Specialized representations in visual cortex: a role for binding?
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Animals↗
Biomedical subjects
J Maunsell
Publications and source records attributed to J Maunsell.
On the relationship between synaptic input and spike output jitter in individual neurons.
What is the relationship between the temporal jitter in the arrival times of individual synaptic inputs to a neuron and the resultant jitter in its output spike? We report that the rise time of firing rates of cells in striate and extrastriate visual cortex in the macaque monkey remain equally sharp at different stages of processing. Furthermore, as observed by others, multiunit recordings from single units in the primate frontal lobe reveal a strong peak in their cross-correlation in the 10-150 msec range with very small temporal jitter (on the order of 1 msec). We explain these results using numerical models to study the relationship between the temporal jitter in excitatory and inhibitory synaptic input and the variability in the spike output timing in integrate-and-fire units and in a biophysically and anatomically detailed model of a cortical pyramidal cell. We conclude that under physiological circumstances, the standard deviation in the output jitter is linearly related to the standard deviation in the input jitter, with a constant of less than one. Thus, the timing jitter in successive layers of such neurons will converge to a small value dictated by the jitter in axonal propagation times.
Action Potentials↗
Magnocellular or parvocellular lesions in the lateral geniculate nucleus of monkeys cause minor deficits of smooth pursuit eye movements.
The effects of unilateral LGN lesions, made with ibotenic acid, on smooth pursuit eye movements were studied in two monkeys (Macaca nemestrina). Both monkeys received unilateral magnocellular (M-) layer lesions 18 months before the study and one monkey received a parvocellular (P-) lesion during the study on the side opposite the magnocellular lesion. The lesions did not affect the accuracy of saccades to stationary or moving targets, but the latencies of saccades to targets in the M-layer lesioned hemifields were significantly longer. Neither M- nor P-layer lesions affected the earliest interval (0-50 msec) of pursuit initiation, but during later intervals (50-150 msec), eye acceleration was less for pursuit initiation in the lesioned hemifield compared to the control hemifield. M-layer lesions created larger deficits in ocular acceleration than P-layer lesions. All deficits, however, were relatively small and accurate pursuit speeds were achieved near the time of the initial "catch-up" saccade. If both M and P layers representing the same part of the visual field were destroyed, the monkey was unable to locate the target or initiate smooth pursuit eye movements. We conclude that smooth pursuit initiation receives contributions from both the M- and P-layers of the LGN and either of these inputs can support pursuit initiation.
Animals↗