INVESTIGADORES
MURER Mario Gustavo
congresos y reuniones científicas
Título:
Research Project: Physiological evidence of striato-nigro-striatal spiraling circuits
Autor/es:
GALIÑANES G; MURER MG
Lugar:
Córdoba
Reunión:
Congreso; I reunion Conjunta de Neurociencia; 2009
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencia
Resumen:
Several aspects of our behavior are thought to depend on complex sensorimotor and cognitive computations performed by parallel corticobasal ganglia circuits. Recent anatomical and behavioral evidence suggest the existence of serial cortico-basal ganglia connections linking ventral to dorsal regions of the striatum through striato-nigro-striatal spiraling loops. These connections are supposed to depend on nigrostriatal dopaminergic inputs and have been proposed to be necessary for the progression of goaldirected instrumental behavior to more habitual instrumental responses. However, physiological evidence of such connections is lacking. We speculate that cortical information would be processed within the striatum across a ventromedial to dorsolateral gradient and that such gradient should be disrupted in the absence of nigrostriatal dopamine neurons. Previous results supporting this hypothesis are presented. Striatal neurons of mice with neonatal dopamine neuron depletion exhibit a less refined tuning to localized cortical ongoing oscillations, a decreased probability of convergent responses to electrical stimulation at separate cortical sites and a disrupted transfer of experimentally induced corticostriatal long term depression to unconditioned motor cortex area after prelimbic cortex conditioning. Statistical tools allowing causal connectivity estimations have been recently applied to physiological data (e.g. Granger Causality). To study serial connectivity within the striatum and dopamine pathways influence, we show preliminary Granger Causality analysis on multisite striatal neuronal activity recorded along a ventromedial-dorsolateteral axis in mice with neonatal dopamine neuron depletion and sham controls.