ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Brain-derived neurotrophic factor controls activity-dependent maturation of CA1 synapses by downregulating tonic activation of presynaptic kainate receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 45 citations in OpenAlex.
- Presynaptic Kainate Receptors onto Somatostatin Interneurons Are Recruited by Activity throughout Development and Contribute to Cortical Sensory Adaptation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Low-frequency electroacupncture improves locomotor function after sciatic crushed nerve injury in rats.Journal of exercise rehabilitation · 2018Article
- Myelination of Purkinje axons is critical for resilient synaptic transmission in the deep cerebellar nucleus.Scientific reports · 2018Article
- Treadmill exercise with bone marrow stromal cells transplantation potentiates recovery of locomotor function after spinal cord injury in rats.Journal of exercise rehabilitation · 2017Article
- Treadmill exercise facilitates recovery of locomotor function through axonal regeneration following spinal cord injury in rats.Journal of exercise rehabilitation · 2016Article
- Activity-dependent upregulation of presynaptic kainate receptors at immature CA3-CA1 synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- TrkB receptor signalling: implications in neurodegenerative, psychiatric and proliferative disorders.International journal of molecular sciences · 2013Review
- Neurotrophin regulation of neural circuit development and function.Nature reviews. Neuroscience · 2013Review
- Deficits in morphofunctional maturation of hippocampal mossy fiber synapses in a mouse model of intellectual disability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Influence of physical exercise on traumatic brain injury deficits: scaffolding effect.Neurotoxicity research · 2012Review
- Expression of GluK1c underlies the developmental switch in presynaptic kainate receptor function.Scientific reports · 2012Article
- Effects of exogenous agents on brain development: stress, abuse and therapeutic compounds.CNS neuroscience & therapeutics · 2011Review
- Running wheel activity restores MPTP-induced functional deficits.Journal of neural transmission (Vienna, Austria : 1996) · 2011Article
- Long-Term Potentiation at CA3-CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress.Frontiers in aging neuroscience · 2011Article
- Wingless-type family member 5A (Wnt-5a) stimulates synaptic differentiation and function of glutamatergic synapses.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- High firing rate of neonatal hippocampal interneurons is caused by attenuation of afterhyperpolarizing potassium currents by tonically active kainate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Developmental changes in presynaptic Ca(2 +) clearance kinetics and synaptic plasticity in mouse Schaffer collateral terminals.The European journal of neuroscience · 2010Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immature hippocampal synapses express presynaptic kainate receptors (KARs), which tonically inhibit glutamate release. Presynaptic maturation involves activity-dependent downregulation of the tonic KAR activity and consequent increase in release probability; however, the molecular mechanisms underlying this developmental process are unknown. Here, we have investigated whether brain derived neurotrophic factor (BDNF), a secreted protein implicated in developmental plasticity in several areas of the brain, controls presynaptic maturation by regulating KARs. Application of BDNF in neonate hippocampal slices resulted in increase in synaptic transmission that fully occluded the immature-type KAR activity in area CA1. Conversely, genetic ablation of BDNF was associated with delayed synaptic maturation and persistent presynaptic KAR activity, suggesting a role for endogenous BDNF in the developmental regulation of KAR function. In addition, our data suggests a critical role for BDNF TrkB signaling in fast activity-dependent regulation of KARs. Selective acute inhibition of TrkB receptors using a chemical-genetic approach prevented rapid change in synapse dynamics and loss of tonic KAR activity that is typically seen in response to induction of LTP at immature synapses. Together, these data show that BDNF-TrkB-dependent maturation of glutamatergic synapses is tightly associated with a loss of endogenous KAR activity. The coordinated action of these two receptor mechanisms has immediate physiological relevance in controlling presynaptic efficacy and transmission dynamics at CA3-CA1 synapses at a stage of development when functional contact already exists but transmission is weak.
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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.