ArticleChonnam medical journal2012
Molecular mechanisms involved in depotentiation and their relevance to schizophrenia.
Article in Chonnam medical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed.
- Overnight neuronal plasticity and adaptation to emotional distress.Nature reviews. Neuroscience · 2024Review
- Reinstatement of nicotine conditioned place preference in a transgenerational model of drug abuse vulnerability in psychosis: Impact of BDNF on the saliency of drug associations.Psychopharmacology · 2023Article
- Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models.Acta neuropathologica communications · 2019Article
- Learning-Induced Metaplasticity? Associative Training for Early Odor Preference Learning Down-Regulates Synapse-Specific NMDA Receptors via mGluR and Calcineurin Activation.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- The reemergence of long-term potentiation in aged Alzheimer's disease mouse model.Scientific reports · 2016Article
- Separate Ionotropic and Metabotropic Glutamate Receptor Functions in Depotentiation vs. LTP: A Distinct Role for Group1 mGluR Subtypes and NMDARs.Frontiers in cellular neuroscience · 2016Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context.
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Registered trials
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