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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: J Physiol. 2020 Jul 24;598(21):4969–4994. doi: 10.1113/JP280243

Table 1.

Summary of model connectivity and its manipulations performed to reproduce and predict experimental observations.

Pre-I/I Early-I Aug-E Post-I (GABA) Late-E Post-I (glycine) Drive
Synaptic Weights a1i b2i b3i b4i a5i b6i ci
1: Pre-I/I 0.15 1.0 0.5 0.7
2: Early-I 0.35 0.05 0.6 0.65
3: Aug-E 0.42b 0.3b 0.1 0.5c
4: Post-I (GABA) 0.18b 0.7c,d
5: Late-E 0.09 0.135 0.31e 0.12*
6: Post-I (glycine) 0.42b 0.6a 0.5c,d
*

increased chemosensitive drive to the late-E population is implemented as a 33% increase in the c5 synaptic weight.

a

the suppression of glycinergic transmission within the BötC is implemented as a 10% reduction in the b36 synaptic weight.

b

the suppression of GABAergic transmission within the BötC is implemented as a 10% reduction in the b23, b24, and b26 synaptic weights as well as a 15% reduction in the b43 synaptic weight.

c

the activation of glutamatergic receptors in the BötC is implemented as a 12% increase in the c3, c4, and c6 synaptic weights.

d

an increase in the excitability of specifically the GABAergic and glycinergic post-I populations of the BötC is implemented as a 5% reduction in the c4 and c6 synaptic weights.

e

the suppression of glycinergic transmission within the pFRG is implemented as an 80% reduction in the b65 synaptic weight.