作者: O. Jaidar , L. Carrillo-Reid , J. Bargas
DOI: 10.5772/21036
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摘要: Experimentally, depriving the basal ganglia (BG) from their dopaminergic innervation, dramatically changes behavior of all circuits, neurons, and synapses in multiple ways. Dopamine afferents are received by BG nuclei (Rommelfanger Wichmann, 2010). In absence DA, generate enhanced pathological oscillatory patterns external segment striatum: globus pallidus (GPe), internal (GPi), subthalamic nucleus (STN) substantia nigra pars reticulata (SNr) (Blandini et al., 2000). These expressed as increased cortical beta frequency coherence (Costa 2006; Fuentes 2009; Kozlov Walters Bergstrom, 2009) reflected inability to select, change or initiate motor actions (Magill 2001; Ni Wilson 2006), though neurons were trapped a massive oscillation that does not allow selection any circuit action. Behaviorally, disfunction is accompanied bradykinesia, akinesia, tremor muscular rigidity (Brown, 2007; Hammond Galvan 2008; Zold 2009). One question what manifestations these at level striatal microcircuitry (Alexander Crutcher, 1990; Middleton Strick, 2002), given its principal entrance DA particularly concentrated this (striatum); more than other (Bjorklund Dunnett, 2007). To answer question, here we show how microcircuit functions before after depletion. The observed may be fundamental understand activity during Parkinsonism.