ArticleeNeuro
Shank Proteins Differentially Regulate Synaptic Transmission.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Hippocampus-targeted BDNF gene therapy to rescue cognitive impairments of Alzheimer's disease in multiple mouse models.Genes & diseases · 2026Article
- HDAC Inhibition Reshapes Splicing of Synaptic Plasticity-Related Genes and Neural Network Dynamics.Cellular and molecular neurobiology · 2026Article
- Hypersynchronous iPSC-derived SHANK2 neuronal networks are rescued by mGluR5 agonism.Stem cell reports · 2025Article
- Review
- Decoding the genetic landscape of autism: A comprehensive review.World journal of clinical pediatrics · 2024Article
- Agonists, Antagonists and Receptors of Somatostatin: Pathophysiological and Therapeutical Implications in Neoplasias.Current issues in molecular biology · 2024Review
- Quantitative proteomics of dorsolateral prefrontal cortex reveals an early pattern of synaptic dysmaturation in children with idiopathic autism.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Spatially Resolved Transcriptomic Signatures of Hippocampal Subregions andbioRxiv : the preprint server for biology · 2024Article
- Dual-specificity protein phosphatase 6 (DUSP6) overexpression reduces amyloid load and improves memory deficits in male 5xFAD mice.Frontiers in aging neuroscience · 2024Article
- Spatially resolved transcriptomic signatures of hippocampal subregions andFrontiers in molecular neuroscience · 2024Article
- Engram cell connectivity as a mechanism for information encoding and memory function.bioRxiv : the preprint server for biology · 2023Article
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- Shank2 identifies a subset of glycinergic neurons involved in altered nociception in an autism model.Molecular autism · 2023Article
- Targeting Shank3 deficiency and paresthesia in autism spectrum disorder: A brief review.Frontiers in molecular neuroscience · 2023Review
- The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Chronic sodium bromide treatment relieves autistic-like behavioral deficits in three mouse models of autism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- SHANK1 facilitates non-small cell lung cancer processes through modulating the ubiquitination of Klotho by interacting with MDM2.Cell death & disease · 2022Article
- Early and Late Transcriptional Changes in Blood, Neural, and Colon Tissues in Rat Models of Stress-Induced and Comorbid Pain Hypersensitivity Reveal Regulatory Roles in Neurological Disease.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- A Maternal High-Fat Diet during Early Development Provokes Molecular Changes Related to Autism Spectrum Disorder in the Rat Offspring Brain.Nutrients · 2021Article
- Pharmacological modulation of AMPA receptors rescues specific impairments in social behavior associated with the A350V Iqsec2 mutation.Translational psychiatry · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Shank proteins, one of the principal scaffolds in the postsynaptic density (PSD) of the glutamatergic synapses, have been associated with autism spectrum disorders and neuropsychiatric diseases. However, it is not known whether different Shank family proteins have distinct functions in regulating synaptic transmission, and how they differ from other scaffold proteins in this aspect. Here, we investigate the role of Shanks in regulating glutamatergic synaptic transmission at rat hippocampal SC-CA1 synapses, using lentivirus-mediated knockdown and molecular replacement combined with dual whole-cell patch clamp in hippocampal slice culture. In line with previous findings regarding PSD-MAGUK scaffold manipulation, we found that loss of scaffold proteins via knockdown of Shank1 or Shank2, but not Shank3, led to a reduction of the number but not the unitary response of AMPAR-containing synapses. Only when both Shank1 and Shank2 were knocked down, were both the number and the unitary response of active synapses reduced. This reduction was accompanied by a decrease in NMDAR-mediated synaptic response, indicating more profound deficits in synaptic transmission. Molecular replacement with Shank2 and Shank3c rescued the synaptic transmission to the basal level, and the intact sterile α-motif (SAM) of Shank proteins is required for maintaining glutamatergic synaptic transmission. We also found that altered neural activity did not influence the effect of Shank1 or Shank2 knockdown on AMPAR synaptic transmission, in direct contrast to the activity dependence of the effect of PSD-95 knockdown, revealing differential interaction between activity-dependent signaling and scaffold protein families in regulating synaptic AMPAR function.
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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.