ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
The role of brain-derived neurotrophic factor receptors in the mature hippocampus: modulation of long-term potentiation through a presynaptic mechanism involving TrkB.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 1 of them a synthesis that pooled it.
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Who cites it
176 citing papers in PubMed, 1 synthesis or guideline pooled it, 404 citations in OpenAlex.
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- Memory-Associated Immediate Early Genes: Roles in Synaptic Function, Memory Processes, and Neurological Diseases.Molecular neurobiology · 2025Review
- A comprehensive review on schizophrenia: epidemiology, pathogenesis, diagnosis, conventional treatments, and proposed natural compounds used for management.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Brain-Derived Neurotrophic Factor (BDNF) and Sex Differences in Metabolic Regulation.Journal of neurochemistry · 2025Review
- BDNF Signaling and Pain Modulation.Cells · 2025Review
- Decoding serotonin: the molecular symphony behind depression.Frontiers in cellular neuroscience · 2025Review
- α-linolenic acid-induced facilitation of GABAergic synaptic transmission is mediated via acid-sensing ion channel (ASIC1a) activity in the basolateral amygdala.Experimental biology and medicine (Maywood, N.J.) · 2025Article
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- The relevance of BDNF for neuroprotection and neuroplasticity in multiple sclerosis.Frontiers in neurology · 2024Review
- Pre- and postsynaptic N-methyl-D-aspartate receptors are required for sequential printing of fear memory engrams.iScience · 2023Article
- Alpha-linolenic acid enhances the facilitation of GABAergic neurotransmission in the BLA and CA1.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Brain-derived neurotrophic factor interplay with oxidative stress: neuropathology approach in potential biomarker of Alzheimer's disease.Dementia & neuropsychologia · 2023Review
- Pimavanserin treatment increases plasma brain-derived neurotrophic factor levels in rats.Frontiers in neuroscience · 2023Article
- Deletion of p75Frontiers in molecular neuroscience · 2023Article
- ProBDNF and its receptors in immune-mediated inflammatory diseases: novel insights into the regulation of metabolism and mitochondria.Frontiers in immunology · 2023Review
- Corticosterone antagonist or TrkB agonist attenuates schizophrenia-like behavior in a mouse model combiningiScience · 2022Article
- Tissue Plasminogen Activator in Central Nervous System Physiology and Pathology: From Synaptic Plasticity to Alzheimer's Disease.Seminars in thrombosis and hemostasis · 2022Review
- High-affinity TrkA and p75 neurotrophin receptor complexes: A twisted affair.The Journal of biological chemistry · 2022Review
116 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The neurotrophin BDNF has been shown to modulate long-term potentiation (LTP) at Schaffer collateral-CA1 hippocampal synapses. Mutants in the BDNF receptor gene trkB and antibodies to its second receptor p75NTR have been used to determine the receptors and cells involved in this response. Inhibition of p75NTR does not detectably reduce LTP or affect presynaptic function, but analyses of newly generated trkB mutants implicate TrkB. One mutant has reduced expression in a normal pattern of TrkB throughout the brain. The second mutant was created by cre-loxP-mediated removal of TrkB in CA1 pyramidal neurons of this mouse. Neither mutant detectably impacts survival or morphology of hippocampal neurons. TrkB reduction, however, affects presynaptic function and reduces the ability of tetanic stimulation to induce LTP. Postsynaptic glutamate receptors are not affected by TrkB reduction, indicating that BDNF does not modulate plasticity through postsynaptic TrkB. Consistent with this, elimination of TrkB in postsynaptic neurons does not affect LTP. Moreover, normal LTP is generated in the mutant with reduced TrkB by a depolarization-low-frequency stimulation pairing protocol that puts minimal demands on presynaptic terminal function. Thus, BDNF appears to act through TrkB presynaptically, but not postsynaptically, to modulate LTP.
Indexed as
Identifiers
10995833PMC2711895W2138497185What 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.