ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Thalamic T-type Ca²+ channels mediate frontal lobe dysfunctions caused by a hypoxia-like damage in the prefrontal cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 34 citations in OpenAlex.
- Age- and sex-dependent effects of stressors on activity of the nucleus reuniens of the thalamus.Schizophrenia research · 2025Article
- Thrombin mediates seizures following cortical injury-induced status epilepticus.Epilepsy research · 2025Article
- Noradrenergic stimulation of αScientific reports · 2023Article
- Synergistic structural and functional alterations in the medial prefrontal cortex of patients with high-grade gliomas infiltrating the thalamus and the basal ganglia.Frontiers in neuroscience · 2023Article
- Activation of the basal ganglia and indirect pathway neurons during frontal lobe seizures.Brain : a journal of neurology · 2021Article
- Corticothalamic Pathways From Layer 5: Emerging Roles in Computation and Pathology.Frontiers in neural circuits · 2021Review
- Neocortical injury-induced status epilepticus.Epilepsia · 2020Article
- Prefrontal cortex modulates firing pattern in the nucleus reuniens of the midline thalamus via distinct corticothalamic pathways.The European journal of neuroscience · 2018Article
- Effect of Hypoxic Injury in Mood Disorder.Neural plasticity · 2017Review
- Protein arginine methylation facilitates KCNQ channel-PIP2 interaction leading to seizure suppression.eLife · 2016Article
- T-type Ca2+ channels in absence epilepsy.Pflugers Archiv : European journal of physiology · 2014Review
- The potential roles of T-type Ca2+ channels in motor coordination.Frontiers in neural circuits · 2013Review
- Amelioration of behavioral abnormalities in BH(4)-deficient mice by dietary supplementation of tyrosine.PloS one · 2013Article
- Anti-epileptic drugs delay age-related loss of spiral ganglion neurons via T-type calcium channel.Hearing research · 2011Article
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12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxic damage to the prefrontal cortex (PFC) has been implicated in the frontal lobe dysfunction found in various neuropsychiatric disorders. The underlying subcortical mechanisms, however, have not been well explored. In this study, we induced a PFC-specific hypoxia-like damage by cobalt-wire implantation to demonstrate that the role of the mediodorsal thalamus (MD) is critical for the development of frontal lobe dysfunction, including frontal lobe-specific seizures and abnormal hyperactivity. Before the onset of these abnormalities, the cross talk between the MD and PFC nuclei at theta frequencies was enhanced. During the theta frequency interactions, burst spikes, known to depend on T-type Ca(2+) channels, were increased in MD neurons. In vivo knockout or knockdown of the T-type Ca(2+) channel gene (Ca(V)3.1) in the MD substantially reduced the theta frequency MD-PFC cross talk, frontal lobe-specific seizures, and locomotor hyperactivity in this model. These results suggest a two-step model of prefrontal dysfunction in which the response to a hypoxic lesion in the PFC results in abnormal thalamocortical feedback driven by thalamic T-type Ca(2+) channels, which, in turn, leads to the onset of neurological and behavioral abnormalities. This study provides valuable insights into preventing the development of neuropsychiatric disorders arising from irreversible PFC damage.
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