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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D <t>for</t> <t>AMPA</t> and <t>NMDA</t> receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with <t>nimodipine</t> (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.
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Image Search Results


a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D for AMPA and NMDA receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Schematics of cerebellar circuit b. UMAP embedding showing normalized expression of gene involved in mGluR1 signaling cascade. c. Same as in D for AMPA and NMDA receptors. d. Same as in D for genes involved in mGluR2 signaling cascade. e. Example spiking responses in different UBCs to a burst of MF input (20 stimuli at 100Hz). f. Instantaneous firing rate for the same cells.

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques: Expressing

a. Examples of instantaneous firing rate from on-cell recordings before (black) and after (gray) the application of AMPA/NMDA receptor antagonist (gray bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. b. Summary of evoked spiking (20×100 Hz) and the effect of AMPA/NMDA receptor antagonist (normalized to baseline, mean±sem, n=5). c. Examples of instantaneous firing rate from on-cell recordings before (black) and after (red) the application of an mGluR1 antagonist (red bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. d. Summary of evoked spiking (20×100 Hz) and the effect of an mGluR1 antagonist (normalized to baseline, mean±sem, n=5). e. Example of instantaneous firing rate before and after 20 minutes of DGK inhibitor II wash-in. f. Summary of half-decay time of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6) g. Summary of peak amplitude of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6)

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Examples of instantaneous firing rate from on-cell recordings before (black) and after (gray) the application of AMPA/NMDA receptor antagonist (gray bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. b. Summary of evoked spiking (20×100 Hz) and the effect of AMPA/NMDA receptor antagonist (normalized to baseline, mean±sem, n=5). c. Examples of instantaneous firing rate from on-cell recordings before (black) and after (red) the application of an mGluR1 antagonist (red bar) in a fast (left) and a slow (right) UBC. Each trace is an average of 8 trials. d. Summary of evoked spiking (20×100 Hz) and the effect of an mGluR1 antagonist (normalized to baseline, mean±sem, n=5). e. Example of instantaneous firing rate before and after 20 minutes of DGK inhibitor II wash-in. f. Summary of half-decay time of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6) g. Summary of peak amplitude of instantaneous firing rate response with DGK inhibitor II (normalized to baseline, mean±sem, n=6)

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques:

a. Sample cell-attached recording (top) instantaneous firing rate (middle) and synaptic current measured with whole-cell voltage clamp (bottom) in a cell with fast response. b. Same as in A but for a cell with intermediate speed response c. Same as in A but for a cell with clear biphasic synaptic current (bottom) d. Same as in A but for a cell with slow biphasic response e. Same as in A but for a cell with only a pause in firing f. Half-decay times of firing rates vs. half-decay times of currents and linear fit on a log-log plot (R adj 2 = 0.91, slope = 0.88, intercept = -0.22, n = 17) g. Peak firing rate vs. peak current amplitude and linear fit on a log-log plot (R adj 2 = 0.69, slope = 0.71, intercept = -0.65, n = 17) h. Pause duration vs. amplitude of the current at stimulation offset, and linear fit with log 10 response variable (black, R adj 2 = 0.44, slope = 0.01, intercept = -0.42, n = 20) i. Heatmap of peak normalized mGluR1-mediated current (n=10) j. Heatmap of peak normalized mGluR2/3-mediated current (n=7) k. Average synaptic response before (black), after (red) mGluR1 antagonist, and after AMPA/NMDA receptor antagonist wash-ins (grey). Each trace is an average of 8 trials. l. Average synaptic response before (top, black) and after (top, blue) mGluR2/3 antagonist washin, and their difference (bottom, black). Each trace is an average of 8 trials.

Journal: bioRxiv

Article Title: Graded heterogeneity of metabotropic signaling underlies a continuum of cell-intrinsic temporal responses

doi: 10.1101/2020.12.27.424473

Figure Lengend Snippet: a. Sample cell-attached recording (top) instantaneous firing rate (middle) and synaptic current measured with whole-cell voltage clamp (bottom) in a cell with fast response. b. Same as in A but for a cell with intermediate speed response c. Same as in A but for a cell with clear biphasic synaptic current (bottom) d. Same as in A but for a cell with slow biphasic response e. Same as in A but for a cell with only a pause in firing f. Half-decay times of firing rates vs. half-decay times of currents and linear fit on a log-log plot (R adj 2 = 0.91, slope = 0.88, intercept = -0.22, n = 17) g. Peak firing rate vs. peak current amplitude and linear fit on a log-log plot (R adj 2 = 0.69, slope = 0.71, intercept = -0.65, n = 17) h. Pause duration vs. amplitude of the current at stimulation offset, and linear fit with log 10 response variable (black, R adj 2 = 0.44, slope = 0.01, intercept = -0.42, n = 20) i. Heatmap of peak normalized mGluR1-mediated current (n=10) j. Heatmap of peak normalized mGluR2/3-mediated current (n=7) k. Average synaptic response before (black), after (red) mGluR1 antagonist, and after AMPA/NMDA receptor antagonist wash-ins (grey). Each trace is an average of 8 trials. l. Average synaptic response before (top, black) and after (top, blue) mGluR2/3 antagonist washin, and their difference (bottom, black). Each trace is an average of 8 trials.

Article Snippet: Sequential drug wash-ins were performed using a computer-controlled solenoid manifold system (ValveLink 8.2, Automate Scientific, Inc., Berkeley, CA) with a flow rate of 1 to 2mL/min, where indicated, with mGluR1 antagonist (100μM LY357385, Tocris Bio-Techne, Minneapolis, MN), AMPA receptor blocker (5μM NBQX), NMDA receptor blocker (2 μM R-CPP), mGluR2/3 antagonist (1μM LY341495, Tocris Bio-Techne, Minneapolis, MN) and DGK inhibitor II (100 μM R59949, MilliporeSigma, St. Louis, MO)

Techniques:

Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.

Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Staining

Hua-Feng-Dan alleviates histopathology injury and apoptosis of nerve cells after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Thin sections of brain tissue after hematoxylin-eosin staining (n = 3). Blue arrows represent macrophage infiltration or vascular stasis; red arrows, necrotic neurons or pyramidal cells; green arrows, glial cell proliferation; yellow arrows, vacuoles or septa; and black arrows, crumpled neurons or pyramidal cells. Scale bar, 100 μm. (B) Thin sections of brain tissue after terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining (n = 3). Scale bar, 100 μm. (C) TUNEL positive cells density (n = 3).

Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan alleviates histopathology injury and apoptosis of nerve cells after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Thin sections of brain tissue after hematoxylin-eosin staining (n = 3). Blue arrows represent macrophage infiltration or vascular stasis; red arrows, necrotic neurons or pyramidal cells; green arrows, glial cell proliferation; yellow arrows, vacuoles or septa; and black arrows, crumpled neurons or pyramidal cells. Scale bar, 100 μm. (B) Thin sections of brain tissue after terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining (n = 3). Scale bar, 100 μm. (C) TUNEL positive cells density (n = 3).

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Histopathology, Staining, End Labeling, TUNEL Assay

Hua-Feng-Dan restores the integrity of the intestinal barrier after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with a high dose of Hua-Feng-Dan (HFD, 0.648 g/kg) and nimodipine (NMDP). (A) Representative photographs of colon H&E staining (n = 3). Red arrows indicate the presence of lymphocytic infiltration; blue arrows, edema or edematous mucosal epithelial cells; black arrows, necrosis of mucosal epithelial cells; yellow arrows, dilated intestinal glands; and purple arrows, vasodilation. Scale bar = 200 and 100 μm. (B–D) Comparison of levels of three indices of intestinal barrier permeability: lipopolysaccharide (LPS), diamine oxidase (DAO) and d -lactate ( d -LA). (E–G) Comparison of levels of three pro-inflammatory factors: tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. (H) Comparison of levels of total cholesterol (T-CHO) as an index of dyslipidemia. (I, J) Comparison of levels of oxidative stress factors total superoxide dismutase (T-SOD) and malondialdehyde (MDA). Data are mean ± SD, n = 6 (excluding H&E staining). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. MCAO group (based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test).

Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan restores the integrity of the intestinal barrier after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with a high dose of Hua-Feng-Dan (HFD, 0.648 g/kg) and nimodipine (NMDP). (A) Representative photographs of colon H&E staining (n = 3). Red arrows indicate the presence of lymphocytic infiltration; blue arrows, edema or edematous mucosal epithelial cells; black arrows, necrosis of mucosal epithelial cells; yellow arrows, dilated intestinal glands; and purple arrows, vasodilation. Scale bar = 200 and 100 μm. (B–D) Comparison of levels of three indices of intestinal barrier permeability: lipopolysaccharide (LPS), diamine oxidase (DAO) and d -lactate ( d -LA). (E–G) Comparison of levels of three pro-inflammatory factors: tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. (H) Comparison of levels of total cholesterol (T-CHO) as an index of dyslipidemia. (I, J) Comparison of levels of oxidative stress factors total superoxide dismutase (T-SOD) and malondialdehyde (MDA). Data are mean ± SD, n = 6 (excluding H&E staining). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. MCAO group (based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test).

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Staining, Comparison, Permeability