We emphasize that these high-frequency oscillations represent the harmonic signal, i.e., they have the same profile as the stimulation signal and differ considerably from the profile of the action potential of the free neuron.
This pial (outer) localization of centrosome and Golgi in vivo also occurred when axon-free neurons were migrating towards the pial side; these organella existed at the base of the leading process.
Scanning electron microscopy with energy-dispersive x-ray spectrometry was used to analyze the elemental content of neurofibrillary tangle (NFT -bearing aNFT -bearingneurons within the Sommer's sector (H1 region) of the hippocandus in Guamanian Chamorros with amyotrophic lateral sclerosis aneuronsinsonism-dementia and in neurologically normal controls.
With this completely xeno-free ES-ACM, xeno-free neurons and astrocytes can repeatedly be produced.
When the neurite-free neurons received larger mechanical force as the indentation was closer, they may have a larger change in membrane potential.
Nevertheless, the neurite-free neurons only altered less than 10 mV of membrane potential when the indentation was displaced in 30 µm distance (Fig. 4).
In contrast, for neurite-free neurons, neither was an AP evoked nor was membrane potential altered during the application of mechanical stimulation at a 100 µm distance from the soma (Fig. 3).
Although glia cells and neurons were side-by-side on PDMS substrate (Fig. 2), when the indentation was displaced adjacent to glia cells, no AP was induced in neurite-free neurons in D2, D1+F, and D2+F groups.
Furthermore, previous studies investigating the molecular mechanisms of mechanotransduction in sensory neurons (by adopting neurite-free neurons to stimulate nerve terminals) used mechanical forces such as compression and hypo-osmotic stretch [5], [6].
Even when the indentation was close to the soma (within 30 µm), the mechanical stimulation only caused limited changes of membrane potential (<10 mV) for neurite-free neurons (Fig. 4).
In the same study, quantitative RT-PCR analysis of AD and control hippocampal neurons, revealed that the expressions of BDNF and TrkB in AD were equally low in Aβ-containing and Aβ-free neurons and lower than that in control brains[24].
