Time course of experience-dependent synaptic potentiation and depression in barrel cortex of adolescent rats.

1. Plasticity could be induced in (S1) barrel cortex of adolescent rats by reducing the complement of vibrissae on one side of the muzzle to a single whisker for a period of 7, 20, or 60 days. The effect of deprivation was assessed by quantitatively by measuring cortical responses to stimulation of the spared and regrown deprived vibrissae. Vibrissa responses were evoked using a standard stimulus generated by an electromechanical stimulator and measured using poststimulus time histogram analysis. 2. Cells located in layers II/III were found to be plastic beyond postnatal day 28 (P28), whereas cells located in layer IV were not. The vibrissa dominance distribution was shifted significantly toward the spared vibrissa after 7, 20, and 60 days of deprivation for cells located in layers II/III of barrel columns surrounding the D1 column (P < 0.0001, 2-factor analysis of variance). The vibrissa dominance distribution did not shift significantly for cells located in layer IV of surrounding barrels for any of the durations of deprivation tested (P > 0.1). After 7 days of deprivation, 37% of the cells located in layers II/III of the columns deprived vibrissae showed greater responses to the spared vibrissae than to their deprived principal vibrissa, compared with 11% in normally reared adolescent animals and 3% in adults. The percentage of cells dominated by the spared vibrissa was 65% after 20 days of deprivation and 43% after 60 days. 3. For cells located in layers II/III, short-term deprivation (7 days) caused a decrease in the absolute magnitude of response to stimulation of the deprived vibrissa (reduction to approximately 28% of control levels). However, no change could be detected in the spared (D1) vibrissa input to the same deprived columns. Therefore the increase in D1 dominance registered in the deprived columns was mainly due to a decrease in principal vibrissa response and no change in the spared D1 vibrissa response. 4. The first increase in spared vibrissa response was seen after 20 days of deprivation. The response magnitude cells located in layers II/III increased to 70% above control levels. Responses to deprived vibrissa stimulation were depressed at 20 days of deprivation (reduction to 35% of control), implying that the vibrissa dominance shift at 20 days was due to both an increase in spared vibrissa response and a decrease in deprived vibrissa response. 5. The spared vibrissa response was increased after 60 days of deprivation (110% above control) in both near and far halves of the barrel columns surrounding D1. On average, the deprived vibrissa response was depressed at 60 days (84% of control), although less than at 20 or 7 days, because of recovery of responsiveness in the far half of the deprived barrel column. Layer II/III cells located in the half of the barrel column farthest from the spared D1 barrel column showed normal levels of deprived vibrissa input, whereas cells located in the half of the barrel column closest to the spared D1 barrel column still exhibited depressed levels of deprived vibrissa input (54% of control). 6. Control experiments suggested that depression of the deprived vibrissa response could not be explained by nonspecific effects. Depression was not a function of animal's age, because normally reared P28 and adult animals showed similar principal vibrissa response levels. It was not a result of nonspecific depression of cortical responses. because the decreased response only occurred in cells of deprived barrel columns and not spared barrel columns (recorded in the same animals). Depression was not due to altered vibrissa mechanics, because the spared vibrissa response was similarly depressed in animals in which the vibrissae had been trimmed rather than removed. Finally, depression was input specific at 7 and 20 days, because only the deprived vibrissa responses were depressed, whereas spared vibrissa responses were either at control levels or at elevated levels for the same cells. 7.