ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
The presynaptic active zone protein RIM1α controls epileptogenesis following status epilepticus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. 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, 24 citations in OpenAlex.
- Variants in BSN, encoding the presynaptic protein Bassoon, result in a distinct neurodevelopmental disorder with a broad phenotypic range.American journal of human genetics · 2025Article
- Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death.International journal of molecular sciences · 2024Article
- Multiomics of early epileptogenesis in mice reveals phosphorylation and dephosphorylation-directed growth and synaptic weakening.iScience · 2024Article
- Highly dynamic inflammatory and excitability transcriptional profiles in hippocampal CA1 following status epilepticus.Scientific reports · 2023Article
- Subcellular analysis of blood-brain barrier function by micro-impalement of vessels in acute brain slices.Nature communications · 2023Article
- Characterisation of NLRP3 pathway-related neuroinflammation in temporal lobe epilepsy.PloS one · 2022Article
- Calcium Channel Subunit α2δ4 Is Regulated by Early Growth Response 1 and Facilitates Epileptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Anti-epileptogenic and Anti-convulsive Effects of Fingolimod in Experimental Temporal Lobe Epilepsy.Molecular neurobiology · 2019Article
- Polyamine Modulation of Anticonvulsant Drug Response: A Potential Mechanism Contributing to Pharmacoresistance in Chronic Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Abnormal Expression of FBXL20 in Refractory Epilepsy Patients and a Pilocarpine-Induced Rat Model.Neurochemical research · 2016Article
- Echinoderm microtubule-associated protein -like protein 5 in anterior temporal neocortex of patients with intractable epilepsy.Iranian journal of basic medical sciences · 2015Article
- De novo insertions and deletions of predominantly paternal origin are associated with autism spectrum disorder.Cell reports · 2014Article
- The Proteome of the Murine Presynaptic Active Zone.Proteomes · 2014Review
- Experience-dependent regulation of presynaptic NMDARs enhances neurotransmitter release at neocortical synapses.Learning & memory (Cold Spring Harbor, N.Y.) · 2014Article
- Molecular mechanisms driving homeostatic plasticity of neurotransmitter release.Frontiers in cellular neuroscience · 2013Review
- Cryo-electron tomography reveals a critical role of RIM1α in synaptic vesicle tethering.The Journal of cell biology · 2013Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To ensure operation of synaptic transmission within an appropriate dynamic range, neurons have evolved mechanisms of activity-dependent plasticity, including changes in presynaptic efficacy. The multidomain protein RIM1α is an integral component of the cytomatrix at the presynaptic active zone and has emerged as key mediator of presynaptically expressed forms of synaptic plasticity. We have therefore addressed the role of RIM1α in aberrant cellular plasticity and structural reorganization after an episode of synchronous neuronal activity pharmacologically induced in vivo [status epilepticus (SE)]. Post-SE, all animals developed spontaneous seizure events, but their frequency was dramatically increased in RIM1α-deficient mice (RIM1α(-/-)). We found that in wild-type mice (RIM1α(+/+)) SE caused an increase in paired-pulse facilitation in the CA1 region of the hippocampus to the level observed in RIM1α(-/-) mice before SE. In contrast, this form of short-term plasticity was not further enhanced in RIM1α-deficient mice after SE. Intriguingly, RIM1α(-/-) mice showed a unique pattern of selective hilar cell loss (i.e., endfolium sclerosis), which so far has not been observed in a genetic epilepsy animal model, as well as less severe astrogliosis and attenuated mossy fiber sprouting. These findings indicate that the decrease in release probability and altered short- and long-term plasticity as present in RIM1α(-/-) mice result in the formation of a hyperexcitable network but act in part neuroprotectively with regard to neuropathological alterations associated with epileptogenesis. In summary, our results suggest that presynaptic plasticity and proper function of RIM1α play an important part in a neuron's adaptive response to aberrant electrical activity.
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