British journal of anaesthesia
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Editorial
Unmasking imposter syndrome: individual responsibility or repercussions of systemic oppression?
In contemporary and popular discourse, imposter syndrome is frequently outlined as an individual problem that can be overcome. Rather than the locus of responsibility being placed on the individual, we posit that neoliberal academic institutions contribute to imposter syndrome by (de)legitimising certain forms of knowledge.
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Administration of subanaesthetic doses of ketamine during isoflurane anaesthesia has been shown in animals to deepen the anaesthetised state, while accelerating emergence. Duan and colleagues have now shown that the addition of subanaesthetic doses of esketamine to isoflurane has a similar effect of increasing the burst suppression ratio, while accelerating emergence. Using c-Fos expression and fibre photometry, they show that esketamine activates glutamatergic neurones in the paraventricular nucleus of the thalamus, a structure that regulates wakefulness. Chemogenetic inhibition of these neurones attenuates the arousal-promoting effects, suggesting a causal role of the paraventricular nucleus of the thalamus in esketamine-mediated acceleration of recovery from anaesthesia.
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The neural mechanisms underlying sevoflurane-induced loss of consciousness and recovery of consciousness after anaesthesia remain unknown. We investigated whether glutamatergic pedunculopontine tegmental nucleus (PPT) neurones are involved in the regulation of states of consciousness under sevoflurane anaesthesia. ⋯ Glutamatergic PPT neurones regulate induction and emergence of sevoflurane anaesthesia.