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Openshaw, R. L. , Thomson, D. M., Bristow, G. C., Mitchell, E. J., Pratt, J. A., Morris, B. J. and Dawson, N. (2023) 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability. Communications Biology, 6, 557. (doi: 10.1038/s42003-023-04891-2) (PMID:37225770) (PMCID:PMC10209099)
Willis, A., Pratt, J. A. and Morris, B. J. (2021) BDNF and JNK signalling modulate cortical interneuron and perineuronal net development: implications for schizophrenia-linked 16p11.2 duplication syndrome. Schizophrenia Bulletin, 47(3), pp. 812-826. (doi: 10.1093/schbul/sbaa139) (PMID:33067994)
Mitchell, E. J., Thomson, D. M., Openshaw, R. L. , Bristow, G. C., Dawson, N., Pratt, J. A. and Morris, B. (2020) Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions. Scientific Reports, 10, 12303. (doi: 10.1038/s41598-020-69130-8) (PMID:32704009) (PMCID:PMC7378168)
Bristow, G. C., Thomson, D. M., Openshaw, R. L. , Mitchell, E. J., Pratt, J. A., Dawson, N. and Morris, B. J. (2020) 16p11 duplication disrupts hippocampal-orbitofrontal-amygdala connectivity, revealing a neural circuit endophenotype for schizophrenia. Cell Reports, 31(3), 107536. (doi: 10.1016/j.celrep.2020.107536) (PMID:32320645)