We have previously reported to the Society that in cats in which monocular retinal lesions were made in adulthood or adolescence cells in the lesion projection zone (LPZ) of area 17 recovered sensitivity to photic stimuli but the receptive fields (RFs) were now ectopic, i.e. outside the lesion (Burke et al. 2000). When the lesions were made in adult cats (AL), stimuli presented via the lesioned eye gave lower peak discharge rates and lower cut-off velocities than those presented via the non-lesioned eye. By contrast, in kitten-lesioned cats (KL) the cut-off velocities and the peak discharge rates were similar for stimuli presented via the lesioned and the non-lesioned eye. There was, however, a difference in the time from lesion to experiment between the AL and KL groups, 2-24 weeks vs. 28-68 weeks. It was, therefore, important to see if this factor could be responsible for the neural effects. Ectopic RFs are believed to be mediated via axon collaterals of pyramidal cells interconnecting mainly in laminae 2 and 3. We, therefore, also investigated the location of the LPZ neurones (supragranular (SG) - laminae 1-3: granular/ infragranular (G/I) - laminae 4-6). In addition to the two groups already described (AL 4 cats; KL 5 cats) we prepared a third group in which the lesion was made in the adult cat but the cat then survived 3.5-4.5 years (AL/L 3 cats). Retinal lesions 8-12 deg in diameter were made in cats anaesthetized with xylazine (3 mg kg-1) and ketamine (30 mg kg-1). Single neurones in area 17 were studied in cats anaesthetized with 0.5-0.7 % halothane in 67/33 N2O/O2, given gallamine triethiodide 7.5 mg kg-1 h-1 I.V. and artificially respired. EEG, ECG, end-tidal CO2, lung pressure and deep body temperature were monitored and kept within normal limits. Animals were humanely killed at the end of the experiments. In the G/I laminae we found no difference between AL and AL/L cats but a significant difference between AL/L and KL cats and between AL and KL cats with regard to peak discharge rates and cut-off velocities (Wilcoxon, P < 0.05). Thus it seems that the interval between lesion and experiment is not a critical factor. By contrast, in the SG laminae there was no difference between AL and KL cats with respect to peak discharge rates and cut-off velocities. Thus following monocular retinal lesions there appears to be a critical period for the LPZ cells recorded from the G/I layers of area 17, after which the presumed cortical mechanisms underlying establishment of ectopic RFs are not capable of good compensation for the loss of the retinal input.
Journal of Physiology: Proceedings of the Physiological Society Vol. 544.P, p. 69P--