Recordings were made from neurons in layers II, III, and IV of rat barrel cortex. The animals were raised either from the day of birth (P0) or from P2, P4, or P7 with just the D1 vibrissa protruding on one side of the face and the contralateral side intact. Follicles were not ablated, but vibrissae were carefully removed by applying steady tension to the base of each vibrissa. Deprivation was continued until the day of recording (P30-P90), though in most cases vibrissae were allowed to regrow for 4-7 d prior to recording. The area of cortex driven by stimulating the spared D1 vibrissa was found to be enlarged in uni-vibrissae animals, but the characteristic anatomical map of the barrel field, defined by cytochrome oxidase staining, retained its normal form. In animals deprived from P0, layer IV cells outside the D1 barrel responded with short latencies (5-10 msec) to D1 stimulation, a condition never observed in normally reared animals. Short-latency responses to stimulation of regrown, deprived vibrissae were still present in layer IV despite the deprivation. Plasticity decreased rapidly in layer IV between P0 and P4 as judged by two measures: first, the percentage of cells in neighboring barrels that showed short-latency responses to D1 fell from 30% in P0 deprived animals to 18% in P2 and 13% in P4 deprived animals. Second, the percentage of cells in barrels surrounding D1 with larger responses to D1 stimulation than to stimulation of their anatomically related vibrissa also fell from 37% in P0 to 23% in P2 and 12% in P4 deprived animals. The percentage of "shifted cells" showed no further reduction in P7 deprived animals (14%). Plasticity in layers II and III showed little sign of decreasing between P2 and P7 after an initial drop between P0 and P2. Therefore, deprivation started at P4 and P7 had a far greater effect on layers II and III than on layer IV. In animals deprived from P4 onward, not only were responses to D1 stimulation greater in barrels neighboring D1 (in layers II/III), but responses were smaller to principal vibrissa stimulation. This suggests increased lateral transmission from the "experienced" barrel and a failure of vertical transmission within the "deprived" barrels. These results show that changes in the balance of experience acquired through vibrissae can affect development of connectivity in the barrel cortex. The main locus of plasticity is cortical when deprivations are started at P4 and beyond.(ABSTRACT TRUNCATED AT 400 WORDS)

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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 ...

We summarize here the results presented and subsequent discussion from the meeting on Integrating Hebbian and Homeostatic Plasticity at the Royal Society in April 2016. We first outline the major themes and results presented at the meeting. We next provide a synopsis of the outstanding questions that emerged from the discussion at the end of the meeting and finally suggest potential directions of research that we believe are most promising to develop an understanding of how these two forms of plasticity interact to facilitate functional changes in the brain.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.