New papers in Nature Communications
Congratulations to first authors Dr Sam Booker and Dr Aleks Domanski and senior authors Profs Peter Kind and David Wyllie who have published two papers in Nature Communications on their findings from investigating the developmental basis of sensory hypersenstivities in Fragile X Syndrome.
Sensory hypersensitivity is a key feature of Fragile X Syndrome (FXS) and autism, and experimental models for these conditions are characterised by cellular and circuit hyperexcitability. This suggests that alterations in intrinsic and synaptic neuronal physiology might underlie these features.
These studies address whether there is a relationship between the function of the spines found on dendrites of neurones (which are responsible for receiving signals from other neurones), the intrinsic properties of the neurones, and the function of the ion channel found in the neuronal spines. These all influence the integration of these signals and, ultimately, the output from the neurones so any changes would alter this integration process.
Researchers used a number of technical approaches (including electrical recordings of individual cells, 2-photon microscopy and computational model) and found that, in a mouse model of FXS, the local neuronal circuits in the somatosensory cortex were more excitable than controls, in response to a stimulus. These studies were performed during an early developmental time-window when experience is shaping cortical connectivity and ultimately sensory function.
These studies demonstrate that the information flow through sensory circuits, during this critical time-window for experience-dependent plasticity, is dramatically altered in a mouse model of FXS; thereby giving valuable insight into the developmental origins of sensory hypersensitivities.
Read 'Altered dendritic spine function and integration in a mouse model of fragile X syndrome' in Nature Communications
Read 'Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex' in Nature Communications