Unbalanced synaptic inhibition can create intensity-tuned auditory cortex neurons

Intensity-tuned auditory cortex neurons may be formed by intensity-tuned synaptic excitation. Synaptic inhibition has also been shown to enhance, and possibly even create intensity-tuned neurons. Here we show, using in vivo whole cell recordings in pentobarbital-anesthetized rats, that some intensity-tuned neurons are indeed created solely through disproportionally large inhibition at high intensities, without any intensity-tuned excitation. Since inhibition is essentially cortical in origin, these neurons provide examples of auditory feature-selectivity arising de novo at the cortex.Comment: 22 pages, 5 figure

Experience-dependent plasticity in S1 caused by noncoincident inputs

Prior work has shown that coincident inputs became corepresented in somatic sensory cortex. In this study, the hypothesis that the corepresentation of digits required synchronous inputs was tested, and the daily development of two-digit receptive fields was observed with cortical implants. Two adult primates detected temporal differences in tap pairs delivered to two adjacent digits. With stimulus onset asynchronies of >= 100 ms, representations changed to include two-digit receptive fields across the first 4 wk of training. In addition, receptive fields at sites responsive to the taps enlarged more than twofold, and receptive fields at sites not responsive to the taps had no significant areal change. Further training did not increase the expression of two-digit receptive fields. Cortical responses to the taps were not dependent on the interval length. Stimuli preceding a hit, miss, false positives, and true negatives differed in the ongoing cortical rate from 50 to 100 ms after the stimulus but did not differ in the initial, principal, response to the taps. Response latencies to the emergent responses averaged 4.3 ms longer than old responses, which occurs if plasticity is cortical in origin. New response correlations developed in parallel with the new receptive fields. These data show corepresentation can be caused by presentation of stimuli across a longer time window than predicted by spike-timing-dependent plasticity and suggest that increased cortical excitability accompanies new task learning

Somatotopically inappropriate projections from thalamocortical neurons to the SI cortex of the cat demonstrated by the use of intracortical microstimulation

Single thalamocortical neurons with receptive fields on the toes were antidromically activated by the passage of 300-microseconds, 0.5- to 10-microA pulses through glass micropipette electrodes placed within somatotopically identified regions of the digit representation of the cat first somatosensory (SI) cortex. The somatotopy of the cortex was determined using recordings from single cortical neurons (see "Methods"), and the positions of the all tracks were marked on an enlarged photograph of the postcruciate cortex. In two of the three protocols, a very precise map of the boundary between two adjacent toes was produced prior to attempting intracortical microstimulation. Slopes of the threshold-distance curves at the sites of the lowest recorded thresholds were on the order of 0.8 microA/10 micron. This value, together with information on the anatomy of the cortical arborizations of thalamocortical neurons (Landry and Deschenes, 1981), suggested that currents of 2 and 5 microA would not activate the cortical processes of thalamocortical neurons at distances greater than 50 and 90 microns, respectively. With currents below 5 microA, thalamocortical neurons could be antidromically activated at a number of sites at depths between 340 and 930 microns (layer IV and upper layer III) and between 1,050 and 1,460 microns (layer VI). A total of 13 thalamocortical neurons could be antidromically activated using current pulses of between 0.8 and 5.0 microA, from within tracks at tangential distances of 250-830 microns from the nearest track through the somatotopically appropriate region. Within somatotopically inappropriate regions, cortical neurons frequently had receptive fields on a toe adjacent to that bearing the receptive field of the thalamic neuron(s) under study. The possible relationship of somatotopically inappropriate projections to the reorganization of cortical somatotopy following digit amputation, paw amputation, and nerve section is discussed

Perceptual learning and sensomotor flexibility: cortical plasticity under attentional control?

Recent research reveals long-lasting cortical plasticity of early sensory cortices even in adults. Sensory signals could be modified under top-down control if necessary quite early in order to optimize their signal-to-noise ratio, leading to ‘low level’ or ‘early’ perceptual learning (PL). For easy tasks, such elaborate top-down influences are usually not required, and learning is restricted to late selection of the appropriate signals on higher cortical levels, which seems easier and faster to achieve. But to reach the absolute limits of sensory performance, PL seems to optimize the entire chain of sensory processing. Hence, improvement for these extreme perceptual abilities is quite specific for a number of stimulus parameters, such as the position in the visual field and sometimes even the trained eye, reflecting the specificity of receptive fields in early sensory cortices. Early PL may be just one example—even if a very extensive one—of the mechanisms of neuronal plasticity and sensomotor flexibility that are constantly updating our sensomotor representations as a result of experience. As an illustration, this review contains some new experimental results on PL and sensory flexibility in the context of adaptation to multifocal intraocular lenses