The directional bias in a 2D slice varies depending on the depth of the slice in the oocyte, ranging from 50.7% of posteriorly oriented MT segments at the cortex to 60.6% in the mid plane.
The concentration of Aβ in the slice approached the concentration in the ACSF within 30 minutes (monomer) to 1 hour (24mer) throughout the depth of the slice (figure 10B and 10C).
The depth of each slice is marked in the upper left corner of each P-wave panel.
The tissue concentrations (averaged throughout the depth of the slice) of monomer and 24mer both declined rapidly towards steady-state concentrations (figure 8A).
With a half-life of 0.64 hours, the normalized tissue concentrations of Aβ (averaged throughout the depth of the slice) were 0.16 and 0.36 for monomer and 24mer, respectively (figure 7C).
Scale to the left indicates the depth of each slice in microns, relative to an image of the hippocampal surface.
Layer IV/V neurons were imaged (from surface to the depth of the slice) in regular aCSF + 1 μM TTX (selective inhibitor of Na+ channels) to avoid spontaneous epileptiform activity that can cause Cl− accumulation.
Exponential fitting was applied to correct for the reduction in fluorescence intensity toward the center of the brain slice due to decreasing antibody penetration as well as the additional reduction imposed by light scattering and light absorption over the complete depth of the slice.
A higher [Cl−]i has been associated with cutting trauma in brain slices, 52 but as shown in Figure 1F, the high [Cl−]i in younger slices extends throughout all depths of the slice and therefore cannot be attributed to trauma.
Confocal micrographs (Figs. 2, 3, 6, 7D, S1, S2) were obtained on a Zeiss LSM510 Axiovert 200 M microscope, with ∼1 2 µm depth of field (optical slice).
Approximately 5 neurons within 100 200 μm depth from the surface of slice were injected.
