Ben-Shalom R et al. (2017). Opposing Effects on NaV1.2 Function Underlie Differences Between SCN2A Variants Observed in Individuals With Autism Spectrum Disorder or Infantile Seizures. Biological psychiatry. 82 [PubMed]
Ferguson KA, Huh CY, Amilhon B, Williams S, Skinner FK. (2013). Experimentally constrained CA1 fast-firing parvalbumin-positive interneuron network models exhibit sharp transitions into coherent high frequency rhythms. Frontiers in computational neuroscience. 7 [PubMed]
Lee SH et al. (2014). Parvalbumin-positive basket cells differentiate among hippocampal pyramidal cells. Neuron. 82 [PubMed]
Royeck M et al. (2008). Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. Journal of neurophysiology. 100 [PubMed]
Spratt PWE et al. (2021). Paradoxical hyperexcitability from NaV1.2 sodium channel loss in neocortical pyramidal cells Cell reports. 36 [PubMed]
Thomas EA, Reid CA, Berkovic SF, Petrou S. (2009). Prediction by modeling that epilepsy may be caused by very small functional changes in ion channels. Archives of neurology. 66 [PubMed]
Thomas EA, Reid CA, Petrou S. (2010). Mossy fiber sprouting interacts with sodium channel mutations to increase dentate gyrus excitability. Epilepsia. 51 [PubMed]
Wimmer VC et al. (2010). Axon initial segment dysfunction in a mouse model of genetic epilepsy with febrile seizures plus. The Journal of clinical investigation. 120 [PubMed]