Midbrain 6-hydroxydopamine lesions modulate blink reflex excitability

Midbrain 6-hydroxydopamine lesions modulate blink reflex excitability 221 94 94 1 1 Michele A. Basso Robert E. Strecker Craig Evinger Department of Psychology SUNY at Stony Brook 11794-2500 Stony Brook NY USA Department of Psychiatry and Behavioral Sciences SUNY at Stony Brook 11794-2500 Stony Brook NY USA Department of Neurobiology Behavior and Ophthalmology SUNY at Stony Brook 11794-2500 Stony Brook NY USA Abstract The blink reflex abnormalities present in the 6 hydroxydopamine (6-OHDA) lesioned rat model of parkinsonism mimicked those of the human with Parkinon's disease. In alert rats, we monitored the long and short latency components of the orbicularis oculi electromyographic (OOemg) response evoked by electrical stimulation of the supraorbital branch of the trigeminal nerve (SO). Two paradigms, habituation and double pulse, provided a measure of blink reflex excitability. In normal rats, repeated stimulation of the SO produced habituation of the R2 component of the blink. In the double pulse paradigm, presentation of two identical SO stimuli resulted in a reduced or suppressed OOemg response to the second stimulus relative to the first. In rats with complete, unilateral lesions of midbrain dopamine neurons, repeated SO stimulation produced facilitation rather than habituation of the R2 component of the blink reflex. This facilitation occurred only with the eyelid contralateral to the lesion. In the double pulse paradigm, the lesioned rats showed increased excitability rather than suppression. This effect occurred bilaterally, although the increased excitability was strongest contralateral to the lesion. Rats with partial lesions of midbrain dopamine neurons exhibited qualitatively similar, but less pronounced blink reflex abnormalities. The R1 component of the blink reflex was unaffected by either the complete or partial lesions. Thus, modification of the blink reflex by 6-OHDA lesions provides a reproducible parkinsonian-like symptom which is amenable to investigations of increases in reflex excitability. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Brain Research Springer Journals

Midbrain 6-hydroxydopamine lesions modulate blink reflex excitability

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Publisher
Springer Journals
Copyright
Copyright © 1993 by Springer-Verlag
Subject
Biomedicine; Neurosciences; Neurology
ISSN
0014-4819
eISSN
1432-1106
D.O.I.
10.1007/BF00230472
Publisher site
See Article on Publisher Site

Abstract

221 94 94 1 1 Michele A. Basso Robert E. Strecker Craig Evinger Department of Psychology SUNY at Stony Brook 11794-2500 Stony Brook NY USA Department of Psychiatry and Behavioral Sciences SUNY at Stony Brook 11794-2500 Stony Brook NY USA Department of Neurobiology Behavior and Ophthalmology SUNY at Stony Brook 11794-2500 Stony Brook NY USA Abstract The blink reflex abnormalities present in the 6 hydroxydopamine (6-OHDA) lesioned rat model of parkinsonism mimicked those of the human with Parkinon's disease. In alert rats, we monitored the long and short latency components of the orbicularis oculi electromyographic (OOemg) response evoked by electrical stimulation of the supraorbital branch of the trigeminal nerve (SO). Two paradigms, habituation and double pulse, provided a measure of blink reflex excitability. In normal rats, repeated stimulation of the SO produced habituation of the R2 component of the blink. In the double pulse paradigm, presentation of two identical SO stimuli resulted in a reduced or suppressed OOemg response to the second stimulus relative to the first. In rats with complete, unilateral lesions of midbrain dopamine neurons, repeated SO stimulation produced facilitation rather than habituation of the R2 component of the blink reflex. This facilitation occurred only with the eyelid contralateral to the lesion. In the double pulse paradigm, the lesioned rats showed increased excitability rather than suppression. This effect occurred bilaterally, although the increased excitability was strongest contralateral to the lesion. Rats with partial lesions of midbrain dopamine neurons exhibited qualitatively similar, but less pronounced blink reflex abnormalities. The R1 component of the blink reflex was unaffected by either the complete or partial lesions. Thus, modification of the blink reflex by 6-OHDA lesions provides a reproducible parkinsonian-like symptom which is amenable to investigations of increases in reflex excitability.

Journal

Experimental Brain ResearchSpringer Journals

Published: May 1, 1993

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