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0 reviewsSUMMARYGlioblastoma (GBM), the most aggressive primary brain tumor, is shaped by its integration into neural networks. While glutamatergic input is linked to tumor progression, the broader architecture and function ofneuron-glioma connectomes remain unclear. Using monosynaptic rabies tracing, we map brain-wide neuralinput to patient-derived xenografts and reveal a consistent organizational logic: local inputs are primarily glutamatergic, while long-range connections exhibit diverse neurotransmitter profiles, with basal forebraincholinergic projections emerging as a conserved input across sites. Functionally, presynaptic acetylcholinerelease promotes GBM progression through muscarinic receptor CHRM3 in a circuit-specific manner. Mechanistically, glutamatergic and cholinergic signals converge to enhance glioma calcium transients but divergein temporal transcriptional control, with their dual blockade producing additive anti-tumor effects. Therapeutically, the anticholinergic drug scopolamine attenuates glioma growth, whereas the acetylcholinesterase inhibitor donepezil exacerbates disease. These findings reveal the complexity of neuron-glioma connectivity,highlighting long-range neuromodulatory pathways as promising therapeutic targets in GBM.
