In this paper we argue that school toilets function as one civilising site [Elias, 1978. The Civilising Process. Oxford: Blackwell] in which children learn that disabled and queer bodies are out of place. This paper is the first to offer queer and crip perspectives on school toilets. The small body of existing school toilet literature generally works from a normative position which implicitly perpetuates dominant and oppressive ideals. We draw on data from Around the Toilet, a collaborative research project with queer, trans and disabled people (aroundthetoilet.wordpress.com) to critically interrogate this work. In doing this we consider 'toilet training' as a form of 'civilisation', that teaches lessons around identity, embodiment and ab/normal ways of being in the world. Furthermore, we show that 'toilet training' continues into adulthood, albeit in ways that are less easily identifiable than in the early years. We therefore call for a more critical, inclusive, and transformative approach to school toilet research. ARTICLE HISTORY
As one of the few explicitly gender-separated spaces, the toilet has become a prominent site of conflict and a focal point for ‘gender-critical’ feminism. In this article we draw upon an AHRC-funded project, Around the Toilet, to reflect upon and critique trans-exclusionary and trans-hostile narratives of toilet spaces. Such narratives include ciscentric, heteronormative and gender essentialist positions within toilet research and activism which, for example, equate certain actions and bodily functions (such as menstruation) to a particular gender, decry the need for all-gender toilets, and cast suspicion upon the intentions of trans women in public toilet spaces. These include explicitly transmisogynist discourses perpetuated largely by those calling themselves ‘gender-critical’ feminists, but also extend to national media, right-wing populist discourses and beyond. We use Around the Toilet data to argue that access to safe and comfortable toilets plays a fundamental role in making trans lives possible. Furthermore, we contend that – whether naive, ignorant or explicitly transphobic – trans-exclusionary positions do little to improve toilet access for the majority, instead putting trans people, and others with visible markers of gender difference, at a greater risk of violence, and participating in the dangerous homogenisation of womanhood.
GABA A receptors (GABA A Rs) are profoundly important for controlling neuronal excitability. Spontaneous and familial mutations to these receptors feature prominently in excitability disorders and neurodevelopmental deficits following disruption to GABA-mediated inhibition. Recent genotyping of an individual with severe epilepsy and Williams-Beuren Syndrome identified a frameshifting de novo variant in a major GABA A R gene, GABRA1. This truncated the α1 subunit between the third and fourth transmembrane domains and introduced 24 new residues forming the mature protein, α1 Lys374Serfs*25. Cell surface expression of mutant murine GABA A Rs is severely impaired compared to wild-type, due to retention in the endoplasmic reticulum. Mutant receptors were differentially co-expressed with β3, but not with β2 subunits in mammalian cells. Reduced surface expression was reflected by smaller inhibitory postsynaptic currents, which may underlie the induction of seizures. The mutant does not have a dominant negative effect on native neuronal GABA A R expression since GABA current density was unaffected in hippocampal neurons, even though mutant receptors exhibited limited GABA sensitivity. To date, the underlying mechanism is unique for epileptogenic variants and involves differential β subunit expression of GABA A R populations, which profoundly affected receptor function and synaptic inhibition. Significance Statement GABA A Rs are critical for controlling neural network excitability. They are ubiquitously distributed throughout the brain and their dysfunction underlies many neurological disorders, especially epilepsy. Here we report the characterisation of an α1-GABA A R variant that results in severe epilepsy. The underlying mechanism is structurally unusual, with the loss of part of the α1 subunit transmembrane domain and part-replacement with nonsense residues. This led to compromised and differential α1-subunit cell surface expression with β subunits resulting in severely reduced synaptic inhibition. Our study reveals that diseaseinducing variants can affect GABA A R structure, and consequently subunit assembly and cell surface expression, critically impacting on the efficacy of synaptic inhibition, a property that will orchestrate the extent and duration of neuronal excitability.
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