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. Author manuscript; available in PMC: 2015 Jan 30.
Published in final edited form as: Curr Neurovasc Res. 2009 Aug 1;6(3):171–180. doi: 10.2174/156720209788970063

Table 1. Effects of Thapsigargin on Neuronal Cell Death.

Region Control Thapsigargin
ChAT nBM 124 ± 15 (7) - 60 ± 11 (5) **
dStr 54 ± 12 (7) - 18 ± 5 (5) **
TH vMes 81±18 (6) - 18 ± 5 (5) ***
DAPI nBM 9 ± 1 (7) - 30 ± 2 (5) ***
vMes 12 ± 2 (7) - 49 ± 3 (5) ***
TUNEL nBM 45 ± 5 (4) - 392 ± 44 (3) ***
vMes 53 ± 7 (4) - 313 ± 16 (4) ***

A 4 week old co-culture brain slice, composed of the basal nucleus of Meynert (nBM), the dorsal striatum (dStr), the cortex (Ctx) and the ventral mesencephalon (vMes), was incubated with 3 μM thapsigargin for 24 hr and then for further 3 days in without. Subsequently, the slices were fixed, stained for choline acetyltransferase (ChAT) or tyrosine hydroxylase (TH) or DAPI or DNA fragments were labelled in situ using the TUNEL assay. The number of ChAT/TH or DAPI-positive nuclei with apoptotic morphology or TUNEL-positive nuclei were counted on a random field (260 μm × 190 μm) per slice are given as mean ± S.E.M.; the values in parenthesis give the number of analyzed slices. Statistical analysis was performed by one way ANOVA with a Fisher PLSD posthoc test (*** p<0.001; ** p<0.01).