Yibin Shao

Visual cortical plasticity after V1 lesion and retina degeneration in macaque monkeys

Introduction and Scientific Aims

Primate visual cortex (V1) is of particular interest as it is the main cortical relay of visual information. It is not surprising that primary visual cortical injuries produce a dense visual scotoma that has long been thought to be irreversible. However, a series of studies performed over the last 25 years has provided strong evidence that primate (human and monkey) subjects still possess some rudimentary residual visual sensitivity in the blind part of their visual field following dense area V1 lesions (blindsight) [1-3]. Macular degeneration (MD) is a common cause of human visual impairment, which often damages the central retina eliminating the normal retinal input to a large region of visual cortex. Human fMRI studies in MD patients and electrophysiological studies in macaques with retinal lesions indicate that V1 might retain a remarkable degree of plasticity into adulthood [4,5]. However a recent fMRI study in rhesus macaques following homonymous retinal lesions suggested that post lesion responses inside the V1 lesion projection zone (LPZ) are weak or absent [6].

The purpose of our experiments is to study how the visual cortex changes to adapt to injury, with particular focus on understanding aspects of plasticity that may help us restore part of the loss functionality.

Methods

We are using fMRI methods to study reorganization in the primary visual cortex of one animal with macular degeneration that was fortuitously found in our colony. We also plan to employ electrophysiological recording and stimulation techniques in the non-human primate to study visual cortex reorganization following area V1 lesions.

Results and Preliminary Conclusions

For the macular degeneration monkey (D06), the size and location of the fMRI defined LPZ in V1 is consistent with the retinotopic projection of the retinal lesion. The retinotopic organization of the non-deafferented V1 periphery is regular without distortion. Higher level visual areas of D06 (V5/MT) show more extensive activation than areas of control monkeys with an artificial scotoma (to obscure part of the stimuli from the visual field as a simulation of the real scotoma) of comparable size. Population receptive field sizes in the non-deafferented V5/MT of monkey D06 are on average slightly smaller than controls.No significant activity was found within V1 LPZ of D06. There is potential reorganization in V5/MT of this monkey.

References

1. Cowey A and Stoerig P (1995) blindsight in monkeys. Nature,373(6511): p. 247-9.

2. Huxlin KR, Martin T, Kelly K, Riley M, Friedman DI, Burgin WS and Hayhoe M (2009) perceptual Relearning of Complex Visual Motion after V1 Damage in Humans. J Neurosci, 29(13):3981-3991

3. Schmid MC, Panagiotaropoulos T, Augath M, Logothetis N K and Smirnakis SM (2009) visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex. PLoS ONE, 4, e5527.

4. Baker C I, Peli E, Knouf N and Kanwisher NG (2005) reorganization of visual processing in macular degeneration. J. Neurosci. 25, 614–618.

5. Gilbert CD and Wiesel TN (1992) receptive field dynamics in adult primary visual cortex. Nature 356, 150–-152.

6. Smirnakis SM, Brewer AA, Schmid MC, Tolias AS, Schüz A, Augath M, Inhoffen W, Wandell BA and Logothetis NK (2005) lack of long-term cortical reorganization after macaque retinal lesions. Nature 435, 300–307.