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Effects of Tetramethylpyrazine on Functional Recovery and Neuronal Dendritic Plasticity after Experimental Stroke.

Lin JB, Zheng CJ, Zhang X, Chen J, Liao WJ, Wan Q - Evid Based Complement Alternat Med (2015)

Bottom Line: TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites.TMP failed to affect the spine density of apical dendrites and the total dendritic length.Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

ABSTRACT
The 2,3,5,6-tetramethylpyrazine (TMP) has been widely used in the treatment of ischemic stroke by Chinese doctors. Here, we report the effects of TMP on functional recovery and dendritic plasticity after ischemic stroke. A classical model of middle cerebral artery occlusion (MCAO) was established in this study. The rats were assigned into 3 groups: sham group (sham operated rats treated with saline), model group (MCAO rats treated with saline) and TMP group (MCAO rats treated with 20 mg/kg/d TMP). The neurological function test of animals was evaluated using the modified neurological severity score (mNSS) at 3 d, 7 d, and 14 d after MCAO. Animals were euthanized for immunohistochemical labeling to measure MAP-2 levels in the peri-infarct area. Golgi-Cox staining was performed to test effect of TMP on dendritic plasticity at 14 d after MCAO. TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites. TMP failed to affect the spine density of apical dendrites and the total dendritic length. Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO. Thus, enhanced dendritic plasticity contributes to TMP-elicited functional recovery after ischemic stroke.

No MeSH data available.


Related in: MedlinePlus

Quantification analyses of effect of TMP on dendritic spine density (basilar dendrites and apical dendrites, resp.). (a) The segments were acquired from layer V pyramidal cells and viewed at ×1000 magnification. Scale bar = 10 μm for all segments. (b) The dendritic spine density was expressed as spines/10 μm and the data were presented as mean ± standard deviation (n = 6). *P < 0.05 and **P < 0.01.
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fig9: Quantification analyses of effect of TMP on dendritic spine density (basilar dendrites and apical dendrites, resp.). (a) The segments were acquired from layer V pyramidal cells and viewed at ×1000 magnification. Scale bar = 10 μm for all segments. (b) The dendritic spine density was expressed as spines/10 μm and the data were presented as mean ± standard deviation (n = 6). *P < 0.05 and **P < 0.01.

Mentions: For layer V pyramidal neurons, a one-way ANOVA of basilar dendrites spine density found difference between groups at 14 d after MCAO (sham: 9.43 ± 0.85 versus model: 7.70 ± 0.73 versus TMP: 9.07 ± 0.84; F = 7.642, P = 0.005) (Figure 9). A following Tukey's test revealed that the dendritic spine density in model group was lower than that of sham group (P = 0.006; decreased 18.35%) and TMP treatment increased the dendritic spine density compared to model group (P = 0.027; increased 17.79%).


Effects of Tetramethylpyrazine on Functional Recovery and Neuronal Dendritic Plasticity after Experimental Stroke.

Lin JB, Zheng CJ, Zhang X, Chen J, Liao WJ, Wan Q - Evid Based Complement Alternat Med (2015)

Quantification analyses of effect of TMP on dendritic spine density (basilar dendrites and apical dendrites, resp.). (a) The segments were acquired from layer V pyramidal cells and viewed at ×1000 magnification. Scale bar = 10 μm for all segments. (b) The dendritic spine density was expressed as spines/10 μm and the data were presented as mean ± standard deviation (n = 6). *P < 0.05 and **P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4563062&req=5

fig9: Quantification analyses of effect of TMP on dendritic spine density (basilar dendrites and apical dendrites, resp.). (a) The segments were acquired from layer V pyramidal cells and viewed at ×1000 magnification. Scale bar = 10 μm for all segments. (b) The dendritic spine density was expressed as spines/10 μm and the data were presented as mean ± standard deviation (n = 6). *P < 0.05 and **P < 0.01.
Mentions: For layer V pyramidal neurons, a one-way ANOVA of basilar dendrites spine density found difference between groups at 14 d after MCAO (sham: 9.43 ± 0.85 versus model: 7.70 ± 0.73 versus TMP: 9.07 ± 0.84; F = 7.642, P = 0.005) (Figure 9). A following Tukey's test revealed that the dendritic spine density in model group was lower than that of sham group (P = 0.006; decreased 18.35%) and TMP treatment increased the dendritic spine density compared to model group (P = 0.027; increased 17.79%).

Bottom Line: TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites.TMP failed to affect the spine density of apical dendrites and the total dendritic length.Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

ABSTRACT
The 2,3,5,6-tetramethylpyrazine (TMP) has been widely used in the treatment of ischemic stroke by Chinese doctors. Here, we report the effects of TMP on functional recovery and dendritic plasticity after ischemic stroke. A classical model of middle cerebral artery occlusion (MCAO) was established in this study. The rats were assigned into 3 groups: sham group (sham operated rats treated with saline), model group (MCAO rats treated with saline) and TMP group (MCAO rats treated with 20 mg/kg/d TMP). The neurological function test of animals was evaluated using the modified neurological severity score (mNSS) at 3 d, 7 d, and 14 d after MCAO. Animals were euthanized for immunohistochemical labeling to measure MAP-2 levels in the peri-infarct area. Golgi-Cox staining was performed to test effect of TMP on dendritic plasticity at 14 d after MCAO. TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites. TMP failed to affect the spine density of apical dendrites and the total dendritic length. Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO. Thus, enhanced dendritic plasticity contributes to TMP-elicited functional recovery after ischemic stroke.

No MeSH data available.


Related in: MedlinePlus