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. Author manuscript; available in PMC: 2008 Dec 1.
Published in final edited form as: Neurotox Res. 2004;6(4):333–342. doi: 10.1007/BF03033444

Table 3.

Bax mRNA Levels Increase After Traumatic Brain Injury

BRAIN REGION MODEL TIME POSTINJURY (days)
SHAMS 0.25 1 3 7
CORTEX bcl-xL mRNA (fg/μg protein)a
IPSILATERAL LFP 5.27±0.51 - 6.67±0.49 7.45±0.85* 7.44±0.46*
LCI 2.04±0.25 2.81±0.32§ 1.92±0.35 1.57±0.38 1.28±0.17
CONTRALATERAL LFP£ 4.39±0.42 - 5.76±0.67# 5.55±0.14^ 3.21±0.44#

LCI£
2.91±0.56^
2.40±0.38
2.35±0.29
2.43±0.65^
1.71±0.26
HIPPOCAMPUS
IPSILATERAL LFP 1.68±0.27 - 1.86±0.17 2.59±0.30* 2.40±0.20*
LCI 3.45±0.86 2.74±0.27 2.76±0.80 5.69±0.62* 7.25±1.35*
CONTRALATERAL LFP 1.69±0.20 - 1.62±0.25 2.18±0.57 2.13±0.12
LCI 5.28±0.71 5.65±1.06# 4.86±0.91 4.38±0.95# 6.18±1.43
a

Messenger RNA levels (mean ± SEM) determined by RNase protection assay (see Methods). Sham controls from multiple time points showed no differences and were combined for each anatomical area. Lateral fluid percussion (LFP) or lateral cortical impact (LCI) injury was performed as described in Methods. “-” not done.

*

p<0.05, ANOVA, Dunnett vs. shams

§

p<0.05, ANOVA, Fisher PLSD vs. shams.

#

p<0.05, paired t-test, contralateral vs. ipsilateral

^

0.05<p<0.10

£

p<0.05, paired t-test, contralateral vs. ipsilateral over time groups combined.