AN EXPLANATION FOR REFLEX BLINK HYPEREXCITABILITY IN PARKINSONS-DISEASE .2. NUCLEUS RAPHE MAGNUS

Hyperexcitable reflex blinks are a cardinal sign of Parkinson's diseas e. The first step in the circuit linking the basal ganglia and brainst em reflex blink circuits is the inhibitory nigrostriatal pathway (Bass o et al., 1996). The current study reports the circuits linking the su perior colliculus (SC) to trigeminal reflex blink circuits. Microstimu lation of the deep layers of the SC suppresses subsequent reflex blink s at a latency of 5.4 msec. This microstimulation does not activate pe riaqueductal gray antinociceptive circuits. The brainstem structure li nking SC to reflex blink circuits must suppress reflex blinks at a sho rter latency than the SC and produce the same effect on reflex blink c ircuits 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 wit h a latency of 4.4 msec. Like SC stimulation, NRM microstimulation red uces the responsiveness of the spinal trigeminal nucleus. Finally, blo cking the receptors for the NRM transmitter serotonin eliminates SG mo dulation of reflex blinks, and muscimol inactivation of the NRM transi ently prevents SC modulation of reflex blinks. Thus, the circuit throu gh which the basal ganglia modulates reflex blinking is (1) the substa ntia nigra pars reticulata inhibits SC neurons, (2) the SC excites ton ically active NRM neurons, and (3) NRM neurons inhibit spinal trigemin al neurons involved in reflex blink circuits.