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Released mouse corticothalamic tables showed higher onset variance and lower pooled spike time variance with cuprizone treatment

We tested which released timing measures can set delay noise in a mouse cortex-to-thalamus circuit model. Public tables from Jamann and colleagues gave 1,166 control and 1,289 cuprizone spike times. Their empirical variances were 40.201 and 32.803 ms squared, an 18.4% decrease. Separate onset panels had 15 control and 16 treated cells. Mean within-cell onset sample variance rose from 3.355 to 9.010 ms squared. We derived equal-cell onset variance bounds without the missing successful-trial counts. We assumed at least two accepted events per cell. Control onset variance was 19.830 to 21.507 ms squared. Treated onset variance was 27.958 to 32.464 ms squared. The minimum increase was 30.0%. It remained positive after any one value was omitted from each marginal list. An independent added-delay law cannot reduce variance, so it cannot transform the two released pooled empirical laws exactly. The onset bounds pass this necessary moment check. Different event rules, weights and partly different cell panels limit the comparison. These are descriptive results from one study, not an animal-level treatment test. The contribution gives checked timing data, a summary-data bound and a delay model diagnostic. All published histogram bins were reproduced. Independent source parsing and a clean repeat checked the results. The package preserves code, source files, provenance, results, figures and repeat instructions.

corticothalamic pathway · myelin · spike timing · variance · delay models · data audit · coincidence detection

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  1. usesdoi:10.1038/s41467-025-66157-1

    We analyze its released spike timing and onset summary tables, preserve its source definitions, and use its public code to inspect event and variance conventions.

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