Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
European Journal of Neuroscience. 2005-11-01; 22(9): 2283-2294
DOI: 10.1111/j.1460-9568.2005.04402.x
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1. Eur J Neurosci. 2005 Nov;22(9):2283-94. doi: 10.1111/j.1460-9568.2005.04402.x.
Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the
subthalamic nucleus and substantia nigra in the rat.
Breit S(1), Lessmann L, Benazzouz A, Schulz JB.
Author information:
(1)Neurodegeneration Department, Center of Neurology and Hertie Institute for
Clinical Brain Research, University of Tübingen, Hoppe-Seyler-Strasse 3, 72076
Tübingen, Germany.
Recent data suggest a role for the pedunculopontine nucleus (PPN) in the
pathophysiology of Parkinson’s disease. Although there is anatomical evidence
that the PPN and the basal ganglia are reciprocally connected, the functional
importance of these connections is poorly understood. Lesioning of the PPN was
shown to induce akinesia in primates, whereas in the 6-hydroxydopamine rat model
the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion
and lesioning of the PPN were shown to induce akinesia and parkinsonism, the
present study was performed in order to investigate the changes in neuronal
activity of the subthalamic nucleus (STN) and the substantia nigra pars
reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after
unilateral 6-hydroxydopamine lesioning of the substantia nigra pars compacta
(SNc). The firing rate of STN neurones significantly increased from 10.2 +/- 6.2
(mean +/- SD) to 14.6 +/- 11.7 spikes/s after lesion of the PPN and to 18.6 +/-
14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly
increased from 19.6 +/- 10.5 to 28.7 +/- 13.4 spikes/s after PPN lesioning and
to 23.5 +/- 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased
the number of spontaneously firing dopaminergic SNc cells, while having no
effect on their firing rate. The results of our study show that lesion of the
PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by
lesion of the SNc. Moreover, the decreased activity of SNc cells observed after
PPN lesion might be at the origin of activity changes in the STN and SNr.
DOI: 10.1111/j.1460-9568.2005.04402.x
PMID: 16262666 [Indexed for MEDLINE]