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. 2013 Nov 12;3(4):1461–1482. doi: 10.3390/brainsci3041461

Figure 6.

Figure 6

Acute NMDA exposure elicits the expression of HSP-90 in the CC and TSC1 neutralizes the NMDA effect. Coronal brain slices 300 μm thick were used for the acute treatment of NMDA alone or in slices pre-incubated with TSC1. After electrophysiology, slices were fixed and immunolabeled for the cell stress marker HSP-90 and the OL marker CNPase. (A–D) representative views of untreated slices, neither nestin (A) nor CNPase-expressing cells (C-arrowheads) were labeled for HSP-90 (B-circle). (D) merged image. After acute NMDA, CNPase-positive OL expressed HSP-90 (E–F). Moreover, cells that were not labeled for either of the two markers also expressed HSP-90 (F,G-thin arrows and circle). In slices pre-incubated with TSC1 followed by acute NMDA treatment (see methods for details) (I–L) the majority of CNPase-positive cells did not express HSP-90 (K). Nestin-positive cells did not express HSP-90 in the presence of TSC1 (I-circle). Some cells co-expressed CNPase and HSP-90 (J,K and L-open arrows). Insets show higher magnification views of the cells pointed by open arrows in (J) and (L). Arrowhead points to a CNPase-positive cell (K) that co-expresses HSP-90 (L). The inset in (J) shows an example on the colocalization of both HSP90 and CNPase both, in the cell body and processes (K,L). Calibration bar in (I) corresponds to 50 μm.