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Neurons responsive to mechanical stimulation of the ocular surface were recorded under barbiturate anesthesia at the trigeminal subnucleus interpolaris\/caudalis (Vi\/Vc) transition and subnucleus caudalis\/cervical cord (Vc\/C1) junction, the main terminal regions for corneal nociceptors. Two days after LPS, Vc\/C1 units had reduced responses to histamine, nicotine, and CO<jats:sub>2<\/jats:sub>gas applied to the ocular surface, whereas unit responses were increased 7 days after LPS. Those units with convergent cutaneous receptive fields at Vc\/C1 were enlarged 7 days after LPS. Units at the Vi\/Vc transition also had reduced responses to histamine and CO<jats:sub>2<\/jats:sub>2 days after LPS but no enhancement was seen at 7 days. Tear volume evoked by CO<jats:sub>2<\/jats:sub>was reduced 2 days after LPS and returned toward control values by 7 days, whereas CO<jats:sub>2<\/jats:sub>-evoked eye blinks were normal at 2 days and increased 7 days after LPS. These results indicate that a single exposure to endotoxin causes long-term changes in the excitability of second-order neurons responsive to noxious ocular stimulation. 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