Target membrane time constants reduced log decay prediction error by 5.1% in a fixed ridge test of 650 mouse cortical connections
We tested whether a target cell membrane time constant helps predict the decay of a measured synaptic voltage response. We used the Allen Synaptic Physiology r2.1 small database. The main panel had 650 mouse V1 connections from 233 inferred donor groups. A nested ridge test excluded whole donor groups from training. The baseline used current kinetics, cell labels, and distance. Adding target membrane time reduced squared log decay error from 1.30508 to 1.23884, or 5.08%. A 10,000-draw donor range with predictions fixed was 0.47% to 9.45%. A later 1,000-draw check that refit the models gave a range from 0.0011% to 9.35%; the lower endpoint was effectively zero at this precision. On the same 644 connections, the gain fell from 4.73% to 0.86% after input resistance adjustment. The refitting range for the adjusted gain was -1.11% to 2.80%. A secondary human panel of 172 connections gave a gain of -0.04%. Removing fits near default limits gave an uncertain mouse gain. All selected stored kinetic fields matched accepted component-fit aggregation exactly. These results concern selected local recording graphs and a fixed model family. They do not establish a general membrane mechanism or a species effect. The package preserves original code, source hashes, selection IDs, coefficients, predictions, loss tables, bootstrap draws, figures, and repeat instructions. Original source measurements remain external.
synaptic physiology · membrane time constant · temporal integration · cortical circuits · structure and function · group validation · ridge regression · reproducible research
References
4- usesdoi:10.1126/science.abj5861
We use the public Allen Synaptic Physiology r2.1 small database from this study. All measurements are extracted again from the hash-checked original file.
- supportsdoi:10.1152/jn.1967.30.5.1138
This prior cell theory explains why target cell properties can alter synaptic potential time courses. We do not claim a new passive circuit law.
- usesA passive current filter gave no clear voltage prediction gain in 197 mouse V1 excitatory connections from Allen r2.1 sci:sha256:8c700a70e37fc5c4a8a4d92530bb5d12eb4e6461c1b761608d9408ac68f1b60a
We follow its pinned database version and inferred donor naming rule. Its outcome was voltage amplitude. Our new outcome is voltage decay, and no prior predictions or result tables are reused.
- supportsAll 14,313 numeric pulse amplitude arrays in Allen Synaptic Physiology r2.1 were flat, and a shared list reproduced the loss of pulse order sci:sha256:989c63646cdf418f9663cb5767fc90245c7cf15182f746f5bef2e1e419d97342
This audit motivates avoiding stored pulse-order arrays. We use separate scalar kinetic fields and verify their accepted-fit aggregation.
Cited by
4 publicationsPublic catalog entries on Sciscape.
- usesA fixed rule gave no clear decay prediction gain from other inputs to the same target in 152 mouse V1 connections
We use its source version, source interpretation, and mouse naming rule. We wrote new code for a different prediction task.
- A membrane time constant matching term gave no clear added gain in a logistic test of 8,667 mouse cortical directions
This prior test links target membrane timing to voltage decay at detected connections. The present study tests connection detection. No code or results were reused.
- usesWith measured membrane times and nonnegative input, a passive one-compartment model needed over 5% changes in 73 of 242 mouse V1 fits within recorded windows
We use its source version records, donor grouping convention, and interpretation of fitted kinetic fields. We extract the data again and test a different question.
- usesReverse decay gave no clear inhibitory decay prediction gain in fixed ridge tests of 114 reciprocal mouse V1 pairs
This prior study supplied the pinned source version, donor naming rule, scalar aggregation audit and default-fit-limit definitions. We independently extract the source and test reverse-edge decay.