CiNet/FBS Seminar
"What limits the visual performance of amblyopic primates: V2 studies"
Date / Time : Friday, October 25, 2013 / 16:00 - 18:00
日時：2013年10月25日（金） 16:00 - 18:00
Place : CiNet Building 1F Conference Hall (A)
場所：CiNet棟１階 大会議室（A）
## Map and directions:
http://cinet.jp/access/index.html
http://www.fbs.osaka-u.ac.jp/eng/general/suita.php
(CiNet Building is [Blue Circle #11] right next to the Nanobiology Building in the map)
Abstract:
Amblyopia is a developmental vision disorder caused by experiencing binocular imbalance during early development. Amblyopic humans and monkeys exhibit a wide range of vision deficits. Despite some interesting theories based on many perceptual and modeling studies, the neural basis of vision deficits associated with amblyopia is poorly understood except for the well established ocular dominance imbalance in V1 of monocularly form deprived animals. This talk will present the results of our new studies in primate models of anisometropic amblyopia, and make a proposal on how some of the more complex monocular deficits may develop. Our earlier studies established that binocular imbalance in infant monkeys immediately initiates interocular suppression in their visual cortex, which persists until adulthood. We also found that the depth of amblyopia in individual strabismic monkeys is highly correlated with the strength of binocular suppression in V1 and V2. I will present our preliminary data to demonstrate that such robust binocular suppression can disrupt the functional development of cortical circuits supporting the spatial map of subunits within the receptive field of a given V2 neuron in amblyopic monkeys, and also, suppression may affect the timing and reliability of spiking by these neurons. Our results give a new insight into the neural mechanisms underlying such comlex spatial deficits as position uncertainty, crowding, and distortion.
"What limits the visual performance of amblyopic primates: V2 studies"
Date / Time : Friday, October 25, 2013 / 16:00 - 18:00
日時：2013年10月25日（金） 16:00 - 18:00
Place : CiNet Building 1F Conference Hall (A)
場所：CiNet棟１階 大会議室（A）
## Map and directions:
http://cinet.jp/access/index.html
http://www.fbs.osaka-u.ac.jp/eng/general/suita.php
(CiNet Building is [Blue Circle #11] right next to the Nanobiology Building in the map)
Abstract:
Amblyopia is a developmental vision disorder caused by experiencing binocular imbalance during early development. Amblyopic humans and monkeys exhibit a wide range of vision deficits. Despite some interesting theories based on many perceptual and modeling studies, the neural basis of vision deficits associated with amblyopia is poorly understood except for the well established ocular dominance imbalance in V1 of monocularly form deprived animals. This talk will present the results of our new studies in primate models of anisometropic amblyopia, and make a proposal on how some of the more complex monocular deficits may develop. Our earlier studies established that binocular imbalance in infant monkeys immediately initiates interocular suppression in their visual cortex, which persists until adulthood. We also found that the depth of amblyopia in individual strabismic monkeys is highly correlated with the strength of binocular suppression in V1 and V2. I will present our preliminary data to demonstrate that such robust binocular suppression can disrupt the functional development of cortical circuits supporting the spatial map of subunits within the receptive field of a given V2 neuron in amblyopic monkeys, and also, suppression may affect the timing and reliability of spiking by these neurons. Our results give a new insight into the neural mechanisms underlying such comlex spatial deficits as position uncertainty, crowding, and distortion.