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. Author manuscript; available in PMC: 2009 Jun 22.
Published in final edited form as: Nat Neurosci. 2008 Jun 22;11(7):807–815. doi: 10.1038/nn.2145

Figure 6. Altered distribution and dynamism of surface AChRs associated with AChR loss after axotomy.

Figure 6

(a) Confocal reconstruction of the surface AChRs (red) and nerve terminal (green) of a ganglion cell 24 h after axotomy. (b) AChRs (red in a), pseudocolored, from the boxed region in a. Synaptic AChRs (circle) appear dimmer than nonsynaptic AChR clusters (square). (c) Pooled data from multiple experiments depicting the half-time of FRAP recovery for synaptic AChRs (S) and nonsynaptic AChRs (N) for control cells (black bars) versus cells 24 h after axotomy (gray bars). Error bars, s.e.m. (d) Confocal stack of a postganglionic neuron 48 h after axotomy. Dim BTX labeling (red) can still be found apposed to presynaptic terminals (green). Inset, enhanced image of BTX labeling from the boxed region in the upper left position of d shows remaining AChRs. (e) Time-lapse imaging of BTX-labeled AChRs 36 h after axotomy shows disequilibrium between removal and insertion of AChRs. (f) Fluorescence decay and relabeling intensity in a control ganglion cell. In control (f) and axotomized cells (e), surface labeling grew dim over the course of hours (compare the first images at time 0 to the second images taken 6 h 30 min later). However, after axotomy, relabeling of newly inserted AChRs produced only a small increase in receptor fluorescence (see 6:45 + relabel), whereas fluorescence intensity recovered to initial levels in control cells (see 6:50 + relabel). Scale bars, 5 µm in all images.