MIDBRAIN 6-HYDROXYDOPAMINE LESIONS MODULATE BLINK REFLEX EXCITABILITY

The blink reflex abnormalities present in the 6 hydroxydopamine (6-OHD A) lesioned rat model of parkinsonism mimicked those of the human with Parkinson's disease. In alert rats, we monitored the long and short l atency components of the orbicularis oculi electromyographic (OOemg) r esponse evoked by electrical stimulation of the supraorbital branch of the trigeminal nerve (SO). Two paradigms, habituation and double puls e, provided a measure of blink reflex excitability. In normal rats, re peated stimulation of the SO produced habituation of the R2 component of the blink. In the double pulse paradigm, presentation of two identi cal SO stimuli resulted in a reduced or suppressed OOemg response to t he second stimulus relative to the first. In rats with complete, unila teral lesions of midbrain dopamine neurons, repeated SO stimulation pr oduced facilitation rather than habituation of the R2 component of the blink reflex. This facilitation occurred only with the eyelid contral ateral to the lesion. In the double pulse paradigm, the lesioned rats showed increased excitability rather than suppression. This effect occ urred bilaterally, although the increased excitability was strongest c ontralateral to the lesion. Rats with partial lesions of midbrain dopa mine neurons exhibited qualitatively similar, but less pronounced blin k reflex abnormalities. The R1 component of the blink reflex was unaff ected by either the complete or partial lesions. Thus, modification of the blink reflex by 6-OHDA lesions provides a reproducible parkinsoni an-like symptom which is amenable to investigations of increases in re flex excitability.