Journal
NEURON
Volume 74, Issue 4, Pages 719-730Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2012.03.032
Keywords
-
Categories
Funding
- Ministerio de Educacion y Ciencia (MEC, Spain)
- Burroughs Wellcome Fund Career Award in Biomedical Sciences
- U.S. National Institutes of Health [K01CA106596, R01 NS055031, R56 NS072142]
- NIH [UL1 RR025758]
- CURE
Ask authors/readers for more resources
Neuronal excitation can be substantially modulated by alterations in metabolism, as evident from the anticonvulsant effect of diets that reduce glucose utilization and promote ketone body metabolism. We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabolism, imparts reciprocal effects on metabolism of glucose and ketone bodies in brain cells. These effects involve phosphoregulation of BAD and are independent of its apoptotic function. BAD modifications that reduce glucose metabolism produce a marked increase in the activity of metabolically sensitive K-ATP channels in neurons, as well as resistance to behavioral and electrographic seizures in vivo. Seizure resistance is reversed by genetic ablation of the K-ATP channel, implicating the BAD-K-ATP axis in metabolic control of neuronal excitation and seizure responses.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available