Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
In this Comment, Riquelme and Gjorgjieva describe why and how individual researchers and the broader neuroscientific community should aim to improve code readability in the field.
Different voltage-gated sodium channels contribute to the transmission of painful information. In this Review, Goodwin and McMahon ask which channels are involved in nociceptor transduction, transmission and transmitter release and why individuals with Nav1.7 null mutations have a painless phenotype.
Ion channel dysfunctions contribute significantly to fragile X pathophysiology. In this Review, Deng and Klyachko discuss the mechanisms underlying the effects of these channelopathies in fragile X syndrome, and the therapeutic potential of pharmacological interventions that target ion channels.
Dysfunctional GABAergic signalling is common to various neurodevelopmental disorders (NDDs). Tang, Jaenisch and Sur give an overview of the contribution of GABA signalling dysfunction to NDD aetiology and examine how mechanistic insights into such disruption can be used to advance treatments for NDDs.
In this Perspective, Koban, Gianaros, Kober and Wager describe neural systems that construct models of the ‘self-in-context’. Such models endow events with personal meaning and enable predictive control over behaviour and peripheral physiology — with implications for health and disease.