While binocularity has been established as an important characteristic of cat visual cortical neurons, neurons in the dorsal lateral geniculate nucleus (LGNd) are commonly believed to be monocular. To test whether binocularity exists at the level of the LGNd, postsynaptic potentials (PSPs) of 101 cells were intracellularly recorded in eight normal and eight monocularly deprived cats while presenting stimuli to either the dominant or non-dominant eyes. The results showed that: (1) About 92% of neurons (45 out of 49) responded to a flashing spot presented to the non-dominant eye. In contrast to the dominant eye responses, the non-dominant eye PSPs usually exhibited the same polarization tendency (hyperpolarization or depolarization) to flashing spot stimuli of light increment or decrement, and most of them were inhibitory (hyperpolarization, 35 out of 45, 78%). (2) The response field (RF) of the non-dominant eye overlapped that of the dominant eye. (3) For most binocular cells, peak-to-peak amplitudes of non-dominant eye PSPs were about half the size (46%) of those of the dominant eye. The peak latencies and half-peak latencies of non-dominant eye PSPs were significantly longer than those of the dominant eye (mean differences were 5.4ms and 5.6ms respectively). (4) Most of the binocular cells responded well to contrast reversing gratings presented to the non-dominant eye, and the responses were clearly spatial-frequency tuned. No null phase could be found for non-dominant eye PSPs, no matter the neuron was classified as X or Y type according to dominant eye elicited responses. Some of the cells responded well to drifting gratings presented to the non-dominant eye. (5) We also recorded 52 cells in monocularly deprived cats, and found that 49 cells (94%) showed significant responses to flashing spots presented to the non-dominant eye, a similar percentage to that found in normal cats (92%). Conclusion: as strongly monocular neurons, most of LGNd cells could also be driven by the non-dominant eye. The responses evoked by non-dominant eye stimulation differ greatly from those evoked by dominant eye stimulation, and remain intact even without visual experience. These observations suggest an important role of the perigeniculate nucleus in providing binocular inputs to LGNd cells.

Pattern adaptation is very important for visual function, while the mechanisms that mediate pattern adaptation, especially in the dorsal lateral geniculate nucleus (LGNd), are still unclear. Iontophoresis of the antagonists and agonists of GABA receptors were employed to separately investigate the contribution of GABA and GABA receptors to pattern adaptation of LGNd cells. When GABA receptors A B A were blocked by bicuculline both the response amplitude of LGNd cells and the degree of adaptation increased significantly. Many neurons showing no pattern adaptation under the normal condition became adapted to a prolonged stimulus. Moreover, the proportion of cells showing adaptation doubled (from 40 to 88%). The mean adaptation index (AI, adapted response amplitude/ original response amplitude) was 0.82 during bicuculline application, compared with 0.92 under the control condition. In additional, iontophoresis of baclofen, a selective GABA receptor agonist, decreased the mean response amplitude to grating stimuli to 53% of normal. Nearly half of B the neurons increased their adaptation index following baclofen administration and the mean AI increased from 0.89 to 1.01. Iontophoresis of GABA receptor antagonist (CGP35348) could abolish this effect, though it had no significant effect on visual response B amplitude and pattern adaptation itself. Iontophoresis of another GABA receptor antagonist, 2-OH-saclofen, also had no significant B effect on visual response amplitude and pattern adaptation. These results suggest that both GABA receptors and GABA receptors A B modulate the pattern adaptation of LGNd cells and are involved in synaptic plasticity.

PURPOSE. To study changes in the dendritic morphology of retinal ganglion cells (RGCs) in cats with experimental chronic glaucoma. METHODS. Chronic elevation of intraocular pressure (IOP) was produced by injecting endogenous ghost red blood cells into the unilateral anterior chamber of the feline eyes for 1 month. The morphologic features of retrograde-labeled RGCs by bilateral injection of horseradish peroxidase (HRP) into layers A and Aa1 of the lateral geniculate nucleus (LGN) were examined and compared between the normal and glaucomatous eyes. Nissl staining was used for measuring the change in cell density in the retina and the LGN. RESULTS. Quantitative analysis of 720 labeled α and β type RGCs showed that the cell density, body size, maximum dendritic field radius, total dendritic length, and number of branch bifurcations of dendrites decreased significantly in glaucomatous eyes compared with normal ones. The cell loss and shrinkage of dendrites in α type ganglion cells in the retina was more pronounced than that in type cells. The cell density of all kinds of cells in the retina and LGN monotonically declined with time while IOP was elevated, and cell loss was more significant in large cells than in small ones. CONCLUSION. Progressive cell loss and dendritic damage by chronic elevation of IOP in RGCs and LGN cells are more pronounced in the Y-channel (large cells) than the X-channel (small cells) in feline glaucomatous eyes. The dendritic structure changes and corresponding physiological deficits of RGCs occur before cell death and thus may provide an opportunity for clinical treatment.

The responses of X and Y type retinal ganglion cells were extracellularly recorded from the cat optic chiasm or tract before and during brief intraocular pressure (IOP) elevation. The responses of both X and Y cells to stimulus flashes decreased monotonically with increase of lOP. Y cells had significantly higher tolerance to lOP than did X cells. This systematic difference was independent of the cell's retinal position. The findings support the conclusion that during brief lOP elevation pressure-induced ischemia is the main factor causing a decrease in ganglion cell responsiveness. Our findings also suggest a means of selectively eliminating the contribution of X cells to visual function. At moderate levels of lOP elevation X cells, but not Y cells, virtually cease to function. Invest Ophthalmol Vis Sci 30: 2093-2098, 1989

Peripheral nerve injury in a limb usually causes functional reorganization of the contralateral motor cortex. However, a dynamic process of the novel transhemispheric functional reorganization in the motor cortex was found in adult rats after transferring the seventh cervical nerve root from the contralateral healthy side to the injured limb. Initially the ipsilateral motor cortex activated the injured forepaw for 5 months after the operation. Then, both hemispheres of the cortex activated the injured forepaw, and finally the contralateral cortex exclusively controlled the injured forepaw. It is concluded an extensive functional shift occurred between two hemispheres based on neural plasticity in the CNS. The experimental results of the later lesions of the ipsilateral cortex suggest that maintaining transhemispheric functional reorganization does not depend on the corpus callosum, but depends on mechanisms involving central axonal sprouting. Possible mechanisms underlying the alternative changes in cortical functions were discussed in rats and in patients having similar operations.