Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
Identifieur interne : 002130 ( Istex/Corpus ); précédent : 002129; suivant : 002131Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
Auteurs : S. Breit ; L. Lessmann ; A. Benazzouz ; J. B. SchulzSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-11.
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- KwdEn :
Abstract
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.
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DOI: 10.1111/j.1460-9568.2005.04402.x
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<front><div type="abstract" xml:lang="en">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.</div>
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<abstract>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.</abstract>
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<refBibs><json:item><author><json:item><name>E.E. Benarroch</name>
</json:item>
<json:item><name>A.M. Schmeichel</name>
</json:item>
<json:item><name>J.E. Parisi</name>
</json:item>
</author>
<host><volume>59</volume>
<pages><last>946</last>
<first>944</first>
</pages>
<author></author>
<title>Neurology</title>
</host>
<title>Depletion of mesopontine cholinergic and sparing of raphe neurons in multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>H. Bergman</name>
</json:item>
<json:item><name>T. Wichmann</name>
</json:item>
<json:item><name>B. Karmon</name>
</json:item>
<json:item><name>M.R. DeLong</name>
</json:item>
</author>
<host><volume>72</volume>
<pages><last>520</last>
<first>507</first>
</pages>
<author></author>
<title>J. Neurophysiol.</title>
</host>
<title>The primate subthalamic nucleus. II. Neuronal activity in the MPTP model of parkinsonism</title>
</json:item>
<json:item><author><json:item><name>M.D. Bevan</name>
</json:item>
<json:item><name>J.P. Bolam</name>
</json:item>
</author>
<host><volume>15</volume>
<pages><last>7120</last>
<first>7105</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Cholinergic, GABAergic, and glutamate‐enriched inputs from the mesopontine tegmentum to the subthalamic nucleus in the rat</title>
</json:item>
<json:item><author><json:item><name>S. Breit</name>
</json:item>
<json:item><name>R. Bouali‐Benazzouz</name>
</json:item>
<json:item><name>A.L. Benabid</name>
</json:item>
<json:item><name>A. Benazzouz</name>
</json:item>
</author>
<host><volume>14</volume>
<pages><last>1842</last>
<first>1833</first>
</pages>
<author></author>
<title>Eur. J. Neurosci.</title>
</host>
<title>Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nu cleus in the rat</title>
</json:item>
<json:item><author><json:item><name>B.S. Bunney</name>
</json:item>
<json:item><name>A.A. Grace</name>
</json:item>
</author>
<host><volume>23</volume>
<pages><last>1727</last>
<first>1715</first>
</pages>
<author></author>
<title>Life Sci.</title>
</host>
<title>Acute and chronic haloperidol treatment: comparison of effects on nigral dopaminergic cell activity</title>
</json:item>
<json:item><author><json:item><name>A. Capozzo</name>
</json:item>
<json:item><name>T. Florio</name>
</json:item>
<json:item><name>R. Cellini</name>
</json:item>
<json:item><name>U. Moriconi</name>
</json:item>
<json:item><name>E. Scarnati</name>
</json:item>
</author>
<host><volume>110</volume>
<pages><last>747</last>
<first>733</first>
</pages>
<author></author>
<title>J. Neural Transm.</title>
</host>
<title>The pedunculopontine nucleus projection to the parafascicular nucleus of the thalamus: an electrophysiological investigation in the rat</title>
</json:item>
<json:item><author><json:item><name>J.D. Carlson</name>
</json:item>
<json:item><name>R.D. Pearlstein</name>
</json:item>
<json:item><name>J. Buchholz</name>
</json:item>
<json:item><name>R.P. Iacono</name>
</json:item>
<json:item><name>G. Maeda</name>
</json:item>
</author>
<host><volume>828</volume>
<pages><last>19</last>
<first>12</first>
</pages>
<author></author>
<title>Brain Res.</title>
</host>
<title>Regional metabolic changes in the pedunculopontine nucleus of unilateral 6‐hydroxydopamine Parkinson's model rats</title>
</json:item>
<json:item><author><json:item><name>A. Charara</name>
</json:item>
<json:item><name>Y. Smith</name>
</json:item>
<json:item><name>A. Parent</name>
</json:item>
</author>
<host><volume>364</volume>
<pages><last>266</last>
<first>254</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Glutamatergic inputs from the pedunculopontine nucleus to midbrain dopaminergic neurons in primates: Phaseolus vulgaris‐leucoagglutinin anterograde labeling combined with postembedding glutamate and GABA immunohistochemistry</title>
</json:item>
<json:item><author><json:item><name>L.A. Chiodo</name>
</json:item>
<json:item><name>B.S. Bunney</name>
</json:item>
</author>
<host><volume>3</volume>
<pages><last>1619</last>
<first>1607</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Typical and atypical neuroleptics: differential effects of chronic administration on the activity of A9 and A10 midbrain dopaminergic neurons</title>
</json:item>
<json:item><author><json:item><name>N.P. Clarke</name>
</json:item>
<json:item><name>M.D. Bevan</name>
</json:item>
<json:item><name>C. Cozzari</name>
</json:item>
<json:item><name>B.K. Hartman</name>
</json:item>
<json:item><name>J.P. Bolam</name>
</json:item>
</author>
<host><volume>81</volume>
<pages><last>385</last>
<first>371</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Glutamate‐enriched cholinergic synaptic terminals in the entopeduncular nucleus and subthalamic nucleus of the rat</title>
</json:item>
<json:item><author><json:item><name>S. Datta</name>
</json:item>
<json:item><name>E.E. Spoley</name>
</json:item>
<json:item><name>V.K. Mavanji</name>
</json:item>
<json:item><name>E.H. Patterson</name>
</json:item>
</author>
<host><volume>114</volume>
<pages><last>164</last>
<first>157</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>A novel role of pedunculopontine tegmental kainate receptors: a mechanism of rapid eye movement sleep generation in the rat</title>
</json:item>
<json:item><author><json:item><name>J. Feger</name>
</json:item>
<json:item><name>M. Bevan</name>
</json:item>
<json:item><name>A.R. Crossman</name>
</json:item>
</author>
<host><volume>60</volume>
<pages><last>132</last>
<first>125</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>The projections from the parafascicular thalamic nucleus to the subthalamic nucleus and the striatum arise from separate neuronal populations: a comparison with the corticostriatal and corticosubthalamic efferents in a retrograde fluorescent double‐labelling study</title>
</json:item>
<json:item><author><json:item><name>M. Filion</name>
</json:item>
<json:item><name>L. Tremblay</name>
</json:item>
</author>
<host><volume>547</volume>
<pages><last>151</last>
<first>142</first>
</pages>
<author></author>
<title>Brain Res.</title>
</host>
<title>Abnormal spontaneous activity of globus pallidus neurons in monkeys with MPTP‐induced parkinsonism</title>
</json:item>
<json:item><author><json:item><name>S.B. Floresco</name>
</json:item>
<json:item><name>C.L. Todd</name>
</json:item>
<json:item><name>A.A. Grace</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>4922</last>
<first>4915</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Glutamatergic afferents from the hippocampus to the nucleus accumbens regulate activity of ventral tegmental area dopamine neurons</title>
</json:item>
<json:item><author><json:item><name>G.L. Forster</name>
</json:item>
<json:item><name>C.D. Blaha</name>
</json:item>
</author>
<host><volume>17</volume>
<pages><last>762</last>
<first>751</first>
</pages>
<author></author>
<title>Eur. J. Neurosci.</title>
</host>
<title>Pedunculopontine tegmental stimulation evokes striatal dopamine efflux by activation of acetylcholine and glutamate receptors in the midbrain and pons of the rat</title>
</json:item>
<json:item><author><json:item><name>E. Garcia‐Rill</name>
</json:item>
</author>
<host><volume>36</volume>
<pages><last>389</last>
<first>363</first>
</pages>
<author></author>
<title>Prog. Neurobiol.</title>
</host>
<title>The pedunculopontine nucleus</title>
</json:item>
<json:item><author><json:item><name>E. Garcia‐Rill</name>
</json:item>
<json:item><name>C.R. Houser</name>
</json:item>
<json:item><name>R.D. Skinner</name>
</json:item>
<json:item><name>W. Smith</name>
</json:item>
<json:item><name>D.J. Woodward</name>
</json:item>
</author>
<host><volume>18</volume>
<pages><last>738</last>
<first>731</first>
</pages>
<author></author>
<title>Brain Res. Bull.</title>
</host>
<title>Locomotion‐inducing sites in the vicinity of the pedunculopontine nucleus</title>
</json:item>
<json:item><author><json:item><name>E. Garcia‐Rill</name>
</json:item>
<json:item><name>Y. Homma</name>
</json:item>
<json:item><name>R.D. Skinner</name>
</json:item>
</author>
<host><volume>143</volume>
<pages><last>290</last>
<first>283</first>
</pages>
<author></author>
<title>Prog. Brain Res.</title>
</host>
<title>Arousal mechanisms related to posture and locomotion: 1. Descending modulation</title>
</json:item>
<json:item><author><json:item><name>A.A. Grace</name>
</json:item>
<json:item><name>B.S. Bunney</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>315</last>
<first>301</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Intracellular and extracellular electrophysiology of nigral dopaminergic neurons — 1. Identification and characterization</title>
</json:item>
<json:item><author><json:item><name>A.R. Granata</name>
</json:item>
<json:item><name>S.T. Kitai</name>
</json:item>
</author>
<host><volume>86</volume>
<pages><last>466</last>
<first>459</first>
</pages>
<author></author>
<title>Exp. Brain Res.</title>
</host>
<title>Inhibitory substantia nigra inputs to the pedunculopontine neurons</title>
</json:item>
<json:item><author><json:item><name>I. Grofova</name>
</json:item>
<json:item><name>M. Zhou</name>
</json:item>
</author>
<host><volume>395</volume>
<pages><last>379</last>
<first>359</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Nigral innervation of cholinergic and glutamatergic cells in the rat mesopontine tegmentum: light and electron microscopic anterograde tracing and immunohistochemical studies</title>
</json:item>
<json:item><author><json:item><name>C. Hammond</name>
</json:item>
<json:item><name>B. Rouzaire‐Dubois</name>
</json:item>
<json:item><name>J. Feger</name>
</json:item>
<json:item><name>A. Jackson</name>
</json:item>
<json:item><name>A.R. Crossman</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>52</last>
<first>41</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Anatomical and electrophysiological studies on the reciprocal projections between the subthalamic nucleus and nucleus tegmenti pedunculopontinus in the rat</title>
</json:item>
<json:item><author><json:item><name>O.K. Hassani</name>
</json:item>
<json:item><name>M. Mouroux</name>
</json:item>
<json:item><name>J. Feger</name>
</json:item>
</author>
<host><volume>72</volume>
<pages><last>115</last>
<first>105</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Increased subthalamic neuronal activity after nigral dopaminergic lesion independent of disinhibition via the globus pallidus</title>
</json:item>
<json:item><author><json:item><name>E.C. Hirsch</name>
</json:item>
<json:item><name>A.M. Graybiel</name>
</json:item>
<json:item><name>C. Duyckaerts</name>
</json:item>
<json:item><name>F. Javoy‐Agid</name>
</json:item>
</author>
<host><volume>84</volume>
<pages><last>5980</last>
<first>5976</first>
</pages>
<author></author>
<title>Proc. Natl Acad. Sci. U.S.A.</title>
</host>
<title>Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy</title>
</json:item>
<json:item><author><json:item><name>W.D. Hutchison</name>
</json:item>
<json:item><name>R.J. Allan</name>
</json:item>
<json:item><name>H. Opitz</name>
</json:item>
<json:item><name>R. Levy</name>
</json:item>
<json:item><name>J.O. Dostrovsky</name>
</json:item>
<json:item><name>A.E. Lang</name>
</json:item>
<json:item><name>A.M. Lozano</name>
</json:item>
</author>
<host><volume>44</volume>
<pages><last>628</last>
<first>622</first>
</pages>
<author></author>
<title>Ann. Neurol.</title>
</host>
<title>Neurophysiological identification of the subthalamic nucleus in surgery for Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>W.L. Inglis</name>
</json:item>
<json:item><name>P. Winn</name>
</json:item>
</author>
<host><volume>47</volume>
<pages><last>29</last>
<first>1</first>
</pages>
<author></author>
<title>Prog. Neurobiol.</title>
</host>
<title>The pedunculopontine tegmental nucleus: where the striatum meets the reticular formation</title>
</json:item>
<json:item><author><json:item><name>W.L. Inglis</name>
</json:item>
<json:item><name>L.F. Allen</name>
</json:item>
<json:item><name>R.B. Whitelaw</name>
</json:item>
<json:item><name>M.P. Latimer</name>
</json:item>
<json:item><name>H.M. Brace</name>
</json:item>
<json:item><name>P. Winn</name>
</json:item>
</author>
<host><volume>58</volume>
<pages><last>833</last>
<first>817</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>An investigation into the role of the pedunculopontine tegmental nucleus in the mediation of locomotion and orofacial stereotypy induced by d‐amphetamine and apomorphine in the rat</title>
</json:item>
<json:item><author><json:item><name>T.A. Jenkins</name>
</json:item>
<json:item><name>M.P. Latimer</name>
</json:item>
<json:item><name>H.L. Alderson</name>
</json:item>
<json:item><name>P. Winn</name>
</json:item>
</author>
<host><volume>322</volume>
<pages><last>48</last>
<first>45</first>
</pages>
<author></author>
<title>Neurosci. Lett.</title>
</host>
<title>Determination of acetylcholine and dopamine content in thalamus and striatum after excitotoxic lesions of the pedunculopontine tegmental nucleus in rats</title>
</json:item>
<json:item><author><json:item><name>M.F. Jeon</name>
</json:item>
<json:item><name>Y. Ha</name>
</json:item>
<json:item><name>Y.H. Cho</name>
</json:item>
<json:item><name>B.H. Lee</name>
</json:item>
<json:item><name>Y.G. Park</name>
</json:item>
<json:item><name>J.W. Chang</name>
</json:item>
</author>
<host><volume>99</volume>
<pages><last>767</last>
<first>762</first>
</pages>
<author></author>
<title>J. Neurosurg.</title>
</host>
<title>Effect of ipsilateral subthalamic nucleus lesioning in a rat parkinsonian model: study of behavior correlated with neuronal activity in the pedunculopontine nucleus</title>
</json:item>
<json:item><author><json:item><name>Y. Kaneoke</name>
</json:item>
<json:item><name>J.L. Vitek</name>
</json:item>
</author>
<host><volume>68</volume>
<pages><last>223</last>
<first>211</first>
</pages>
<author></author>
<title>J. Neurosci. Meth.</title>
</host>
<title>Burst and oscillation as disparate neuronal properties</title>
</json:item>
<json:item><author><json:item><name>S. Kasashima</name>
</json:item>
<json:item><name>Y. Oda</name>
</json:item>
</author>
<host><volume>105</volume>
<pages><last>124</last>
<first>117</first>
</pages>
<author></author>
<title>Acta Neuropathol. (Berl.)</title>
</host>
<title>Cholinergic neuronal loss in the basal forebrain and mesopontine tegmentum of progressive supranuclear palsy and corticobasal degeneration</title>
</json:item>
<json:item><author><json:item><name>S.T. Kitai</name>
</json:item>
<json:item><name>P.D. Shepard</name>
</json:item>
<json:item><name>J.C. Callaway</name>
</json:item>
<json:item><name>R. Scroggs</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>697</last>
<first>690</first>
</pages>
<author></author>
<title>Curr. Opin. Neurobiol.</title>
</host>
<title>Afferent modulation of dopamine neuron firing patterns</title>
</json:item>
<json:item><author><json:item><name>W.R. Klemm</name>
</json:item>
</author>
<host><volume>65</volume>
<pages><last>471</last>
<first>453</first>
</pages>
<author></author>
<title>Prog. Neurobiol.</title>
</host>
<title>Behavioral arrest: in search of the neural control system</title>
</json:item>
<json:item><author><json:item><name>S. Kobayashi</name>
</json:item>
<json:item><name>Y. Nakamura</name>
</json:item>
</author>
<host><volume>980</volume>
<pages><last>91</last>
<first>80</first>
</pages>
<author></author>
<title>Brain Res.</title>
</host>
<title>Synaptic organization of the rat parafascicular nucleus, with special reference to its afferents from the superior colliculus and the pedunculopontine tegmental nucleus</title>
</json:item>
<json:item><author><json:item><name>J. Kojima</name>
</json:item>
<json:item><name>Y. Yamaji</name>
</json:item>
<json:item><name>M. Matsumura</name>
</json:item>
<json:item><name>A. Nambu</name>
</json:item>
<json:item><name>M. Inase</name>
</json:item>
<json:item><name>H. Tokuno</name>
</json:item>
<json:item><name>M. Takada</name>
</json:item>
<json:item><name>H. Imai</name>
</json:item>
</author>
<host><volume>226</volume>
<pages><last>114</last>
<first>111</first>
</pages>
<author></author>
<title>Neurosci. Lett.</title>
</host>
<title>Excitotoxic lesions of the pedunculopontine tegmental nucleus produce contralateral hemiparkinsonism in the monkey</title>
</json:item>
<json:item><author><json:item><name>S.R. Laviolette</name>
</json:item>
<json:item><name>T.O. Alexson</name>
</json:item>
<json:item><name>D. Van Der Kooy</name>
</json:item>
</author>
<host><volume>22</volume>
<pages><last>8660</last>
<first>8653</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Lesions of the tegmental pedunculopontine nucleus block the rewarding effects and reveal the aversive effects of nicotine in the ventral tegmental area</title>
</json:item>
<json:item><author><json:item><name>B. Lavoie</name>
</json:item>
<json:item><name>A. Parent</name>
</json:item>
</author>
<host><volume>344</volume>
<pages><last>231</last>
<first>210</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Pedunculopontine nucleus in the squirrel monkey: projections to the basal ganglia as revealed by anterograde tract‐tracing methods</title>
</json:item>
<json:item><author><json:item><name>M. Matsumura</name>
</json:item>
</author>
<host><volume>77</volume>
<pages><last>97</last>
<first>91</first>
</pages>
<author></author>
<title>Stereotact. Funct. Neurosurg.</title>
</host>
<title>Experimental parkinsonism in primates</title>
</json:item>
<json:item><author><json:item><name>M. Matsumura</name>
</json:item>
<json:item><name>J. Kojima</name>
</json:item>
</author>
<host><volume>77</volume>
<pages><last>115</last>
<first>108</first>
</pages>
<author></author>
<title>Stereotact. Funct. Neurosurg.</title>
</host>
<title>The role of the pedunculopontine tegmental nucleus in experimental parkinsonism in primates</title>
</json:item>
<json:item><author><json:item><name>M. Matsumura</name>
</json:item>
<json:item><name>A. Nambu</name>
</json:item>
<json:item><name>Y. Yamaji</name>
</json:item>
<json:item><name>K. Watanabe</name>
</json:item>
<json:item><name>H. Imai</name>
</json:item>
<json:item><name>M. Inase</name>
</json:item>
<json:item><name>H. Tokuno</name>
</json:item>
<json:item><name>M. Takada</name>
</json:item>
</author>
<host><volume>98</volume>
<pages><last>110</last>
<first>97</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Organization of somatic motor inputs from the frontal lobe to the pedunculopontine tegmental nucleus in the macaque monkey</title>
</json:item>
<json:item><author><json:item><name>I.J. Mitchell</name>
</json:item>
<json:item><name>C.E. Clarke</name>
</json:item>
<json:item><name>S. Boyce</name>
</json:item>
<json:item><name>R.G. Robertson</name>
</json:item>
<json:item><name>D. Peggs</name>
</json:item>
<json:item><name>M.A. Sambrook</name>
</json:item>
<json:item><name>A.R. Crossman</name>
</json:item>
</author>
<host><volume>32</volume>
<pages><last>226</last>
<first>213</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Neural mechanisms underlying parkinsonian symptoms based upon regional uptake of 2‐deoxyglucose in monkeys exposed to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</title>
</json:item>
<json:item><author><json:item><name>S. Moon‐Edley</name>
</json:item>
<json:item><name>A.M. Graybiel</name>
</json:item>
</author>
<host><volume>217</volume>
<pages><last>215</last>
<first>187</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>The afferent and efferent connections of the feline nucleus tegmenti pedunculopontinus, pars compacta</title>
</json:item>
<json:item><author><json:item><name>M. Mouroux</name>
</json:item>
<json:item><name>O.K. Hassani</name>
</json:item>
<json:item><name>J. Feger</name>
</json:item>
</author>
<host><volume>67</volume>
<pages><last>407</last>
<first>399</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Electrophysiological study of the excitatory parafascicular projection to the subthalamic nucleus and evidence for ipsi‐ and contralateral controls</title>
</json:item>
<json:item><author><json:item><name>M. Mouroux</name>
</json:item>
<json:item><name>O.K. Hassani</name>
</json:item>
<json:item><name>J. Feger</name>
</json:item>
</author>
<host><volume>81</volume>
<pages><last>397</last>
<first>387</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Electrophysiological and Fos immunohistochemical evidence for the excitatory nature of the parafascicular projection to the globus pallidus</title>
</json:item>
<json:item><author><json:item><name>L. Munro‐Davies</name>
</json:item>
<json:item><name>J. Winter</name>
</json:item>
<json:item><name>T.Z. Aziz</name>
</json:item>
<json:item><name>J. Stein</name>
</json:item>
</author>
<host><volume>16</volume>
<pages><last>151</last>
<first>150</first>
</pages>
<author></author>
<title>Mov. Disord.</title>
</host>
<title>Kainate acid lesions of the pedunculopontine region in the normal behaving primate</title>
</json:item>
<json:item><author><json:item><name>D. Nandi</name>
</json:item>
<json:item><name>T.Z. Aziz</name>
</json:item>
<json:item><name>N. Giladi</name>
</json:item>
<json:item><name>J. Winter</name>
</json:item>
<json:item><name>J.F. Stein</name>
</json:item>
</author>
<host><volume>125</volume>
<pages><last>2430</last>
<first>2418</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>Reversal of akinesia in experimental parkinsonism by GABA antagonist microinjections in the pedunculopontine nucleus</title>
</json:item>
<json:item><author><json:item><name>D. Nandi</name>
</json:item>
<json:item><name>X. Liu</name>
</json:item>
<json:item><name>J.L. Winter</name>
</json:item>
<json:item><name>T.Z. Aziz</name>
</json:item>
<json:item><name>J.F. Stein</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>174</last>
<first>170</first>
</pages>
<author></author>
<title>J. Clin. Neurosci.</title>
</host>
<title>Deep brain stimulation of the pedunculopontine region in the normal non‐ human primate</title>
</json:item>
<json:item><author><json:item><name>G. Orieux</name>
</json:item>
<json:item><name>C. Francois</name>
</json:item>
<json:item><name>J. Feger</name>
</json:item>
<json:item><name>J. Yelnik</name>
</json:item>
<json:item><name>M. Vila</name>
</json:item>
<json:item><name>M. Ruberg</name>
</json:item>
<json:item><name>Y. Agid</name>
</json:item>
<json:item><name>E.C. Hirsch</name>
</json:item>
</author>
<host><volume>97</volume>
<pages><last>88</last>
<first>79</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Metabolic activity of excitatory parafascicular and pedunculopontine inputs to the subthalamic nucleus in a rat model of Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>P.A. Pahapill</name>
</json:item>
<json:item><name>A.M. Lozano</name>
</json:item>
</author>
<host><volume>123</volume>
<pages><last>1783</last>
<first>1767</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>The pedunculopontine nucleus and Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>E. Palombo</name>
</json:item>
<json:item><name>L.J. Porrino</name>
</json:item>
<json:item><name>K.S. Bankiewicz</name>
</json:item>
<json:item><name>A.M. Crane</name>
</json:item>
<json:item><name>L. Sokoloff</name>
</json:item>
<json:item><name>I.J. Kopin</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>869</last>
<first>860</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Local cerebral glucose utilization in monkeys with hemiparkinsonism induced by intracarotid infusion of the neurotoxin MPTP</title>
</json:item>
<json:item><author><json:item><name>D. Pare</name>
</json:item>
<json:item><name>Y. Smith</name>
</json:item>
<json:item><name>A. Parent</name>
</json:item>
<json:item><name>M. Steriade</name>
</json:item>
</author>
<host><volume>25</volume>
<pages><last>86</last>
<first>69</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Projections of brainstem core cholinergic and non‐cholinergic neurons of cat to intralaminar and reticular thalamic nuclei</title>
</json:item>
<json:item><author><json:item><name>A. Parent</name>
</json:item>
<json:item><name>A. Mackey</name>
</json:item>
<json:item><name>L. De Bellefeuille</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>1150</last>
<first>1137</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>The subcortical afferents to caudate nucleus and putamen in primate: a fluorescence retrograde double labeling study</title>
</json:item>
<json:item><author><json:item><name>M. Parent</name>
</json:item>
<json:item><name>M. Levesque</name>
</json:item>
<json:item><name>A. Parent</name>
</json:item>
</author>
<host><volume>439</volume>
<pages><last>175</last>
<first>162</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Two types of projection neurons in the internal pallidum of primates: single‐axon tracing and three‐dimensional reconstruction</title>
</json:item>
<json:item><host><author></author>
<title>Paxinos, G. & Watson, C. (1996) The Rat Brain in Stereotaxic Coordinates. Academic Press, Sydney.</title>
</host>
</json:item>
<json:item><author><json:item><name>B. Piallat</name>
</json:item>
<json:item><name>A. Benazzouz</name>
</json:item>
<json:item><name>A.L. Benabid</name>
</json:item>
</author>
<host><volume>8</volume>
<pages><last>1414</last>
<first>1408</first>
</pages>
<author></author>
<title>Eur. J. Neurosci.</title>
</host>
<title>Subthalamic nucleus lesion in rats prevents dopaminergic nigral neuron degeneration after striatal 6‐OHDA injection: behavioural and immunohistochemical studies</title>
</json:item>
<json:item><author><json:item><name>J. Rohrbacher</name>
</json:item>
<json:item><name>N. Ichinohe</name>
</json:item>
<json:item><name>S.T. Kitai</name>
</json:item>
</author>
<host><volume>97</volume>
<pages><last>714</last>
<first>703</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Electrophysiological characteristics of substantia nigra neurons in organotypic cultures: spontaneous and evoked activities</title>
</json:item>
<json:item><author><json:item><name>D.B. Rye</name>
</json:item>
<json:item><name>C.B. Saper</name>
</json:item>
<json:item><name>H.J. Lee</name>
</json:item>
<json:item><name>B.H. Wainer</name>
</json:item>
</author>
<host><volume>259</volume>
<pages><last>528</last>
<first>483</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Pedunculopontine tegmental nucleus of the rat: cytoarchitecture, cytochemistry, and some extrapyramidal connections of the mesopontine tegmentum</title>
</json:item>
<json:item><author><json:item><name>T. Schallert</name>
</json:item>
<json:item><name>J.L. Tillerson</name>
</json:item>
</author>
<host><pages><last>151</last>
<first>131</first>
</pages>
<author></author>
<title>Central Nervous System Disease</title>
</host>
<title>Interventioning strategies for degeneration of dopamine neurons in parkinsonism: optimizing behavioral assessment of outcome</title>
</json:item>
<json:item><author><json:item><name>U. Scherer‐Singler</name>
</json:item>
<json:item><name>S.R. Vincent</name>
</json:item>
<json:item><name>H. Kimura</name>
</json:item>
<json:item><name>E.G. McGeer</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>234</last>
<first>229</first>
</pages>
<author></author>
<title>J. Neurosci. Meth.</title>
</host>
<title>Demonstration of a unique population of neurons with NADPH‐diaphorase histochemistry</title>
</json:item>
<json:item><author><json:item><name>K. Semba</name>
</json:item>
<json:item><name>H.C. Fibiger</name>
</json:item>
</author>
<host><volume>323</volume>
<pages><last>410</last>
<first>387</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Afferent connections of the laterodorsal and the pedunculopontine tegmental nuclei in the rat: a retro‐ and antero‐grade transport and immunohistochemical study</title>
</json:item>
<json:item><author><json:item><name>E. Shink</name>
</json:item>
<json:item><name>M. Sidibe</name>
</json:item>
<json:item><name>Y. Smith</name>
</json:item>
</author>
<host><volume>382</volume>
<pages><last>363</last>
<first>348</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Efferent connections of the internal globus pallidus in the squirrel monkey. II. Topography and synaptic organization of pallidal efferents to the pedunculopontine nucleus</title>
</json:item>
<json:item><author><json:item><name>B.M. Spann</name>
</json:item>
<json:item><name>I. Grofova</name>
</json:item>
</author>
<host><volume>283</volume>
<pages><last>27</last>
<first>13</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Origin of ascending and spinal pathways from the nucleus tegmenti pedunculopontinus in the rat</title>
</json:item>
<json:item><author><json:item><name>B.M. Spann</name>
</json:item>
<json:item><name>I. Grofova</name>
</json:item>
</author>
<host><volume>311</volume>
<pages><last>388</last>
<first>375</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Nigropedunculopontine projection in the rat: an anterograde tracing study with phaseolus vulgaris‐leucoagglutinin (PHA‐L)</title>
</json:item>
<json:item><author><json:item><name>T.L. Steininger</name>
</json:item>
<json:item><name>D.B. Rye</name>
</json:item>
<json:item><name>B.H. Wainer</name>
</json:item>
</author>
<host><volume>321</volume>
<pages><last>543</last>
<first>515</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Afferent projections to the cholinergic pedunculopontine tegmental nucleus and adjacent midbrain extrapyramidal area in the albino rat. I. Retrograde tracing studies</title>
</json:item>
<json:item><author><json:item><name>M. Steriade</name>
</json:item>
<json:item><name>S. Datta</name>
</json:item>
<json:item><name>D. Pare</name>
</json:item>
<json:item><name>G. Oakson</name>
</json:item>
<json:item><name>R.C. Curro Dossi</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>2559</last>
<first>2541</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Neuronal activities in brain‐stem cholinergic nuclei related to tonic activation processes in thalamocortical systems</title>
</json:item>
<json:item><author><json:item><name>T. Sugimoto</name>
</json:item>
<json:item><name>T. Hattori</name>
</json:item>
</author>
<host><volume>11</volume>
<pages><last>946</last>
<first>931</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Organization and efferent projections of nucleus tegmenti pedunculopontinus pars compacta with special reference to its cholinergic aspects</title>
</json:item>
<json:item><author><json:item><name>M. Takada</name>
</json:item>
<json:item><name>M. Matsumura</name>
</json:item>
<json:item><name>J. Kojima</name>
</json:item>
<json:item><name>Y. Yamaji</name>
</json:item>
<json:item><name>M. Inase</name>
</json:item>
<json:item><name>H. Tokuno</name>
</json:item>
<json:item><name>A. Nambu</name>
</json:item>
<json:item><name>H. Imai</name>
</json:item>
</author>
<host><volume>12</volume>
<pages><last>1780</last>
<first>1771</first>
</pages>
<author></author>
<title>Eur. J. Neurosci.</title>
</host>
<title>Protection against dopaminergic nigrostriatal cell death by excitatory input ablation</title>
</json:item>
<json:item><author><json:item><name>J. Ulloor</name>
</json:item>
<json:item><name>V. Mavanji</name>
</json:item>
<json:item><name>S. Saha</name>
</json:item>
<json:item><name>D.F. Siwek</name>
</json:item>
<json:item><name>S. Datta</name>
</json:item>
</author>
<host><volume>31</volume>
<pages><first>31</first>
</pages>
<author></author>
<title>J. Neurophysiol.</title>
</host>
<title>Spontaneous REM sleep is modulated by the activation of the pedunculopontine tegmental GABA‐B receptors in the freely moving rat</title>
</json:item>
<json:item><author><json:item><name>M. Vila</name>
</json:item>
<json:item><name>R. Levy</name>
</json:item>
<json:item><name>M.T. Herrero</name>
</json:item>
<json:item><name>B. Faucheux</name>
</json:item>
<json:item><name>J.A. Obeso</name>
</json:item>
<json:item><name>Y. Agid</name>
</json:item>
<json:item><name>E.C. Hirsch</name>
</json:item>
</author>
<host><volume>71</volume>
<pages><last>912</last>
<first>903</first>
</pages>
<author></author>
<title>Neuroscience</title>
</host>
<title>Metabolic activity of the basal ganglia in parkinsonian syndromes in human and non‐human primates: a cytochrome oxidase histochemistry study</title>
</json:item>
<json:item><author><json:item><name>M. Vila</name>
</json:item>
<json:item><name>R. Levy</name>
</json:item>
<json:item><name>M.T. Herrero</name>
</json:item>
<json:item><name>M. Ruberg</name>
</json:item>
<json:item><name>B. Faucheux</name>
</json:item>
<json:item><name>J.A. Obeso</name>
</json:item>
<json:item><name>Y. Agid</name>
</json:item>
<json:item><name>E.C. Hirsch</name>
</json:item>
</author>
<host><volume>17</volume>
<pages><last>773</last>
<first>765</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Consequences of nigrostriatal denervation on the functioning of the basal ganglia in human and nonhuman primates: an in situ hybridization study of cytochrome oxidase subunit I mRNA</title>
</json:item>
<json:item><author><json:item><name>A.R. West</name>
</json:item>
<json:item><name>A.A. Grace</name>
</json:item>
</author>
<host><volume>83</volume>
<pages><last>1808</last>
<first>1796</first>
</pages>
<author></author>
<title>J. Neurophysiol.</title>
</host>
<title>Striatal nitric oxide signaling regulates the neuronal activity of midbrain dopamine neurons in vivo</title>
</json:item>
<json:item><author><json:item><name>F.J. White</name>
</json:item>
<json:item><name>R.Y. Wang</name>
</json:item>
</author>
<host><volume>221</volume>
<pages><last>1057</last>
<first>1054</first>
</pages>
<author></author>
<title>Science</title>
</host>
<title>Differential effects of classical and atypical antipsychotic drugs on A9 and A10 dopamine neurons</title>
</json:item>
<json:item><author><json:item><name>P. Winn</name>
</json:item>
<json:item><name>V.J. Brown</name>
</json:item>
<json:item><name>W.L. Inglis</name>
</json:item>
</author>
<host><volume>11</volume>
<pages><last>261</last>
<first>241</first>
</pages>
<author></author>
<title>Crit. Rev. Neurobiol.</title>
</host>
<title>On the relationships between the striatum and the pedunculopontine tegmental nucleus</title>
</json:item>
<json:item><author><json:item><name>Y. Yasui</name>
</json:item>
<json:item><name>D.F. Cechetto</name>
</json:item>
<json:item><name>C.B. Saper</name>
</json:item>
</author>
<host><volume>517</volume>
<pages><last>24</last>
<first>19</first>
</pages>
<author></author>
<title>Brain Res.</title>
</host>
<title>Evidence for a cholinergic projection from the pedunculopontine tegmental nucleus to the rostral ventrolateral medulla in the rat</title>
</json:item>
<json:item><author><json:item><name>F.M. Zhou</name>
</json:item>
<json:item><name>C. Wilson</name>
</json:item>
<json:item><name>J.A. Dani</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>36</last>
<first>23</first>
</pages>
<author></author>
<title>Neuroscientist</title>
</host>
<title>Muscarinic and nicotinic cholinergic mechanisms in the mesostriatal dopamine systems</title>
</json:item>
<json:item><author><json:item><name>R.M. Zweig</name>
</json:item>
<json:item><name>W.R. Jankel</name>
</json:item>
<json:item><name>J.C. Hedreen</name>
</json:item>
<json:item><name>R. Mayeux</name>
</json:item>
<json:item><name>D.L. Price</name>
</json:item>
</author>
<host><volume>26</volume>
<pages><last>46</last>
<first>41</first>
</pages>
<author></author>
<title>Ann. Neurol.</title>
</host>
<title>The pedunculopontine nucleus in Parkinson's disease</title>
</json:item>
</refBibs>
<genre><json:string>article</json:string>
</genre>
<host><volume>22</volume>
<publisherId><json:string>EJN</json:string>
</publisherId>
<pages><total>12</total>
<last>2294</last>
<first>2283</first>
</pages>
<issn><json:string>0953-816X</json:string>
</issn>
<issue>9</issue>
<genre><json:string>journal</json:string>
</genre>
<language><json:string>unknown</json:string>
</language>
<eissn><json:string>1460-9568</json:string>
</eissn>
<title>European Journal of Neuroscience</title>
<doi><json:string>10.1111/(ISSN)1460-9568</json:string>
</doi>
</host>
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<abstract xml:lang="en"><p>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.</p>
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<correspondenceTo>Dr Sorin Breit, as above.
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<p>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.</p>
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<p> S.B. and L.L. contributed equally to this work.</p>
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<namePart type="family">Benazzouz</namePart>
<affiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J. B.</namePart>
<namePart type="family">Schulz</namePart>
<affiliation>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
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<originInfo><publisher>Blackwell Science Ltd</publisher>
<place><placeTerm type="text">Oxford, UK</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2005-11</dateIssued>
<edition>Received 8 March 2005, revised 9 July 2005, accepted 9 August 2005</edition>
<copyrightDate encoding="w3cdtf">2005</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">8</extent>
<extent unit="references">76</extent>
<extent unit="words">5725</extent>
</physicalDescription>
<abstract lang="en">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.</abstract>
<subject lang="en"><genre>keywords</genre>
<topic>akinesia</topic>
<topic>extracellular recordings</topic>
<topic>6‐hydroxydopamine</topic>
<topic>pedunculopontine nucleus</topic>
<topic>substantia nigra</topic>
<topic>subthalamic nucleus</topic>
</subject>
<relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title>
</titleInfo>
<genre type="journal">journal</genre>
<identifier type="ISSN">0953-816X</identifier>
<identifier type="eISSN">1460-9568</identifier>
<identifier type="DOI">10.1111/(ISSN)1460-9568</identifier>
<identifier type="PublisherID">EJN</identifier>
<part><date>2005</date>
<detail type="volume"><caption>vol.</caption>
<number>22</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>9</number>
</detail>
<extent unit="pages"><start>2283</start>
<end>2294</end>
<total>12</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">00E15A4979A2F6AA59D6167776ECA03A9FAE5467</identifier>
<identifier type="DOI">10.1111/j.1460-9568.2005.04402.x</identifier>
<identifier type="ArticleID">EJN4402</identifier>
<recordInfo><recordContentSource>WILEY</recordContentSource>
<recordOrigin>Blackwell Science Ltd</recordOrigin>
</recordInfo>
</mods>
</metadata>
<serie></serie>
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