Increased Receptive Field Size in the Surround of Chronic Lesions in the Adult Cat Visual Cortex

Abstract

Visual cortical lesions destroy the target cells for geniculocortical fibers from a certain retinotopic region. This leads to a cortical scotoma. We have investigated the receptive fields of cells in the visual cortex before, 2 days and 2 months after focal ibotenic acid lesions in the adult cat visual cortex and have found signs of receptive field plasticity in the surroundings of the chronic but not the acute and subacute excitotoxic lesions. In the subacute state (first two days post lesion) receptive field sizes of cells at the border of the lesion were reduced in size or remained unchanged. Remapping of cortical receptive fields 2 months later revealed a number of cells with multifold enlarged receptive fields at the border of the lesion. The cells with enlarged receptive fields displayed orientation and direction selectivity like normal cells. The size increase appeared not specifically directed towards the scotoma; however, the enlarged receptive fields can reduce the extent of a cortical scotoma, since previously unresponsive regions of the visual field activate cortical cells at the border of the lesion. This late receptive field plasticity could serve as a mechanism for the filling-in of cortical scotomata observed in patients with visual cortex lesions.

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

“…Other work using electrophysiological techniques also finds that peri-infarct tissue moves relative to the infarct location. (Eysel and Schweigart, 1999;Frost et al, 2003;Jenkins and Merzenich, 1987;Reinecke et al, 2003;Schiene et al, 1999;Zepeda et al, 2004).…”

“…In addition, it has been suggested that the compensatory improvements in skilled behavior that occur in the chronic period may be associated with long-lasting plastic changes in residual tissue including changes in neuronal structure, cortical organization, neurotrophic factor regulation, and electrophysiological responsiveness (Eysel and Schweigart, 1999;Schiene et al, 1999;Frost et al, 2003;Gonzalez and Kolb, 2003;Reinecke et al, 2003;Fridman et al, 2004;Zepeda et al, 2004).…”

The second face of blindness: Processing speed deficits in the intact visual field after pre- and post-chiasmatic lesions

“…Firstly, partial optic nerve damage or cortical tissue loss may lead to a reduced physiological signaling power and to a loss of firing synchrony of neuronal assemblies, thus increasing processing time. Secondly, there is an extensive remapping and reorganization of the visual field representation after pre-and post-chiasmatic damage as shown in animal model studies [34][35][36][37], as well as behavioral [38] and fMRI studies in patients [31][32][33]39]. Such receptive field reorganization is believed to be mediated by mechanisms involving plasticity of intrinsic cortical horizontal connections [40].…”

Population receptive field analysis of the primary visual cortex complements perimetry in patients with homonymous visual field defects

“…Less is known about how the visual system remaps to cover the visual field after injury to area V1 or its input projection from the lateral geniculate nucleus (LGN). Enlarged receptive fields have been found in areas surrounding chronic V1 lesions in cats (20)(21)(22), and visual point spread functions were seen to enlarge over time in the areas surrounding focal V1 lesions in kittens (23). Smaller, shortterm changes (2 d after the lesion) have been reported as well (24).…”