and (3) to recommend consensus modelling approaches to obtain reliable and robust log K OW estimates for hazard and risk assessment, accounting for different types of chemicals
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and (2) presynaptic M1 autoreceptor blockade on vagal nerve terminals , which removes negative feedback and transiently increases acetylcholine release (Kawashima et al 1988)
Collectively, our study demonstrates that SLC1A4 mutations lead to dysregulation of multiple solute carrier protein genes causing metabolic stress, excitability defects, and synaptic abnormalities, providing a molecular framework for understanding SLC1A4 -related neurodevelopmental disorders and identifying potential therapeutic targets