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Volume 16, Number 22, Issue of November 15, 1996 pp. 7318-7330
Copyright ©1996 Society for NeuroscienceAn Explanation for Reflex Blink Hyperexcitability in Parkinson's Disease. II. Nucleus Raphe Magnus
Received March 18, 1996; revised July 31, 1996; accepted Aug. 27, 1996.
Michele A. Basso1 and Craig Evinger2 1 Department of Psychology, and 2 Departments of Neurobiology and Behavior and Ophthalmology, SUNY Stony Brook, Stony Brook, New York 11794-5230
Hyperexcitable reflex blinks are a cardinal sign of Parkinson's disease. The first step in the circuit linking the basal ganglia and brainstem reflex blink circuits is the inhibitory nigrostriatal pathway (). The current study reports the circuits linking the superior colliculus (SC) to trigeminal reflex blink circuits. Microstimulation of the deep layers of the SC suppresses subsequent reflex blinks at a latency of 5.4 msec. This microstimulation does not activate periaqueductal gray antinociceptive circuits. The brainstem structure linking SC to reflex blink circuits must suppress reflex blinks at a shorter latency than the SC and produce the same effect on reflex blink circuits as SC stimulation, and removal of the structure must block SC modulation of reflex blinks. Only the nucleus raphe magnus (NRM) meets these requirements. NRM microstimulation suppresses reflex blinks with a latency of 4.4 msec. Like SC stimulation, NRM microstimulation reduces the responsiveness of the spinal trigeminal nucleus. Finally, blocking the receptors for the NRM transmitter serotonin eliminates SC modulation of reflex blinks, and muscimol inactivation of the NRM transiently prevents SC modulation of reflex blinks. Thus, the circuit through which the basal ganglia modulates reflex blinking is (1) the substantia nigra pars reticulata inhibits SC neurons, (2) the SC excites tonically active NRM neurons, and (3) NRM neurons inhibit spinal trigeminal neurons involved in reflex blink circuits.
Key words: Parkinson's disease; blink reflex; superior colliculus; trigeminal complex; rats
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