Separable actions of acetylcholine and noradrenaline on neuronal ensemble formation in hippocampal CA3 circuits
Fig 2
The mechanism of carbachol and noradrenaline action on excitatory and inhibitory feed-forward mossy fiber transmission determined by short-term plasticity models.
A) Irregular stimulation protocol modelled on naturalistic granule cell spike patterns. GC spike patterns recorded in vivo during a spatial memory task, with a bimodal inter-spike interval (ISI) distribution (top right). Bimodal ISI distribution modelled as a doubly stochastic Cox process (middle right), with irregular stimulation protocol a sample drawn from this process (bottom right). B-C) Experimentally recorded EPSCs and IPSCs evoked by irregular stimulation protocol in hippocampal slices under control or presence of 5 μM CCH or 20 μM NA. Evoked peaks highlighted by white dots. The same example burst is shown on expanded timescales. D) Tsodyks-Markram short-term plasticity model schematic illustrating facilitating (f) and depressing (d) presynaptic components with time constants (τf, τd) and postsynaptic scaling factor (g). E-F) Model selection and fitting for EPSCs (E) and IPSCs (F). Left: AIC and BIC weights for each fitted model. Model selection by highest AIC and BIC weights and evidence ratios. Right: Modulation by CCh or NA assessed by effect on parameter fits normalized by time-matched control. Error bars are standard deviations, * denotes significant parameter change.