ArticleScientific reports2016
Premature changes in neuronal excitability account for hippocampal network impairment and autistic-like behavior in neonatal BTBR T+tf/J mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Article
- Insights into the structure and function of the hippocampus: implications for the pathophysiology and treatment of autism spectrum disorder.Frontiers in psychiatry · 2024Review
- Comparing synaptic proteomes across five mouse models for autism reveals converging molecular similarities including deficits in oxidative phosphorylation and Rho GTPase signaling.Frontiers in aging neuroscience · 2023Article
- Seizure susceptibility to various convulsant stimuli in the BTBR mouse model of autism spectrum disorders.Frontiers in pharmacology · 2023Article
- NKCC1 Deficiency in Forming Hippocampal Circuits Triggers Neurodevelopmental Disorder: Role of BDNF-TrkB Signalling.Brain sciences · 2022Review
- Loss of neurodevelopmental-associated miR-592 impairs neurogenesis and causes social interaction deficits.Cell death & disease · 2022Article
- Autistic-like behavior, spontaneous seizures, and increased neuronal excitability in a Scn8a mouse model.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- GABAergic System Dysfunction in Autism Spectrum Disorders.Frontiers in cell and developmental biology · 2021Review
- Topographic heterogeneity of intrinsic excitability in mouse hippocampal CA3 pyramidal neurons.Journal of neurophysiology · 2020Article
- Immature Dentate Granule Cells Require Ntrk2/Trkb for the Formation of Functional Hippocampal Circuitry.iScience · 2020Article
- [A review on the role of γ-aminobutyric acid signaling pathway in autism spectrum disorder].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018Review
- INTERNEURONOPATHIES AND THEIR ROLE IN EARLY LIFE EPILEPSIES AND NEURODEVELOPMENTAL DISORDERS.Epilepsia open · 2017Article
- Article
- Early-life febrile seizures worsen adult phenotypes in Scn1a mutants.Experimental neurology · 2017Article
- The BTBR mouse model of idiopathic autism - Current view on mechanisms.Neuroscience and biobehavioral reviews · 2017Review
- Early Correlated Network Activity in the Hippocampus: Its Putative Role in Shaping Neuronal Circuits.Frontiers in cellular neuroscience · 2017Review
- Modulation of Neocortical Development by Early Neuronal Activity: Physiology and Pathophysiology.Frontiers in cellular neuroscience · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coherent network oscillations (GDPs), generated in the immature hippocampus by the synergistic action of GABA and glutamate, both depolarizing and excitatory, play a key role in the construction of neuronal circuits. In particular, GDPs-associated calcium transients act as coincident detectors for enhancing synaptic efficacy at emerging GABAergic and glutamatergic synapses. Here, we show that, immediately after birth, in the CA3 hippocampal region of the BTBR T+tf/J mouse, an animal model of idiopathic autism, GDPs are severely impaired. This effect was associated with an increased GABAergic neurotransmission and a reduced neuronal excitability. In spite its depolarizing action on CA3 pyramidal cells (in single channel experiments EGABA was positive to Em), GABA exerted at the network level an inhibitory effect as demonstrated by isoguvacine-induced reduction of neuronal firing. We implemented a computational model in which experimental findings could be interpreted as the result of two competing effects: a reduction of the intrinsic excitability of CA3 principal cells and a reduction of the shunting activity in GABAergic interneurons projecting to principal cells. It is therefore likely that premature changes in neuronal excitability within selective hippocampal circuits of BTBR mice lead to GDPs dysfunction and behavioral deficits reminiscent of those found in autistic patients.
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