Experiments were conducted in rats to determine the molecular basis of widespread chronic pain that is frequently reported in veterans of the 1991 Gulf War. Building upon a previous behavioral model, we found that increasing the frequency of exposure to anticholinesterase components (pyridostigmine bromide, chlorpyrifos) could produce a pattern of behavior consistent with an emerging myalgia. Recordings from muscle and vascular pain sensing neurons, 12 weeks post-exposure to permethrin, pyridostigmine bromide and chlorpyrifos, revealed a diminished activity level in certain KsubV ion channel proteins (KsubV7, KsubDsubR) that oppose neural excitability. Chronic exposure to Gulf war neurotoxicants also altered muscarinic receptor coupling to these KsubDsubR and KsubV7 channel proteins in a manner that reduced the capacity of neurons to resist excitation. Molecular maladaptations were prominent in muscle nociceptors.