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Results: 5

2.
Fig. 1

Fig. 1. From: Neuroprotection by Acetyl-l-Carnitine after Traumatic Injury to the Immature Rat Brain.

Beam walking traverse time in seconds tested on days 3–7 after sham surgery or CCI followed by treatment with ALCAR or normal saline. Data are presented as means ± SEM. n = 7 rats/group.

Susanna Scafidi, et al. Dev Neurosci. 2011 February;32(5-6):480-487.
3.
Fig. 3

Fig. 3. From: Neuroprotection by Acetyl-l-Carnitine after Traumatic Injury to the Immature Rat Brain.

Effect of ALCAR treatment on NOR test performance 7 days after CCI injury. CCI rats treated with saline had significantly impaired 24-hour delay NOR task performance (p < 0.001) compared to both sham groups and the CCI + ALCAR rats. The performance of CCI + ALCAR rats was significantly better than that of CCI + saline rats and was not different from that of either sham group. Values are expressed as percentage of time spent exploring the novel object (means ± SEM). n = 7 rats/group. ∗ p < 0.001.

Susanna Scafidi, et al. Dev Neurosci. 2011 February;32(5-6):480-487.
4.
Fig. 2

Fig. 2. From: Neuroprotection by Acetyl-l-Carnitine after Traumatic Injury to the Immature Rat Brain.

Effect of ALCAR treatment on sensorimotor coordination after CCI. CCI injury resulted in an increased number of foot slips during the beam walking task on days 3–7 after injury (▴) in comparison to sham-operated rats in both vehicle- () and ALCAR-treated (○) groups (p < 0.001). CCI rats treated with ALCAR during the first 24 h after CCI (▪) had significantly fewer foot slips (p < 0.005; ANOVA) compared to CCI + saline rats and were not different from the sham groups. Data are presented as means ± SEM. n = 7 rats/group. ∗ p < 0.001.

Susanna Scafidi, et al. Dev Neurosci. 2011 February;32(5-6):480-487.
5.
Fig. 4

Fig. 4. From: Neuroprotection by Acetyl-l-Carnitine after Traumatic Injury to the Immature Rat Brain.

Effect of ALCAR treatment on lesion volume after CCI. a Histological analysis of brain sections (cresyl violet staining) at day 7 after injury shows that the CCI + ALCAR rats had less tissue loss than the CCI + saline rats. Dashed lines approximate upper border of necrotic lesion. b Higher magnification shows the presence of both injured (shrunken neurons with condensed nucleus and lacking nucleolus; white arrows) and noninjured neurons (nucleolus intact with regular distribution of Nissl bodies throughout cytoplasm; black arrows) in cortical regions of saline- (left panel) and ALCAR-treated (right panel) animals following CCI. Scale bar = 25 μm. c Quantified lesion volume using stereologic analysis measured at day 7 after CCI + ALCAR versus CCI + saline. Data are presented as means ± SEM of the percent lesion volume. n = 7 rats/group. ∗ p < 0.05.

Susanna Scafidi, et al. Dev Neurosci. 2011 February;32(5-6):480-487.

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