GABA action in immature neocortical neurons directly depends on the availability of ketone bodies. - Test2 - elhamkhani - TriplyDB

GABA action in immature neocortical neurons directly depends on the availability of ketone bodies.

GABA action in immature neocortical neurons directly depends on the availability of ketone bodies.

http://www.wikidata.org/entity/Q34989280

about

Role of the neuronal K-Cl co-transporter KCC2 in inhibitory and excitatory neurotransmission Differences in cortical versus subcortical GABAergic signaling: a candidate mechanism of electroclinical uncoupling of neonatal seizures.Remodeling of inhibitory synaptic connections in developing ferret visual cortex.The depolarizing action of GABA in cultured hippocampal neurons is not due to the absence of ketone bodies.GABAergic synaptic scaling in embryonic motoneurons is mediated by a shift in the chloride reversal potential.Questioning the depolarizing effects of GABA during early brain development.GABAergic transmission and chloride equilibrium potential are not modulated by pyruvate in the developing optic tectum of Xenopus laevis tadpoles.Non-cell-autonomous factor induces the transition from excitatory to inhibitory GABA signaling in retina independent of activity GABA depolarizes immature neurons and inhibits network activity in the neonatal neocortex in vivo.Emerging themes in GABAergic synapse development Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis.Synaptic activity-induced Ca(2+) signaling in avian cochlear nucleus magnocellularis neurons.Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain.GABA is excitatory in adult vasopressinergic neuroendocrine cells.Kinases SPAK and OSR1 are upregulated by estradiol and activate NKCC1 in the developing hypothalamus.Partial Amelioration of Peripheral and Central Symptoms of Huntington's Disease via Modulation of Lipid Metabolism.Synaptic inhibition, excitation, and plasticity in neurons of the cerebellar nuclei.Molecular and physiological responses to juvenile traumatic brain injury: focus on growth and metabolism.The metamorphosis of the developing cerebellar microcircuit.Spike-timing dependent plasticity in inhibitory circuits.GABAergic depolarization during early cortical development and implications for anticonvulsive therapy in neonates.Excitatory action of GABA on immature neurons is not due to absence of ketone bodies metabolites or other energy substrates.Development of the GABAergic system from birth to adolescence.Ketone bodies in epilepsy Cellular Links between Neuronal Activity and Energy Homeostasis.GABA metabolism and transport: effects on synaptic efficacy.Recent progress in GABAergic excitation from mature brain.The use of ultrasound-guided regional anaesthetic techniques in neonates and young infants.Control of seizures by ketogenic diet-induced modulation of metabolic pathways.Mammalian retinal horizontal cells are unconventional GABAergic neurons.Another Look at Early GABAergic Neurotransmission: Maybe It's Not So Exciting After All!Immature brains don't need GABA to get 'hyper'-excited.Methodological standards for in vitro models of epilepsy and epileptic seizures. A TASK1-WG4 report of the AES/ILAE Translational Task Force of the ILAE.Chronic inhibition of brain glycolysis initiates epileptogenesis.Dietary energy substrates reverse early neuronal hyperactivity in a mouse model of Alzheimer's disease.Glucose is an adequate energy substrate for the depolarizing action of GABA and glycine in the neonatal rat spinal cord in vitro.Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization.The metabolic impact of β-hydroxybutyrate on neurotransmission: Reduced glycolysis mediates changes in calcium responses and KATP channel receptor sensitivity.Commentary: GABA Depolarizes Immature Neurons and Inhibits Network Activity in the Neonatal Neocortex In vivo.

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GABA action in immature neocortical neurons directly depends on the availability of ketone bodies.

http://www.wikidata.org/entity/Q34989280

description

2009 nî lūn-bûn

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2009 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2009 թվականի հունիսին հրատարակված գիտական հոդված

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2009年の論文

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GABA action in immature neocor ...... availability of ketone bodies.

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GABA action in immature neocor ...... availability of ketone bodies.

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GABA action in immature neocor ...... availability of ketone bodies.

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GABA action in immature neocor ...... availability of ketone bodies.

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GABA action in immature neocor ...... availability of ketone bodies.

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GABA action in immature neocor ...... availability of ketone bodies.

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J.1471-4159.2009.06230.X

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Journal of Neurochemistry

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GABA action in immature neocor ...... availability of ketone bodies

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Carl D Holmgren

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Genevieve Chazal

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Tanya Zilberter

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Tibor Harkany

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Yuri Zilberter

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P2860

The Ketogenic Diet: One Decade Later

Mice with a targeted disruption of the Cl-/HCO3- exchanger AE3 display a reduced seizure threshold

Neuroprotective and disease-modifying effects of the ketogenic diet

The SLC4 family of HCO 3 - transporters

GABA: a pioneer transmitter that excites immature neurons and generates primitive oscillations

Cl- uptake promoting depolarizing GABA actions in immature rat neocortical neurones is mediated by NKCC1

Regulation of the rat brain Na+ -driven Cl-/HCO3 - exchanger involves protein kinase A and a multiprotein signaling complex

The course of ketosis and the activity of key enzymes of ketogenesis and ketone-body utilization during development of the postnatal rat

Activities of enzymes of ketone-body utilization in brain and other tissues of suckling rats

Excitatory actions of gaba during development: the nature of the nurture

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1330-1338

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10.1111/J.1471-4159.2009.06230.X

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19558450

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