A novel class of neurons at the trigeminal subnucleus interpolaris/caudalis transition region monitors ocular surface fluid status and modulates tear production.
Reflex tears are produced by many conditions, one of which is drying of the ocular surface. Although peripheral neural control of the lacrimal gland is well established, the afferent pathways and properties of central premotor neurons necessary for this reflex are not known. Male rats under barbiturate anesthesia were used to determine whether neurons at the ventral trigeminal subnucleus interpolaris- caudalis (Vi/Vc) transition or the trigeminal subnucleus caudalis-cervical cord (Vc/C1) junction region in the lower brainstem were necessary for tears evoked by noxious chemical stimulation (CO2 pulses) or drying of the ocular surface. Both the Vi/Vc transition and Vc/C1 junction regions receive a dense direct projection from corneal nociceptors. Synaptic blockade of the Vi/Vc transition, but not the Vc/C1 junction, by the GABA(A) receptor agonist muscimol inhibited CO2-evoked tears. Glutamate excitation of the Vi/Vc transition, but not the Vc/C1 junction, increased tear volume. Single units recorded at the Vi/Vc transition, but not at the Vc/C1 junction, were inhibited by wetting and excited by drying the ocular surface. Nearly all moisture-sensitive Vi/Vc units displayed an initial inhibitory phase to noxious concentrations of CO2 followed by delayed excitation and displayed an inhibitory surround receptive field from periorbital facial skin. Drying of the ocular surface produced many Fos-positive neurons at the Vi/Vc transition, but not at the Vc/C1 junction. This is the first report of a unique class of moisture-sensitive neurons that exist only at the ventral Vi/Vc transition, and not at more caudal portions of Vc, that may underlie fluid homeostasis of the ocular surface.
Hirata
Harumitsu
H
Department of Surgery, Brown Medical School, Rhode Island Hospital, Providence, Rhode Island 02903-4970, USA.
Okamoto
Keiichiro
K
Tashiro
Akimasa
A
Bereiter
David A
DA
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D003228:Conjunctiva / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D003315:Cornea / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018755:GABA Agonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology; D007765:Lacrimal Apparatus / Q000294:innervation* / Q000378:metabolism / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000145:classification* / Q000187:drug effects / Q000502:physiology*; D009883:Ophthalmic Solutions / Q000494:pharmacology; D010812:Physical Stimulation / Q000379:methods; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000502:physiology; D013268:Stimulation, Chemical; D013666:Tears / Q000378:metabolism*; D014279:Trigeminal Nucleus, Spinal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D009883:Ophthalmic Solutions; D016760:Proto-Oncogene Proteins c-fos; D002245:Carbon Dioxide; D018698:Glutamic Acid