Dynamic changes in the cortex-basal ganglia network after dopamine depletion in the rat.
It is well established that 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. This 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 (HVSs) 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 and 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 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 overactivation 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.
Dejean
Cyril
C
Basal Gang, Laboratoire Mouvement, Adaptation, Cognition, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5227, Université Victor Segalen Bordeaux 2, Bordeaux, France.
Gross
Christian E
CE
Bioulac
Bernard
B
Boraud
Thomas
T
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D018663:Adrenergic Agents / Q000633:toxicity; D000704:Analysis of Variance; D000818:Animals; D001479:Basal Ganglia / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000172:deficiency*; D004569:Electroencephalography / Q000379:methods; D007839:Functional Laterality; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D017711:Nonlinear Dynamics; D016627:Oxidopamine / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D013057:Spectrum Analysis
D018663:Adrenergic Agents; D016627:Oxidopamine; D004298:Dopamine