ArticleThalamus & related systems2008
Anterior thalamic lesions produce chronic and profuse transcriptional de-regulation in retrosplenial cortex: A model of retrosplenial hypoactivity and covert pathology.
Article in Thalamus & related systems, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Psychedelic neuroplasticity of cortical neurons lacking 5-HT2A receptors.Molecular psychiatry · 2026Article
- Article
- Deconstructing the Direct Reciprocal Hippocampal-Anterior Thalamic Pathways for Spatial Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2020Article
- Thalamic pathology and memory loss in early Alzheimer's disease: moving the focus from the medial temporal lobe to Papez circuit.Brain : a journal of neurology · 2016Review
- Olfactory dysfunction: its early temporal relationship and neural correlates in the pathogenesis of Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2015Review
- Why do lesions in the rodent anterior thalamic nuclei cause such severe spatial deficits?Neuroscience and biobehavioral reviews · 2015Review
- Retrosplenial Cortex and Long-Term Memory: Molecules to Behavior.Neural plasticity · 2015Review
- Eosinophils and mast cells as therapeutic targets in pediatric functional dyspepsia.World journal of gastrointestinal pharmacology and therapeutics · 2013Review
- Anterior thalamic nuclei lesions in rats disrupt markers of neural plasticity in distal limbic brain regions.Neuroscience · 2012Article
- Unraveling the contributions of the diencephalon to recognition memory: a review.Learning & memory (Cold Spring Harbor, N.Y.) · 2011Review
- Selective genomic targeting by FRA-2/FOSL2 transcription factor: regulation of the Rgs4 gene is mediated by a variant activator protein 1 (AP-1) promoter sequence/CREB-binding protein (CBP) mechanism.The Journal of biological chemistry · 2011Article
- Early-onset dysfunction of retrosplenial cortex precedes overt amyloid plaque formation in Tg2576 mice.Neuroscience · 2011Article
- Sequential relationships between grey matter and white matter atrophy and brain metabolic abnormalities in early Alzheimer's disease.Brain : a journal of neurology · 2010Article
- Article
- Hippocampal-anterior thalamic pathways for memory: uncovering a network of direct and indirect actions.The European journal of neuroscience · 2010Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Anterior thalamic lesions are thought to produce 'covert pathology' in retrosplenial cortex, but the causes are unknown. Microarray analyses tested the hypothesis that thalamic damage causes a chronic, hypo-function of metabolic and plasticity-related pathways (Experiment 1). Rats with unilateral, anterior thalamic lesions were exposed to a novel environment for 20 minutes, and granular retrosplenial tissue sampled from both hemispheres 30 minutes, 2h, or 8h later. Complementary statistical approaches (analyses of variance, predictive patterning and gene set enrichment analysis) revealed pervasive gene expression differences between retrosplenial cortex ipsilateral to the thalamic lesion and contralateral to the lesion. Selected gene differences were validated by QPCR, immunohistochemistry (Experiment 1), and in situ hybridisation (Experiment 2). Following thalamic lesions, the retrosplenial cortex undergoes profuse cellular transcriptome changes including lower relative levels of specific mRNAs involved in energy metabolism and neuronal plasticity. These changes in functional gene expression may be largely driven by decreases in the expression of multiple transcription factors, including brd8, c-fos, fra-2, klf5, nfix, nr4a1, smad3, smarcc2, and zfp9, with a much smaller number (nfat5, neuroD1, RXRγ) showing increases. These findings have implications for conditions such as diencephalic amnesia and Alzheimer's disease, where both anterior thalamic pathology and retrosplenial cortex hypometabolism are prominent.
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