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We constructed average histograms from responses evoked by flashing stimuli and noted previously described variations in the shape of the response profile, particularly with respect to sharpness of the peak. To express this variable, we measured the half-rise latency, which is the latency from stimulus onset required to reach half the maximum response. A short half-rise latency, which is characteristic of nonlagged cells, is associated with a brisk response and sharp peak; a long half-rise latency, characteristic of lagged cells, is associated with a sluggish response and broad peak. Nonlagged cells were readily seen; we attempted to identify cells with long latencies as lagged, but we were unable to do so unambiguously due to failure to observe lagged properties other than latency. We thus refer to these latter cells as having “lagged-like” responses to indicate that we are not certain whether these are indeed lagged cells. In addition to the histograms, we analyzed the individual response trials that were summed to create each histogram, and we used spike density analysis to estimate the initial response latency to the flashing spot for each trial. We found that lagged-like responses were associated with more variability in initial response latency than were nonlagged responses. We then employed an alignment procedure to eliminate latency variation from individual trials; that is, responses during individual trials were shifted in time as needed so that each had a latency equal to the average latency of all trials. We used these “aligned” trials to create a second, “aligned” response histogram for each cell. The alignment procedure had little effect on nonlagged responses, because these were already well aligned due to consistent response latencies amongst trials. For lagged-like responses, however, the alignment made a dramatic difference. The aligned histograms looked very much like those for nonlagged responses: the responses appeared brisk, with a sharply rising peak that was fairly high in amplitude. We thus conclude that the slow build up to a relatively low peak of firing of the lagged-like response histogram is not an accurate reflection of responses on single trials. Instead, the sluggishness of lagged-like responses inferred from average response histograms results from temporal smearing due to latency variability amongst trials. We thus conclude that there is relatively little difference in briskness between nonlagged and lagged-like responses to single stimuli.

Previous studies have shown that functional compensation is present in the cat's posteromedial lateral suprasylvian (PMLS) area of cortex after damage to areas 17, 18, and 19 (visual cortex) early in life but not after damage in adults. These studies all have investigated animals with a unilateral visual cortex lesion, whereas all behavioral studies of compensation for early visual cortex damage have investigated animals with a bilateral lesion. In the present experiment, we investigated whether functional compensation also is present in PMLS cortex after a bilateral visual cortex lesion early in life. We recorded from single neurons in the PMLS cortex of adult cats that had received a bilateral lesion of areas 17, 18, and 19 on the day of birth or at 8 weeks of age. We found that PMLS cells in both groups of cats had functional compensation (normal direction selectivity and ocular dominance) similar to that seen after a unilateral lesion at the same ages. These results are consistent with the hypothesis that PMLS cortex is involved in the behavioral compensation seen after early visual cortex damage. In addition, the results indicate that inputs from contralateral visual cortex are not necessary for the development of functional compensation seen in PMLS cortex.

Prolonged periods of monocular paralysis alter the physiology of the dorsal lateral geniculate nucleus (LGN), shifting the X/Y cell ratio so that X cells are encountered less frequently than Y cells. The shift in the LGN X/Y cell ratio is observed in both the A-layers of both geniculates whether the innervating eye is paralyzed or mobile. This change in the LGN has been attributed to a mechanism that is sensitive to disruptions in binocular cues. The effects of monocular paralysis in the LGN were used to demonstrate that LGN cells possess a sensitivity to binocular cues of an extraretinal and retinal source. The removal of extraretinal signals, in the form of proprioceptive feedback from the extraocular muscles of the mobile eye, by section of the ophthalmic branch of the Vth cranial nerve, resulted in an immediate and long-lasting reversal in the effects of monocular paralysis. The LGN X/Y ratio was restored to a normal value in the layers innervated by the eye with intact proprioceptive inputs as well as in the layers innervated by the eye in which proprioceptive inputs were removed. In contrast to this, the removal of proprioceptive inputs from the paralyzed eye had no effect on the LGN X/Y ratio. The removal of visual inputs from the mobile eye by section of the optic nerve resulted in an immediate, but somewhat transient reversal in the effects of monocular paralysis. Within the first 25 h after optic nerve section, the LGN X/Y ratio was restored to a normal value in the layers innervated by the eye with intact visual inputs. A transient reversal was also observed when both visual and proprioceptive inputs from the mobile eye were removed. These results are consistent with the belief that the LGN is one site in the visual pathway where proprioceptive and visual signals from the two eyes converge.

Adult-onset stimulus modifications, such as monocular paralysis, alter the physiology of the lateral geniculate nucleus (LGN), reducing the encounter rate for X-latency cells in all of the principal layers of both LGNs whether the innervating eye is paralyzed or mobile. These reductions in encounter rate for X-latency cells are confined to those portions of the LGN representing central binocular visual space and are sensitive to the level of anesthesia in that, while these effects are evident in subjects sedated during recording, no such reductions are found when subjects are anesthetized with sodium pentobarbital during recording. Finally, conduction velocity and receptive field classification data from these experiments confirm, as the shifts in OX latency distributions would indicate, that chronic monocular paralysis does have a selective impact upon the recordability of LGN X-cells. These observations together with earlier ones involving monocular paralysis suggest that this adult-onset modification reduces the encounter rate for X-cells by disrupting a binocular mechanism which controls the relative excitability of X- and Y-cells which represent central visual space.