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Effects of apomorphine on globus pallidus neurons in parkinsonian patients

Effects of apomorphine on globus pallidus neurons in parkinsonian patients Current hypotheses of basal ganglia dysfunction in Parkinson's disease (PD) propose that neuronal hypoactivity in the globus pallidus externus (GPe), and hyperactivity in the output nuclei and the external and internal portions of the globus pallidus internus (GPi, e and GPi, i, respectively), result in the cardinal symptoms of PD. To test this theory, the nonselective D1‐ and D2‐dopamine receptor agonist apomorphine (30–100 μg/kg SC) was administered to 14 levodoparesponsive PD patients who were off medication (“of” state) while recording neurons in GP. For 15 neurons that were continuously monitored, apomorphine was found to increase the firing rate of 3 neurons in GPe, and decrease the rate of 12 in GPi. The mean firing rates of many different neurons were determined before (n = 285) and at various intervals after (n = 184) the injection of the drug. The mean rates before apomorphine were as follows: GPe, 45 Hz (SD 15, n = 85); GPi, e, 67 Hz (SD 14, n = 125); and GPi, i, 85 Hz (SD 19, n = 75). At 25 to 35 minutes after APO, the rate of GPe neurons had increased to 72 Hz (SD 18, n = 7), the rate of GPi, e neurons had decreased to 39 Hz (SD 15, n = 15), and in GPi, i the rate decreased to 34 Hz (SD 22, n = 18). Eighty minutes after apomorphine administration, the mean firing rates returned to preadministration values. This study supports current models of basal ganglia dysfunction in PD and suggests that the thereapeutic effect of apomorphine results from a normalization of the imbalance of neuronal activity in the direct and indirect pathways. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Effects of apomorphine on globus pallidus neurons in parkinsonian patients

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References (42)

Publisher
Wiley
Copyright
Copyright © 1997 the American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410420513
pmid
9392576
Publisher site
See Article on Publisher Site

Abstract

Current hypotheses of basal ganglia dysfunction in Parkinson's disease (PD) propose that neuronal hypoactivity in the globus pallidus externus (GPe), and hyperactivity in the output nuclei and the external and internal portions of the globus pallidus internus (GPi, e and GPi, i, respectively), result in the cardinal symptoms of PD. To test this theory, the nonselective D1‐ and D2‐dopamine receptor agonist apomorphine (30–100 μg/kg SC) was administered to 14 levodoparesponsive PD patients who were off medication (“of” state) while recording neurons in GP. For 15 neurons that were continuously monitored, apomorphine was found to increase the firing rate of 3 neurons in GPe, and decrease the rate of 12 in GPi. The mean firing rates of many different neurons were determined before (n = 285) and at various intervals after (n = 184) the injection of the drug. The mean rates before apomorphine were as follows: GPe, 45 Hz (SD 15, n = 85); GPi, e, 67 Hz (SD 14, n = 125); and GPi, i, 85 Hz (SD 19, n = 75). At 25 to 35 minutes after APO, the rate of GPe neurons had increased to 72 Hz (SD 18, n = 7), the rate of GPi, e neurons had decreased to 39 Hz (SD 15, n = 15), and in GPi, i the rate decreased to 34 Hz (SD 22, n = 18). Eighty minutes after apomorphine administration, the mean firing rates returned to preadministration values. This study supports current models of basal ganglia dysfunction in PD and suggests that the thereapeutic effect of apomorphine results from a normalization of the imbalance of neuronal activity in the direct and indirect pathways.

Journal

Annals of Neurology – Wiley

Published: Nov 1, 1997

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