We are currently involved in the implementation of an joint Education and Research Initiative with Harvard Medical School. One of the partners will be the Department of Ophthalmology from Harvard Medical School. This institution has already manifested its willingness to participate.
In this collaboration, we will focus on two main areas: 1. mechanisms of short and long term visual plasticity in health and disease 2. mechanisms of motion perception and multimodal auditory and visual integration.
1. Mechanisms of short and long term visual plasticity in health and disease
A. Short term plasticity
This Research collaboration will focus on neuronal mechanisms of vision from receptor cell level to cortical visual centres. Physiological as well as pathophysiological neuronal mechanisms should be addressed in multiple visual pathways. As a final goal we aim to set a firm scientific ground for improvement of visual perception by low vision aids and training.
As a model of short term plasticity, we will study visual filling-in. This refers to the phenomenon that occurs when, after a few seconds, a figure steadily presented in peripheral vision becomes perceptually filled-in by its background, as if it ‘‘disappeared’’.
This visual illusion referred to as perceptual filling-in, occurs because the visual system interpolates information across regions of the visual field where physical evidence of that information is lacking,
Perceptual filling-in occurs quasi-instantaneously across the blind spot, as has been described in physiological studies (e.g., Komatsu, Kinoshita, & Murakami, 2000, 2002; Fiorani, Rosa, Gattass, & Rocha- Miranda, 1992). This is also the case also for pathological scotomas (Sergent, 1988; Bender & Teuber, 1946) as well as across entopic images of vasculature (Coppola & Purves, 1996). Slower filling-in within the range of a few seconds has been reported under conditions of artificial retinal stabilization (Yarbus, 1967; Gerrits, de Haan, & Vendrik, 1966; Ratliff, 1958), and during stabilization of peripheral images under natural fixation (Riggs, Ratliff, Cornsweet, & Cornsweet, 1953; Troxler, 1804).
It is an open question whether similar neural interpolation mechanisms that underlie perceptual filling-in also play a role during normal surface perception (Paradiso & Nakayama, 1991; Gerritts & Vendrik, 1970; Walls, 1954). The time required before perceptual filling-in depends on level of retinal staibilization and ensuing adaptation of boundary representations, figure size and the length of its boundaries projected on the retinotopic cortex, the relative sizes of figure and background (Sakaguchi, 2001; De Weerd, Desimone, & Ungerleider, 1998), and salience of the figure (Stuerzel & Spillmann, 2001; Welchman & Harris, 2001).
Fast (on a time scale of milliseconds) filling-in of brightness during normal surface perception has been demonstrated with a masking procedure by Paradiso and Nakayama (1991). The basic finding has been replicated im other experimental (Paradiso & Hahn, 1996; Rossi & Paradiso, 1996; Todorovic, 1987) and theoretical (Neumann et al., 2001; Arrington, 1994; Grossberg & Todorovic, 1988) studies. It is believed that neural interpolation is a consequence of activity increases resulting from an adaptation of inhibitory inputs to the neurons with classical RFs overlapping with the figure, such that ordinarily ineffective excitatory inputs from the background in the RF surround became effective in driving these neurons (for review, Tremere, Pinaud, & De Weerd, 2003).
It is likely that mechanisms of figure–ground segregation and interpolation are in part carried out by distinct feature dependent mechanisms in different cortical áreas (Gattass, Pessoa, De Weerd, & Fiorani, 1998; Ramachandran & Gregory, 1991). Interpolation mechanisms are likely to involve horizontal connections (Gilbert & Wiesel, 1989) as well as feedback connections. Indeed, long-range horizontal connections have a tendency to connect orientation columns with similar preferred orientations (Gilbert & Wiesel, 1989) may contribute to the perceived similarity of filled-in line texture across the figure and background.
B. Mechanisms of long term plasticity upon visual impairment
We will focus on two main disease models
Retinits pigmentosa and annular impairment of peripheral vision.
Glaucoma and piecemeal impairment of peripheral vision.
Genetic and acquired macular degeneration as models to study impairment of central vision, and remediation strategies (eg. Training of novel preferred fixation loci).
In order to understand mechanisms of cortical reorganization we will study the dynamics of filling-in processes in long term scotomas and study their remapping in cortical retinotopic maps.
2. Mechanisms of motion perception and multimodal auditory and visual integration.
We will continue our ongoing collaboration to study the neural correlates of local/global visual motion perception.
We will further extend this collaboration on ongoing work that attempts to understand how visual and auditory motion signals are integrated by the human brain.
· Projects within the 7th Framework Program with an emphasis on Ageing and Medical Imaging
- MIRROR: Multi-modal non-invasive in vivo imaging of the ocular fundus as a predictor for morbidity in older adults (7FP - Collaborative Project)
- EuroVisionNet: Visual Impairment and Degeneration: A Road-map for Vision Research within Europe (7FP – Coordination Action)