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Experience-Dependent, Layer-Specific Development of Divergent Thalamocortical Connectivity.

Crocker-Buque A, Brown SM, Kind PC, Isaac JT, Daw MI - Cereb. Cortex (2014)

Bottom Line: Here, we show that, in neonates, the input to layer 6 is as strong as that to layer 4.This strengthening consists of an increase in axon branching and the divergence of connectivity in layer 4 without a change in the strength of individual connections.We propose that experience-driven LTP stabilizes transient TC synapses in layer 4 to increase strength and divergence specifically in layer 4 over layer 6.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrative Physiology, University of Edinburgh, Edinburgh, UK.

No MeSH data available.


TC EPSCs evoked by minimal stimulation do not alter with age not true. (A) Example traces (average of 20 traces) showing paired stimuli at 100 Hz at different ages. Dotted line in top trace shows peak-scaled EPSC from interleaved trails. Gray line shows subtracted trace used to calculate peak of second EPSC. (B) Summary graph showing paired-pulse ratio at 100 Hz at P3–P5, P6–P7, and P8–P9. (C) Traces from 10 consecutive trials in an L4 cell with minimal TC stimulation intensity. In this case, 3 of the 10 trials evoked an EPSC. (D) Amplitude versus time plot for the experiment shown in (C). Points show peak amplitude for individual trials. Solid line shows stimulation intensity. (E) Summary graph showing EPSC amplitude from all minimal stimulation experiments in L4 (black) and L6 (gray) cells (L4 P3–P5 37 ± 6 pA, n = 18, P6–P7 43 ± 9 pA, n = 16, P8–P9 37 ± 6 pA, n = 26; L6 P3–P5 29 ± 4 pA, n = 35, P6–P7 31 ± 4 pA, n = 40, P8–P9 27 ± 4 pA, n = 36). (F) Amplitude distributions of msEPSC amplitude in all L4 (black) and L6 (gray) cells.
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BHU031F4: TC EPSCs evoked by minimal stimulation do not alter with age not true. (A) Example traces (average of 20 traces) showing paired stimuli at 100 Hz at different ages. Dotted line in top trace shows peak-scaled EPSC from interleaved trails. Gray line shows subtracted trace used to calculate peak of second EPSC. (B) Summary graph showing paired-pulse ratio at 100 Hz at P3–P5, P6–P7, and P8–P9. (C) Traces from 10 consecutive trials in an L4 cell with minimal TC stimulation intensity. In this case, 3 of the 10 trials evoked an EPSC. (D) Amplitude versus time plot for the experiment shown in (C). Points show peak amplitude for individual trials. Solid line shows stimulation intensity. (E) Summary graph showing EPSC amplitude from all minimal stimulation experiments in L4 (black) and L6 (gray) cells (L4 P3–P5 37 ± 6 pA, n = 18, P6–P7 43 ± 9 pA, n = 16, P8–P9 37 ± 6 pA, n = 26; L6 P3–P5 29 ± 4 pA, n = 35, P6–P7 31 ± 4 pA, n = 40, P8–P9 27 ± 4 pA, n = 36). (F) Amplitude distributions of msEPSC amplitude in all L4 (black) and L6 (gray) cells.

Mentions: For LTP experiments, a pairing protocol was delivered after determining first that perforation had stabilized by monitoring series resistance then that the EPSC amplitude had been stable for at least 5 min. The pairing protocol consisted of 50 stimuli at 0.2 Hz while holding the postsynaptic cell held at 0 mV. For paired-pulse ratio, experiments 2 stimuli were delivered at 100 Hz interleaved with single stimuli at 0.2 Hz. Paired-pulse ratio was calculated as the peak amplitude of EPSC2/EPSC1. The peak of EPSC2 was determined by subtracting a peak-scaled EPSC from interleaved single-stimulus trials (see Fig. 4A). This is important for EPSCs with slow rise times when decay of EPSC1 significantly affects the observed peak of EPSC2. For minimal stimulation experiments, stimulus intensity was turned down until no EPSC was seen then increased until the minimum intensity at which an EPSC was observed. About 12–36 trials were recorded, depending on failure rate, and amplitude calculated from the peak amplitude of the average EPSC from all trials excluding failures (average of 11 ± 1 traces). Small increases in stimulation intensity typically resulted in a decrease in failure rate without a change in EPSC amplitude (see Fig. 4B), demonstrating that failures represent failures of axon stimulation. For dual minimal stimulation experiments, the intensity was that at which an EPSC was first seen in either cell. The average failure rate in these experiments of 0.47 and each experiment consisted of an average of 21 trials. The same axon was deemed to contact both cells if >65% of successes and 65% of failures were coincident. This level of coincidence was chosen as, assuming that all failures are failures of axon transmission, the false-positive rate for an experiment in which separate axons were stimulated contacting each cell would be <0.05 [given 11/21 successes and 10/21 failures in cell 1; P (≥7/11 coincident successes and ≥6/10 coincident failures in cell 2) = 0.04]. Coincident successes = 0.97 ± 0.02 when axon was deemed to contact both cells, n = 20; coincident successes = 0.11 ± 0.03 when same axon was not deemed to contact both cells. Signals were filtered at 4 kHz, digitized at 10 kHz, and stored on computer using the Signal 2 or Signal 4 software (Cambridge Electronic Design). We did not correct for junction potential. Series resistance (5–25 MΩ for whole cell, 20–50 M for perforated patch) was analyzed in the voltage clamp throughout the experiments and displayed on-line. Cells were rejected if series resistance changed by >20% during data collection. For perforated patch recordings, any sudden step change was taken as indicative of break-in and the recording discarded.


Experience-Dependent, Layer-Specific Development of Divergent Thalamocortical Connectivity.

Crocker-Buque A, Brown SM, Kind PC, Isaac JT, Daw MI - Cereb. Cortex (2014)

TC EPSCs evoked by minimal stimulation do not alter with age not true. (A) Example traces (average of 20 traces) showing paired stimuli at 100 Hz at different ages. Dotted line in top trace shows peak-scaled EPSC from interleaved trails. Gray line shows subtracted trace used to calculate peak of second EPSC. (B) Summary graph showing paired-pulse ratio at 100 Hz at P3–P5, P6–P7, and P8–P9. (C) Traces from 10 consecutive trials in an L4 cell with minimal TC stimulation intensity. In this case, 3 of the 10 trials evoked an EPSC. (D) Amplitude versus time plot for the experiment shown in (C). Points show peak amplitude for individual trials. Solid line shows stimulation intensity. (E) Summary graph showing EPSC amplitude from all minimal stimulation experiments in L4 (black) and L6 (gray) cells (L4 P3–P5 37 ± 6 pA, n = 18, P6–P7 43 ± 9 pA, n = 16, P8–P9 37 ± 6 pA, n = 26; L6 P3–P5 29 ± 4 pA, n = 35, P6–P7 31 ± 4 pA, n = 40, P8–P9 27 ± 4 pA, n = 36). (F) Amplitude distributions of msEPSC amplitude in all L4 (black) and L6 (gray) cells.
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BHU031F4: TC EPSCs evoked by minimal stimulation do not alter with age not true. (A) Example traces (average of 20 traces) showing paired stimuli at 100 Hz at different ages. Dotted line in top trace shows peak-scaled EPSC from interleaved trails. Gray line shows subtracted trace used to calculate peak of second EPSC. (B) Summary graph showing paired-pulse ratio at 100 Hz at P3–P5, P6–P7, and P8–P9. (C) Traces from 10 consecutive trials in an L4 cell with minimal TC stimulation intensity. In this case, 3 of the 10 trials evoked an EPSC. (D) Amplitude versus time plot for the experiment shown in (C). Points show peak amplitude for individual trials. Solid line shows stimulation intensity. (E) Summary graph showing EPSC amplitude from all minimal stimulation experiments in L4 (black) and L6 (gray) cells (L4 P3–P5 37 ± 6 pA, n = 18, P6–P7 43 ± 9 pA, n = 16, P8–P9 37 ± 6 pA, n = 26; L6 P3–P5 29 ± 4 pA, n = 35, P6–P7 31 ± 4 pA, n = 40, P8–P9 27 ± 4 pA, n = 36). (F) Amplitude distributions of msEPSC amplitude in all L4 (black) and L6 (gray) cells.
Mentions: For LTP experiments, a pairing protocol was delivered after determining first that perforation had stabilized by monitoring series resistance then that the EPSC amplitude had been stable for at least 5 min. The pairing protocol consisted of 50 stimuli at 0.2 Hz while holding the postsynaptic cell held at 0 mV. For paired-pulse ratio, experiments 2 stimuli were delivered at 100 Hz interleaved with single stimuli at 0.2 Hz. Paired-pulse ratio was calculated as the peak amplitude of EPSC2/EPSC1. The peak of EPSC2 was determined by subtracting a peak-scaled EPSC from interleaved single-stimulus trials (see Fig. 4A). This is important for EPSCs with slow rise times when decay of EPSC1 significantly affects the observed peak of EPSC2. For minimal stimulation experiments, stimulus intensity was turned down until no EPSC was seen then increased until the minimum intensity at which an EPSC was observed. About 12–36 trials were recorded, depending on failure rate, and amplitude calculated from the peak amplitude of the average EPSC from all trials excluding failures (average of 11 ± 1 traces). Small increases in stimulation intensity typically resulted in a decrease in failure rate without a change in EPSC amplitude (see Fig. 4B), demonstrating that failures represent failures of axon stimulation. For dual minimal stimulation experiments, the intensity was that at which an EPSC was first seen in either cell. The average failure rate in these experiments of 0.47 and each experiment consisted of an average of 21 trials. The same axon was deemed to contact both cells if >65% of successes and 65% of failures were coincident. This level of coincidence was chosen as, assuming that all failures are failures of axon transmission, the false-positive rate for an experiment in which separate axons were stimulated contacting each cell would be <0.05 [given 11/21 successes and 10/21 failures in cell 1; P (≥7/11 coincident successes and ≥6/10 coincident failures in cell 2) = 0.04]. Coincident successes = 0.97 ± 0.02 when axon was deemed to contact both cells, n = 20; coincident successes = 0.11 ± 0.03 when same axon was not deemed to contact both cells. Signals were filtered at 4 kHz, digitized at 10 kHz, and stored on computer using the Signal 2 or Signal 4 software (Cambridge Electronic Design). We did not correct for junction potential. Series resistance (5–25 MΩ for whole cell, 20–50 M for perforated patch) was analyzed in the voltage clamp throughout the experiments and displayed on-line. Cells were rejected if series resistance changed by >20% during data collection. For perforated patch recordings, any sudden step change was taken as indicative of break-in and the recording discarded.

Bottom Line: Here, we show that, in neonates, the input to layer 6 is as strong as that to layer 4.This strengthening consists of an increase in axon branching and the divergence of connectivity in layer 4 without a change in the strength of individual connections.We propose that experience-driven LTP stabilizes transient TC synapses in layer 4 to increase strength and divergence specifically in layer 4 over layer 6.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrative Physiology, University of Edinburgh, Edinburgh, UK.

No MeSH data available.