The same plasticity rule rescues networks built from one conductance set and destabilises networks built from another
- 1Luviner
Abstract
Whether synaptic plasticity stabilises or destabilises a recurrent circuit is usually treated as a question about the rule. We find that in a conductance-based model it is not answered by the rule alone. The model is a simulated bursting culture: 48 excitatory and 12 inhibitory stomatogastric-ganglion neurons, sparsely and recurrently connected. The recurrent synapses carry pair-based spike-timing-dependent plasticity under a fixed homeostatic budget on each cell's total incoming excitatory conductance. We ran one net-depressing rule, at one inhibition level, on unselected random wirings, with a survival criterion fixed before the runs. Two excitatory populations built from different published conductance sets gave opposite outcomes. In one, the network collapsed without the rule in 33 of 36 wirings and the rule rescued 31 of those 33. In the other, the network survived without the rule in 11 of 12 wirings and the rule eliminated 6 of those 11. The only model parameter changed between the two is the excitatory conductance set, and that change also alters their intrinsic dynamics. We then asked what carries the reversal. Across seven conductance sets, elimination increases with a cell's own firing rate, and cell identity does not predict it: a follower-type cell firing at pacemaker rates behaves like a pacemaker. But moving the firing rate inside a single set by injected current reverses the same quantity, which rules out firing rate as a sufficient explanation. Substituting one conductance at a time from the rescued set into the other, over the six channels that differ, no single substitution transferred the rescue (2 of 42 pooled) while substituting all eight did so in 6 of 6 (Fisher exact p = 2.3 x 10^-6). The sign reversal cannot be attributed to any single tested conductance, and firing rate alone cannot account for it. All results are computational and concern one circuit model, one plasticity rule and one homeostatic constraint. Predictions and falsifiers were committed to a version-controlled record before the corresponding runs, with three departures from that order recorded in the manuscript's pre-registration index.
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BibTeX
@misc{groppi2026same,
title = {{The same plasticity rule rescues networks built from one conductance set and destabilises networks built from another}},
author = {F. Groppi and J. Ferrari},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.15.751713},
url = {https://www.biorxiv.org/content/10.64898/2026.09.15.751713v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - The same plasticity rule rescues networks built from one conductance set and destabilises networks built from another
AU - F. Groppi
AU - J. Ferrari
PY - 2026
DA - 2026/09/15
PB - bioRxiv
DO - 10.64898/2026.09.15.751713
UR - https://www.biorxiv.org/content/10.64898/2026.09.15.751713v1
AB - Whether synaptic plasticity stabilises or destabilises a recurrent circuit is usually treated as a question about the rule. We find that in a conductance-based model it is not answered by the rule alone. The model is a simulated bursting culture: 48 excitatory and 12 inhibitory stomatogastric-ganglion neurons, sparsely and recurrently connected. The recurrent synapses carry pair-based spike-timing-dependent plasticity under a fixed homeostatic budget on each cell's total incoming excitatory conductance. We ran one net-depressing rule, at one inhibition level, on unselected random wirings, with a survival criterion fixed before the runs. Two excitatory populations built from different published conductance sets gave opposite outcomes. In one, the network collapsed without the rule in 33 of 36 wirings and the rule rescued 31 of those 33. In the other, the network survived without the rule in 11 of 12 wirings and the rule eliminated 6 of those 11. The only model parameter changed between the two is the excitatory conductance set, and that change also alters their intrinsic dynamics. We then asked what carries the reversal. Across seven conductance sets, elimination increases with a cell's own firing rate, and cell identity does not predict it: a follower-type cell firing at pacemaker rates behaves like a pacemaker. But moving the firing rate inside a single set by injected current reverses the same quantity, which rules out firing rate as a sufficient explanation. Substituting one conductance at a time from the rescued set into the other, over the six channels that differ, no single substitution transferred the rescue (2 of 42 pooled) while substituting all eight did so in 6 of 6 (Fisher exact p = 2.3 x 10^-6). The sign reversal cannot be attributed to any single tested conductance, and firing rate alone cannot account for it. All results are computational and concern one circuit model, one plasticity rule and one homeostatic constraint. Predictions and falsifiers were committed to a version-controlled record before the corresponding runs, with three departures from that order recorded in the manuscript's pre-registration index.
ER -