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Volume 16, Number 22,
Issue of November 15, 1996
pp. 7308-7317
Copyright ©1996 Society for Neuroscience
An Explanation for Reflex Blink Hyperexcitability in Parkinson's
Disease. I. Superior Colliculus
Received March 18, 1996; revised Aug. 27, 1996; accepted Aug. 31, 1996.
Michele A. Basso1,
Alice S. Powers3, and
Craig Evinger2
1 Department of Psychology, and
2 Departments of Neurobiology and Behavior and
Ophthalmology, SUNY Stony Brook, Stony Brook, New York 11794, and
3 Department of Psychology, St. John's University,
Jamaica, New York 11439
Hyperexcitable reflex blinks are a cardinal sign of Parkinson's
disease. We investigated the neural circuit through which a loss of
dopamine in the substantia nigra pars compacta (SNc) leads to increased
reflex blink excitability. Through its inhibitory inputs to the
thalamus, the basal ganglia could modulate the brainstem reflex blink
circuits via descending cortical projections. Alternatively, with its
inhibitory input to the superior colliculus, the basal ganglia could
regulate brainstem reflex blink circuits via tecto-reticular
projections. Our study demonstrated that the basal ganglia utilizes its
GABAergic input to the superior colliculus to modulate reflex blinks.
In rats with previous unilateral 6-hydroxydopamine (6-OHDA) lesions of
the dopamine neurons of the SNc, we found that microinjections of
bicuculline, a GABA antagonist, into the superior colliculus of both
alert and anesthetized rats eliminated the reflex blink
hyperexcitability associated with dopamine depletion. In normal, alert
rats, decreasing the basal ganglia output to the superior colliculus by
injecting muscimol, a GABA agonist, into the substantia nigra pars
reticulata (SNr) markedly reduced blink amplitude.
Finally, brief trains of microstimulation to the superior colliculus
reduced blink amplitude. Histological analysis revealed
that effective muscimol microinjection and microstimulation sites in
the superior colliculus overlapped the nigro-tectal projection from the
basal ganglia. These data support models of Parkinsonian symtomatology
that rely on changes in the inhibitory drive from basal ganglia output
structures. Moreover, they support a model of Parkinsonian reflex blink
hyperexcitability in which the SNr-SC target projection is
critical.
Key words:
Parkinson's disease;
blink reflex;
6-hydroxydopamine;
superior colliculus;
rats
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