Publications by authors named "Natasha Anstey"
Mutations in SYNGAP1 are a common genetic cause of intellectual disability (ID) and a risk factor for autism. SYNGAP1 encodes a synaptic GTPase-activating protein (GAP) that has both signaling and scaffolding roles. Most pathogenic variants of SYNGAP1 are predicted to result in haploinsufficiency.
View Article and Find Full Text PDFBackground: Mutations in the postsynaptic transmembrane protein neuroligin-3 are highly correlative with autism spectrum disorders (ASDs) and intellectual disabilities (IDs). Fear learning is well studied in models of these disorders, however differences in fear response behaviours are often overlooked. We aim to examine fear behaviour and its cellular underpinnings in a rat model of ASD/ID lacking Nlgn3.
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- Dysregulated protein synthesis is a key issue in Fragile X Syndrome (FX), with the mGluR Theory suggesting that too much translation of certain mRNAs leads to problematic synaptic changes.
- Researchers used TRAP-seq and proteomics to discover that mGlu stimulation in FX mice causes increased translation of ribosomal proteins while decreasing the translation of longer mRNAs for synaptic proteins.
- Inhibiting the translation of ribosomal proteins hinders mGluR-induced synaptic changes, pointing to a problematic shift in the type of mRNAs being translated as a core issue in FX pathology.
Cellular hyperexcitability is a salient feature of fragile X syndrome animal models. The cellular basis of hyperexcitability and how it responds to changing activity states is not fully understood. Here, we show increased axon initial segment length in CA1 of the Fmr1 mouse hippocampus, with increased cellular excitability.
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