Although maintaining the tear film on the cornea is the most important role of blinking, information about the organization and modification of cornea-evoked blinks is sparse. This study characterizes cornea-evoked blinks and their modification in urethane-anesthetized rats. Cornea-evoked blinks typically begin 16.2 ms after an electrical stimulus to the cornea and last an average of 50.2 ms. In anesthetized rats, the blink only occurs ipsilateral to the stimulus. In response to cornea stimulation, the orbicularis oculi EMG activity typically exhibits two bursts that correlate with the arrival of A delta and C-fiber inputs to the spinal trigeminal complex. In the paired-stimulus paradigm, suppression of the blink evoked by the second cornea stimulus occurs for interstimulus intervals less than 300 ms and is exclusively unilateral. Stimulation of the contralateral cornea does not affect subsequent blinks evoked from stimulation of the ipsilateral cornea. To determine whether activation of cornea-related neurons in the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) inhibits the second blink in the paired-stimulus paradigm, we examine the suppression of cornea-evoked blinks caused by microstimulation in this region. This suppression of orbicularis oculi EMG activity begins 8.3 ms after Vc/C1 stimulation. Activation of this region, however, is unlike suppression in the paired-stimulus paradigm because Vc/C1 activation bilaterally inhibits cornea-evoked blinks. Thus, activation of Vc/C1 is a previously unidentified mechanism for modulating cornea-evoked blinks.
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http://dx.doi.org/10.1007/s00221-004-2200-y | DOI Listing |
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