FIGURE 1.

Blocking sodium channels and the reverse mode of NCX at the site of injury prevents axotomy-induced spine loss. (A) Inverted gray scale images of 15 DIV rat hippocampal neurons cultured within microfluidic devices that were retrogradely labeled using G-deleted mCherry rabies virus added to axonal compartment. (B) Representative images of dendrites before and 24 h after axotomy treated with either vehicle or reversible NCX blocker (KB-R7943; 10 μM). Asterisks indicate eliminated spines. Scale bars, 5 μm. (C,D) Quantification of dendritic spine density before and 24 h after axotomy with application of either vehicle or KBR or TTX (1 μM) that was applied only to the axonal compartment for 1 h during injury. (E) Quantification of spine density before and 24 h after treatment of axonal compartment with either vehicle or sodium channel activator (veratridine, 10 μM) for 10 min in the absence of injury. n = 15 dendrites for each condition over 2 independent experiments. Paired two-tailed t-test, ^∗p ≤ 0.05. Error bars, s.e.m.