Signaling models for dopamine-dependent temporal contiguity in striatal synaptic plasticity
Fig 2
Requirements of AC1 coincidence detection in the D1 RP model.
(A) Schematics of PKA signaling in the somas and spines. The symbol ⨂ denotes the product of two inputs. (B) Spine PKA activity (AKAR2-CR) highly correlates with spine enlargement (r = 0.94, Spearman's correlation coefficient) [4]. From Yagishita et al., Science 26 Sep 2014:Vol. 345, Issue 6204, pp. 1616–1620 (DOI:10.1126/science.1255514). Reprinted with permission from AAAS. (C) Time courses of PKA activity in the experiment (left; DA delay: 0.6 s) [4] and model (right; DA delay: 1 s). From Yagishita et al., Science 26 Sep 2014:Vol. 345, Issue 6204, pp. 1616–1620 (DOI:10.1126/science.1255514). Reprinted with permission from AAAS. (D) Critical time windows for PKA activity in the experiment and model (left and right, respectively). The peak amplitudes of active AKAR2-CR (left) and PKA-free catalytic subunits (right) were plotted. (E) DA-delay dependence of PKA activity. Gray shaded area denotes the periods of pre–post pairing, and red shaded area indicates the periods of DA bursts.
doi: https://doi.org/10.1371/journal.pcbi.1008078.g002