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Published on: September 21, 2015
Endotoxin-induced uveitis causes long-term changes in trigeminal subnucleus caudalis neurons
David A Bereiter1, Keiichiro Okamoto, Akimasa Tashiro
1Department of Surgery, Brown Medical School, Rhode Island Hospital, Providence, 02903, USA. David_Bereiter@brown.edu
Journal of Neurophysiology
|July 29, 2005
Summary
Endotoxin-induced uveitis (EIU) alters central neural responses to ocular stimuli. Inflammation changes neuronal excitability, affecting pain perception and reflexes like eye blinking.
Area of Science:
- Neuroscience
- Ophthalmology
- Pain Research
Background:
- Endotoxin-induced uveitis (EIU) models human ocular inflammation.
- Central neural effects of anterior eye inflammation are poorly understood.
- EIU involves inflammatory responses affecting the eye.
Purpose of the Study:
- Investigate central neural changes in response to anterior eye inflammation.
- Examine the effects of endotoxin on trigeminal neurons processing ocular pain.
- Determine long-term alterations in neuronal excitability following EIU.
Main Methods:
- Induced EIU in male rats using lipopolysaccharide (LPS).
- Recorded neuronal activity in the trigeminal nucleus (Vi/Vc and Vc/C1).
- Stimulated ocular surface with mechanical, chemical (histamine, nicotine, CO2), and thermal stimuli.
Main Results:
- EIU reduced neuronal responses to stimuli 2 days post-LPS, with increased responses at 7 days.
- Convergent cutaneous receptive fields enlarged in Vc/C1 units 7 days post-LPS.
- EIU differentially affected tear volume and CO2-evoked eye blinks.
Conclusions:
- A single LPS exposure induces lasting changes in ocular pain-sensing neurons.
- EIU alters the excitability of second-order neurons in the trigeminal system.
- Ocular-sensitive neurons mediate distinct aspects of pain during intraocular inflammation.
