Responses of lateral geniculate neurons that survive long-term visual cortex damage in kittens and adult cats

Abstract

Damage to visual cortex (areas 17-19) in kittens or adult cats produces severe retrograde degeneration of neurons in the dorsal lateral geniculate nucleus (LGN). However, some neurons survive in otherwise degenerated portions of the LGN after a visual cortex lesion at any age. Previous studies have shown that there are well-defined differences in potential retinal inputs, soma size, synaptic connections, outputs, and physiological properties of output targets of the surviving LGN cells in cats that received visual cortex damage at different ages. The present experiment investigated the relationships between these differences and the responses of surviving LGN neurons to visual stimulation. Recordings were made from surviving neurons in the degenerated A- and C-layers of the LGN in cats that had received a visual cortex lesion on the day of birth, at 8 weeks of age, or as adults (survival was 11.5-36 months). Normal adult cats were studied for comparison. The visual receptive field was mapped, and tests were carried out to classify each cell as X, Y, or W. In addition, quantitative methods were used to assess response amplitude, strength of receptive-field surround inhibition, spatial-frequency tuning to drifting or counterphased sine-wave gratings, and response to nondominant-eye stimulation for each cell. We found that surviving cells in all LGN layers respond to light, have normal receptive-field organization, and have normal eye dominance following a lesion at any age tested. In addition, gross retinotopic organization of the LGN is normal. However, 2 main abnormalities were observed following a lesion at all 3 ages. First, there is a reduction in the percentage of X cells in the A layers, from 62% in normal LGNs to about 15% in degenerated LGNs. Second, many surviving cells in both the A- and C-layers have abnormally large receptive-field centers. Other differences that were observed between normal A-layer cells and surviving A-layer cells could be attributed to the loss of X cells. These results indicate that cells within a structure that shows severe retrograde degeneration after brain damage can maintain relatively normal function and can take part in potentially important residual neural pathways. Previous studies indicate that these residual pathways can show both anatomical and physiological compensation for the brain damage, and the present findings bear on the consequences and mechanisms of this compensation.

On Sensory Eye Dominance Revealed by Binocular Integrative and Binocular Competitive Stimuli

“…Neurophysiologic studies have shown that binocular suppression begins as early as dLGN. 43 – 46 From modeling work, Ding and Levi 47 suggested that the interocular inhibition in the LGN, which lacks of orientation selectivity, could provide the neurophysiologic substrate for the interocular gain-control in binocular combination. This would predict that an imbalance of interocular inhibition at dLGN can affect SED combo .…”

Binocular combination of luminance profiles

“…The origin of the nondominant inhibition of the LGN cells remains uncertain. It could conceivably be due to direct inhibitory interaction between right-eye and left-eye laminae of the LGN, via inhibitory interneurons (Guillery, 1966 ), which is supported by the fact that the visual cortex removal does not reduce nondominant influences on LGN cells (Pape & Eysel, 1986 ; Sanderson et al, 1971 ; Singer, 1970 ; Tumosa, McCall, Guido, & Spear, 1989 ). However, Ding and Sperling ( 2006 , 2007 ) found that, although essentially orientation independent, the interocular gain control was somewhat more effective for vertical and horizontal gratings than diagonal ones, which suggests that some of the gain control is likely of cortical origin, i.e., arises beyond the LGN, because the LGN cells are essentially indifferent to orientation.…”

Differential expression patterns of OCC1-related, extracellular matrix proteins in the lateral geniculate nucleus of macaque monkeys

“…This circuitry is normally formed and maintained through neuronal activity (Shatz, 1996). Even in adult animals, dLGN neurons are capable of eliciting plastic changes in their morphology and connectivity, as revealed by experiments where the dLGN target in the cortex is severely damaged (Tumosa et al, 1989).…”