Teleri Clark

Abstract Chronic pain caused by peripheral nerve injury involves altered spinal pain transduction, where enhanced excitatory and/or reduced inhibitory pathways can drive pain. The cellular transcriptional changes that sustain entrenched neuropathic pain remain poorly understood. Here we use single-nucleus and spatial transcriptomic approaches in male mice to investigate spinal cellular and molecular programs associated with entrenched and treated neuropathic pain.

Highlights Clustered regularly interspaced short palindromic repeats (CRISPR) activation (CRISPRa) technology allows pooled or targeted upregulation of gene expression. This new technical capacity helps to identify genes that, when upregulated, modify cell physiology and/or disease progression. Various CRISPR activation strategies have been described, with single and combinatorial activator domains enhancing gene activation efficiency.