulin-induced hypoglycemia
ventrolateral ventromedial hypothalamic nucleus-ventrolateral part
Journal
AIMS neuroscience
ISSN: 2373-7972
Titre abrégé: AIMS Neurosci
Pays: United States
ID NLM: 101665668
Informations de publication
Date de publication:
2021
2021
Historique:
received:
01
04
2021
accepted:
05
08
2021
entrez:
8
12
2021
pubmed:
9
12
2021
medline:
9
12
2021
Statut:
epublish
Résumé
Gamma-aminobutyric acid (GABA) acts on ventromedial hypothalamic targets to suppress counter-regulatory hormone release, thereby lowering blood glucose. Maladaptive up-regulation of GABA signaling is implicated in impaired counter-regulatory outflow during recurring insulin-induced hypoglycemia (RIIH). Ventromedial hypothalamic nucleus (VMN) GABAergic neurons express the sensitive energy gauge 5'-AMP-activated protein kinase (AMPK). Current research used high-neuroanatomical resolution single-cell microdissection tools to address the premise that GABAergic cells in the VMNvl, the primary location of 'glucose-excited' metabolic-sensory neurons in the VMN, exhibit attenuated sensor activation during RIIH. Data show that during acute hypoglycemia, VMNvl glutamate decarboxylase
Identifiants
pubmed: 34877402
doi: 10.3934/Neuroscience.2021027
pii: neurosci-08-04-027
pmc: PMC8611193
doi:
Types de publication
Journal Article
Langues
eng
Pagination
510-525Informations de copyright
© 2021 the Author(s), licensee AIMS Press.
Déclaration de conflit d'intérêts
Conflict of interest: The authors declare no conflict of interest.
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