2024-03-29T08:51:22Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1113122021-11-22T12:49:26Zcom_10261_79com_10261_1com_10261_54col_10261_332col_10261_307
Altered postnatal development of cortico-hippocampal neuronal electric activity in mice deficient for the mitochondrial aspartate-glutamate transporter
Gómez-Galán, M.
Marakova, Julia
Llorente-Folch, Irene
Saheki, Takeyori
Pardo, Beatriz
Satrústegui, Jorgina
Herreras, Óscar
Ministerio de Educación y Ciencia (España)
Comunidad de Madrid
Fundación Mutua Madrileña
Fundación Ramón Areces
Centro de Investigación Biomédica en Red Enfermedades Raras (España)
OmniBank
Local field potential
Electroencephalographic activity
Aspartate–glutamate mitochondrial carrier
Aralar/AGC1
The deficiency in the mitochondrial aspartate/glutamate transporter Aralar/AGC1 results in a loss of the malate-aspartate NADH shuttle in the brain neurons, hypomyelination, and additional defects in the brain metabolism. We studied the development of cortico/hippocampal local field potential (LFP) in Aralar/AGC1 knockout (KO) mice. Laminar profiles of LFP, evoked potentials, and unit activity were recorded under anesthesia in young (P15 to P22) Aralar-KO and control mice as well as control adults. While LFP power increased 3 to 7 times in both cortex and hippocampus of control animals during P15 to P22, the Aralar-KO specimens hardly progressed. The divergence was more pronounced in the CA3/hilus region. In parallel, spontaneous multiunit activity declined severely in KO mice. Postnatal growth of hippocampal-evoked potentials was delayed in KO mice, and indicated abnormal synaptic and spike electrogenesis and reduced output at P20 to P22. The lack of LFP development in KO mice was accompanied by the gradual appearance of epileptic activity in the CA3/hilus region that evolved to status epilepticus. Strikingly, CA3 bursts were poorly conducted to the CA1 field. We conclude that disturbed substrate supply to neuronal mitochondria impairs development of cortico-hippocampal LFPs. Aberrant neuronal electrogenesis and reduced neuron output may explain circuit dysfunction and phenotype deficiencies. © 2012 ISCBFM All rights reserved.
2015-02-26T09:34:51Z
2015-02-26T09:34:51Z
2012
2015-02-26T09:34:51Z
artículo
Journal of Cerebral Blood Flow and Metabolism; 32: 306- 317 (2012)
http://hdl.handle.net/10261/111312
10.1038/jcbfm.2011.129
http://dx.doi.org/10.13039/100008061
http://dx.doi.org/10.13039/100008054
http://dx.doi.org/10.13039/100012818
21934695
eng
closedAccess
Lippincott Williams & Wilkins