ArticleMolecular and cellular neurosciences2018
Deletion of the endogenous TrkB.T1 receptor isoform restores the number of hippocampal CA1 parvalbumin-positive neurons and rescues long-term potentiation in pre-symptomatic mSOD1(G93A) ALS mice.
Article in Molecular and cellular neurosciences, 2018. 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.
- A comprehensive review of electrophysiological techniques in amyotrophic lateral sclerosis research.Frontiers in cellular neuroscience · 2024Review
- Global research hotspots and trends of theta burst stimulation from 2004 to 2023: a bibliometric analysis.Frontiers in neurology · 2024Article
- Article
- A Truncated Receptor TrkB Isoform (TrkB.T1) in Mechanisms of Genetically Determined Depressive-like Behavior of Mice.Biomedicines · 2023Article
- Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Human-Induced Pluripotent Stem Cell-Based Models for Studying Sex-Specific Differences in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2022Review
- Delayed onset of inherited ALS by deletion of the BDNF receptor TrkB.T1 is non-cell autonomous.Experimental neurology · 2021Article
- MRI-guided histology of TDP-43 knock-in mice implicates parvalbumin interneuron loss, impaired neurogenesis and aberrant neurodevelopment in amyotrophic lateral sclerosis-frontotemporal dementia.Brain communications · 2021Article
- Review
- Dysregulation of BDNF/TrkB signaling mediated by NMDAR/CaJournal of neuroinflammation · 2020Article
- Effects of Exercise on Long-Term Potentiation in Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2020Review
- Disinhibition-assisted long-term potentiation in the prefrontal-amygdala pathway via suppression of somatostatin-expressing interneurons.Neurophotonics · 2020Article
- Future Portrait of the Athletic Brain: Mechanistic Understanding of Human Sport PerformanceFrontiers in systems neuroscience · 2020Article
- NT-4/5 antagonizes the BDNF modulation of corticostriatal transmission: Role of the TrkB.T1 receptor.CNS neuroscience & therapeutics · 2019Article
- The Role of Altered BDNF/TrkB Signaling in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2019Review
- Neuroprotection: Pro-survival and Anti-neurotoxic Mechanisms as Therapeutic Strategies in Neurodegeneration.Frontiers in cellular neuroscience · 2019Review
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Abstract
Amyotrophic lateral sclerosis (ALS) causes rapidly progressive paralysis and death within 5 years from diagnosis due to degeneration of the motor circuits. However, a significant population of ALS patients also shows cognitive impairments and progressive hippocampal pathology. Likewise, the mutant SOD1(G93A) mouse model of ALS (mSOD1), in addition to loss of spinal motor neurons, displays altered spatial behavior and hippocampal abnormalities including loss of parvalbumin-positive interneurons (PVi) and enhanced long-term potentiation (LTP). However, the cellular and molecular mechanisms underlying these morpho-functional features are not well understood. Since removal of TrkB.T1, a receptor isoform of the brain-derived neurotrophic factor, can partially rescue the phenotype of the mSOD1 mice, here we tested whether removal of TrkB.T1 can normalize the number of PVi and the LTP in this model. Stereological analysis of hippocampal PVi in control, TrkB.T1
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