ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Focal cortical infarcts alter intrinsic excitability and synaptic excitation in the reticular thalamic nucleus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 83 citations in OpenAlex.
- Large-scale neural slowing measured with electroencephalography indexes secondary thalamic degeneration in stroke.medRxiv : the preprint server for health sciences · 2026Article
- Adversarial AI reveals mechanisms and treatments for disorders of consciousness.Nature neuroscience · 2026Article
- Characterisation of the axon initial segment and intrinsic excitability in the sub-acute phase post-ischaemic stroke.Brain communications · 2026Article
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
- Modified human mesenchymal stromal/stem cells restore cortical excitability after focal ischemic stroke in rats.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Secondary thalamic dysfunction underlies abnormal large-scale neural dynamics in chronic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Conditioning and pseudoconditioning differently change intrinsic excitability of inhibitory interneurons in the neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Pallidal GABA B receptors: involvement in cortex beta dynamics and thalamic reticular nucleus activity.The journal of physiological sciences : JPS · 2023Article
- Elevation of GABA levels in the globus pallidus disinhibits the thalamic reticular nucleus and desynchronized cortical beta oscillations.The journal of physiological sciences : JPS · 2022Article
- Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents.Science translational medicine · 2022Article
- Differences in hippocampal plasticity and memory outcomes in anterior versus posterior cerebellar stroke.Neurobiology of disease · 2022Article
- Secondary thalamic neuroinflammation after focal cortical stroke and traumatic injury mirrors corticothalamic functional connectivity.The Journal of comparative neurology · 2022Article
- The mechanism and effect of repetitive transcranial magnetic stimulation for post-stroke pain.Frontiers in molecular neuroscience · 2022Review
- Rapid and Bihemispheric Reorganization of Neuronal Activity in Premotor Cortex after Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Amazon rainforest rodents (Proechimys) are resistant to post-stroke epilepsy.Scientific reports · 2021Article
- Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Morphological alterations of the reticular thalamic nucleus in Engrailed-2 knockout mice.Journal of anatomy · 2020Article
- Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke.Frontiers in neurology · 2020Review
- Low oxygen post conditioning prevents thalamic secondary neuronal loss caused by excitotoxicity after cortical stroke.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Focal cortical injuries result in death of cortical neurons and their efferents and ultimately in death or damage of thalamocortical relay (TCR) neurons that project to the affected cortical area. Neurons of the inhibitory reticular thalamic nucleus (nRT) receive excitatory inputs from corticothalamic and thalamocortical axons and are thus denervated by such injuries, yet nRT cells generally survive these insults to a greater degree than TCR cells. nRT cells inhibit TCR cells, regulate thalamocortical transmission, and generate cerebral rhythms including those involved in thalamocortical epilepsies. The survival and reorganization of nRT after cortical injury would determine recovery of thalamocortical circuits after injury. However, the physiological properties and connectivity of the survivors remain unknown. To study possible alterations in nRT neurons, we used the rat photothrombosis model of cortical stroke. Using in vitro patch-clamp recordings at various times after the photothrombotic injury, we show that localized strokes in the somatosensory cortex induce long-term reductions in intrinsic excitability and evoked synaptic excitation of nRT cells by the end of the first week after the injury. We find that nRT neurons in injured rats show (1) decreased membrane input resistance, (2) reduced low-threshold calcium burst responses, and (3) weaker evoked excitatory synaptic responses. Such alterations in nRT cellular excitability could lead to loss of nRT-mediated inhibition in relay nuclei, increased output of surviving TCR cells, and enhanced thalamocortical excitation, which may facilitate recovery of thalamic and cortical sensory circuits. In addition, such changes could be maladaptive, leading to injury-induced epilepsy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.