In cells showing delayed initiation of Ca2+ transients with field stimulation, action potential onset was delayed and the rate of rise was slower than in healthy cells.
By using an MEA to robustly detect and track changes in the propagation of electrically evoked action potentials, we found that variation of a low frequency patterned stimulation modulated action potential propagation delays and amplitudes.
We first determined that neuronal afferent stimulation elicits action potential-dependent currents in VTA astrocytes (Fig. 1, and Supplementary Fig. 1).
Although recorded at different time points, the stitched-together configurations were compatible because voltage stimulation evoked action potentials reliably with high precision, time-locked to the downswing of the biphasic stimulation pulse4.
As shown in these experiments, patterning of cardiac myocyte monolayers solved several inherent problems of multielectrode recordings, increased the temporal resolution of conduction velocity measurements, and made the synchronization of external stimulation with action potential propagation possible for refractory period measurements.
Vrest resting membrane potential, Vthresh threshold potential, Vmin minimum of membrane potential drop, Vss steady‐state membrane potential under long‐lasting hyperpolarizing stimulation, APampl action potential amplitude.
Optical stimulation evoked action potentials in CINs and produced postsynaptic responses in medium spiny neurons that were blocked by glutamate receptor antagonists.
Li et al (2009 [20] showed that an ER localized PC1 fragment, QIF38 (identical to our P100), directly associates with IP3R to inhibit Ca2+ release from ER stores upon IP3 stimulation, an action that results in attenuated responses to exogenous ATP application in MDCK cells [20].
We therefore suggest repeating at least some of the key experiments using stimulation by action potentials (at least for Figure 1).
As AMPA receptor stimulation generates action potentials that result in increased pre-synaptic calcium concentrations, evoking vesicle release [ 20], we hypothesized a role for calcium in regulating neuronal tau release.
