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眼球運動
Oculomotor System

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開催日
2010年09月04日(土)
時 間
13:00 - 14:00
会 場
Poster Room 2

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Modeling saccades through NMDAR-mediated bursting with reciprocal inhibition in the Superior Colliculus

演題番号 : P3-h12

Jan Moren:1 Tomohiro Shibata:2 Aurelien Cassagnes:1,3 Junichiro Yoshimoto:3 Kenji Doya:1,2,3,4 

1:Graduate School of Informatics, Kyoto University, Japan 2:NAIST, Nara, Japan 3:OIST, Okinawa, Japan 4:RIKEN, Saitama, Japan 

 

The saccade perception-action loop consists of the retina, the superior colliculus (SC) and the brainstem motoneuron systems, and supporting areas. The SC is the site of early sensorimotor integration. It is retinotopically organized, and projects on to the motoneuron system.
Current theories [1] posit that the SC bursting output directly drives the motoneuron systems and gives rise to several aspects of the main sequence of saccadic eye movements. In this view, each spike encodes a tiny movement segment, with the spike rate pattern shaping the velocity profile and the downstream weights determining the total distance.
We investigate how this theoretical model might be instantiated in the neuronal substrate, by building a spiking neuron-level model of the SC and the motoneuron systems. We have augmented a conductance-based neuron model by Brette and Gerstner with a membrane potential-dependent synaptic current modeling NMDA-type glutamate receptors (NMDAR).
The intermediate SC consists of several sublayers and distinct neuron types. Burst neurons form the output population, driven by buildup and quasivisual neurons. Burst neurons do not burst intrinsically, but through a combination of NMDA and non-NMDA glutamatergic inputs. The burst is projected to the motoneuron system and the eye position integrator. It is also projected to an area in the central mesencephalic reticular formation (cMRF) that acts as a short-term spike integrator that reciprocally inhibits the burst neuron population.
We propose that cMRF activity suppresses inhibitory interneurons and allow the buildup neuron population activity to spread across the surface, eventually triggering deep layer inhibitory neurons that reset the system. We show that NMDAR-mediated bursting with inhibitory feedback from the cMRF integrator can indeed produce the expected gamma-shaped activation profile and spatial rate distribution in the burst neuron output.
1. Goossens, van Opstal. J. Neuro. 83(6), 2000

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