Correlative intracellular recording and electron microscopy reveals not only that a single thalamic excitatory postsynaptic potential in a cortical neuron can be sufficient to discharge the cell but also that the number of thalamic boutons received by a cortical cell may in fact represent no more than about 5% of its total complement of synapses (Peters and Payne 1993; Douglas and Martin 2004).
Fluorescence microscopy revealed that DB75 did not penetrate into brain parenchyma, however, but was sequestered within cells lining the blood brain and blood cerebrospinal fluid barriers.
Immunoelectron microscopy revealed that anti-S-T1FimH 1-25 C anti-S-T1FimH 1-25 C anti-S-T1FimH 1-25 C anti-S-T1FimH 1-25 Cof E. coli at the fimbutal tips anotat anti-S-T1FimG 1-16 anti-S-T1FimG 1-16 anti-S-T1FimG 1-16 anti-S-T1FimG 1-16
EMSA and immunofluorescence microscopy revealed that Nef does not affect the quantity of nuclear p65.
Differential interference contrast (DIC) microscopy revealed that activated (but not quiescent) macrophages engulfed SWCNTs (129 + 12.7 particles per cell and 2.7 + 0.2 particles per cell, respectively).
High-resolution confocal microscopy revealed that Rgs16::GFP is not expressed in normal acinar cells, consistent with fluorescence microscopy of dissected pancreata (Figs 1, 2).
Interestingly, visualization by confocal microscopy revealed that paxillin and vinculin not only localized to FA but also to podosome-like adhesion rings surrounding actively degrading cortactin- or actin-containing invadopodia (Fig. 1A,B; supplementary material Fig. S1).
Immunocytochemistry and fluorescence microscopy revealed that untreated cells did not show more than 1 or 2 centrosomes, with the exception of the HCTp53KO cells which showed 7% of cells with more than 2 centrosomes.
Moreover, immunofluorescence microscopy revealed that 11-oxo-ETE not only inhibited BrdU incorporation into the HUVECs but also caused a dramatic change in the shape and morphology of these cells.
Although confocal microscopy revealed that N-glycosylation was not required to target AC8 to the PM (Fig. 4 B ), fractionation studies showed that, unlike AC8, the AC8 N-glycosylation-deficient mutant was excluded from lipid rafts (Fig. 4 C ).
