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J Neurophysiol (May 21, 2008). doi:10.1152/jn.90466.2008
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Submitted on April 14, 2008
Revised on May 11, 2008
Accepted on May 14, 2008

Dynamic changes in the cortex-basal ganglia network after dopamine depletion in the rat

Cyril Dejean1, Christian Eric Gross2, Bernard Bioulac2, and Thomas Boraud2*

1 Universitordeaux 2
2 CNRS

* To whom correspondence should be addressed. E-mail: tboraud{at}u-bordeaux2.fr.

It is well established that the parkinsonian syndrome is associated with alterations in the temporal pattern of neuronal activity and local field potentials in the basal ganglia (BG). An increase in synchronized oscillations has been observed in different BG nuclei in parkinsonian patients and animal models of this disease. However the mechanisms underlying this phenomenon remain unclear. The present study investigates the functional connectivity in the cortex-BG network of a rodent model of Parkinson's disease. Single neurons and local field potentials were simultaneously recorded in the motor cortex, the striatum and the substantia nigra pars reticulata (SNr) of freely moving rats, and high-voltage spindles (HVS) were used to compare signal transmission before and after dopaminergic depletion. It is shown that dopaminergic lesion results in a significant enhancement of oscillatory synchronization in the BG: the coherence between pairs of structures increased significantly as well as the percentage of oscillatory auto- and cross-correlograms. HVS episodes were also more numerous and longer. These changes were associated with a shortening of the latency of SNr response to cortical activation, from 40.5 ± 4.8 ms to 10.2±1.07 ms. This result suggests that in normal conditions SNr neurons are likely to be driven by late inputs from the indirect pathway, however after the lesion their shorter latency also indicates an over-activation of the hyperdirect pathway. This study confirms that neuronal signal transmission is altered in the BG after dopamine depletion but also provides qualitative evidence for these changes at the cellular level.




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