The three-neuron corneal reflex circuit and modulation of second-order corneal responsive neurons.
Neurons located in the border region between the interpolaris and caudalis subdivisions of the spinal trigeminal nucleus (Vi/Vc) are second order neurons of the corneal reflex, receiving corneal afferents and projecting to the lid closing, orbicularis oculi (OO) motoneurons. Recordings of Vi/Vc neurons identified by antidromic activation from stimulation of the facial nucleus and non-identified Vi/Vc neurons reveal two neuron types, phasic and tonic. Corneal stimulation elicits Adelta latency action potentials that occur early enough to initiate OO contraction and C-fiber latency action potentials that can modulate the end of the blink in phasic Vi/Vc neurons. Tonic Vi/Vc neurons exhibit a constant irregular, low frequency discharge as well as the cornea-evoked activity exhibited by phasic neurons. For both phasic and tonic neurons, blink amplitude increases with the total number of spikes evoked by the corneal stimulus. Peak firing frequency predicts peak orbicularis oculi EMG activity. Paradigms that suppress cornea-evoked blinks differentially affect Vi/Vc neurons. Microstimulation of the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) significantly reduces the number of spikes evoked by corneal stimulation and suppresses blink amplitude. In the paired stimulus paradigm, a blink evoked by a corneal stimulus 150 ms after an identical corneal stimulus is significantly smaller than the blink elicited by the first stimulus. Vi/Vc neuron discharge, however, is slightly larger for the second blink. Our data indicate that second-order Vi/Vc neurons do not determine the specific pattern of OO muscle activity; rather Vi/Vc neurons initiate OO motoneuron discharge and program the activity of another circuit that generates the late phase of the blink. The Vc/C1 suppression of Vi/Vc neurons suggests that the Vc/C1 region provides an "internal model" of the intended blink.
Henriquez
Victor M
VM
Laryngeal and Speech Section, Medical Neurology Branch, NINDS, Bethesda, MD 20892-1416, USA.
Evinger
Craig
C
D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D001767:Blinking / Q000502:physiology*; D003315:Cornea / Q000294:innervation / Q000502:physiology*; D004525:Efferent Pathways / Q000502:physiology*; D004576:Electromyography; D005143:Eyelids / Q000294:innervation / Q000502:physiology; D005152:Facial Muscles / Q000294:innervation / Q000502:physiology; D005154:Facial Nerve / Q000502:physiology; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000502:physiology; D014276:Trigeminal Nerve / Q000502:physiology; D014278:Trigeminal Nuclei / Q000502:physiology