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All in vitro data are expressed as means ± SEM, all in vivo data as means ± SD.
In vitro data were compared using a one-way ANOVA.
The model is suggested by in silico experiments and is validated using in vitro data.
The cells were characterized by cell surface immunophenotyping, as well as in vitro (data not shown).
We developed a CA1 pyramidal cell model calibrated with a broad spectrum of in vitro data.
To corroborate the in vitro data, we also examined the effect of PRR7 gene deletion in vivo on excitatory synapses.
However, our in vitro data clearly show that primary myoblasts express Col25a1 transcripts as they proliferate and differentiate (Fig. 2).
Our in vitro data prompted us to measure the infection of PIM/AM-like cells during in vivo PRRSV infection.
However, metabolic labeling of mitochondrial protein synthesis in human cells is at odds (Fig. 1c) with the in vitro data.
Thus, we derived a complete model of dopamine and spike-timing dependent cortico-striatal plasticity from in vitro data.
Such differences in operating conditions can compromise extrapolation of in vitro data to explain neuronal operation in vivo.
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