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Effect of midazolam on the proliferation of neural stem cells isolated from rat hippocampus.

Zhao S, Zhu Y, Xue R, Li Y, Lu H, Mi W - Neural Regen Res (2012)

Bottom Line: Pretreatment with the gamma-aminobutyric acid A receptor antagonist bicuculline or Na-K-2Cl cotransport inhibitor furosemide partially rescued this inhibition.In addition, midazolam triggered a calcium influx into neural stem cells.The calcium influx triggered by midazolam may be a trigger factor leading to further downstream events.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, the General Hospital of Chinese PLA, Beijing 100853, China.

ABSTRACT
In many recent studies, the inhibitory transmitter gamma-aminobutyric acid has been shown to modulate the proliferation, differentiation and survival of neural stem cells. Most general anesthetics are partial or allosteric gamma-aminobutyric acid A receptor agonists, suggesting that general anesthetics could alter the behavior of neural stem cells. The neuroprotective efficacy of general anesthetics has been recognized for decades, but their effects on the proliferation of neural stem cells have received little attention. This study investigated the potential effect of midazolam, an extensively used general anesthetic and allosteric gamma-aminobutyric acid A receptor agonist, on the proliferation of neural stem cells in vitro and preliminarily explored the underlying mechanism. The proliferation of neural stem cells was tested using both Cell Counting Kit 8 and bromodeoxyuridine incorporation experiments. Cell distribution analysis was performed to describe changes in the cell cycle distribution in response to midazolam. Calcium imaging was employed to explore the molecular signaling pathways activated by midazolam. Midazolam (30-90 μM) decreased the proliferation of neural stem cells in vitro. Pretreatment with the gamma-aminobutyric acid A receptor antagonist bicuculline or Na-K-2Cl cotransport inhibitor furosemide partially rescued this inhibition. In addition, midazolam triggered a calcium influx into neural stem cells. The suppressive effect of midazolam on the proliferation of neural stem cells can be partly attributed to the activation of gamma-aminobutyric acid A receptor. The calcium influx triggered by midazolam may be a trigger factor leading to further downstream events.

No MeSH data available.


Related in: MedlinePlus

Cell Counting Kit 8 cell proliferation test.(A) Dose response studies indicated that mid significantly decreased the proliferation of neural stem cells at a concentration of 30 μM and 90 μM.The repeated administration of 30 μM mid decreased the proliferation of neural stem cells. Pretreatment with 300 μM furo (B) or 10 μM bic (C) partly reversed this repressed proliferation.Data are expressed as mean ± SEM (n = 5 wells/group in A; n = 8 wells/group in B and C). aP < 0.05, vs. veh group; bP < 0.05, vs. mid group using one-way analysis of variance followed by Newman-Keuls multiple comparison test.mid: Midazolam; veh: vehicle; furo: furosemide; bic: bicuculline.
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Figure 2: Cell Counting Kit 8 cell proliferation test.(A) Dose response studies indicated that mid significantly decreased the proliferation of neural stem cells at a concentration of 30 μM and 90 μM.The repeated administration of 30 μM mid decreased the proliferation of neural stem cells. Pretreatment with 300 μM furo (B) or 10 μM bic (C) partly reversed this repressed proliferation.Data are expressed as mean ± SEM (n = 5 wells/group in A; n = 8 wells/group in B and C). aP < 0.05, vs. veh group; bP < 0.05, vs. mid group using one-way analysis of variance followed by Newman-Keuls multiple comparison test.mid: Midazolam; veh: vehicle; furo: furosemide; bic: bicuculline.

Mentions: Repeated administration of 30 μM midazolam significantly decreased the proliferation of neural stem cells, as revealed by the CCK8 proliferation assay. Pretreatment with the gamma-aminobutyric acid A receptor receptor antagonist bicuculline (10 μM; P < 0.05) or the Na-K-2Cl cotransport (NKCC1) inhibitor furosemide (300 μM; P < 0.05) partly rescued the depressed proliferation (Figure 2).


Effect of midazolam on the proliferation of neural stem cells isolated from rat hippocampus.

Zhao S, Zhu Y, Xue R, Li Y, Lu H, Mi W - Neural Regen Res (2012)

Cell Counting Kit 8 cell proliferation test.(A) Dose response studies indicated that mid significantly decreased the proliferation of neural stem cells at a concentration of 30 μM and 90 μM.The repeated administration of 30 μM mid decreased the proliferation of neural stem cells. Pretreatment with 300 μM furo (B) or 10 μM bic (C) partly reversed this repressed proliferation.Data are expressed as mean ± SEM (n = 5 wells/group in A; n = 8 wells/group in B and C). aP < 0.05, vs. veh group; bP < 0.05, vs. mid group using one-way analysis of variance followed by Newman-Keuls multiple comparison test.mid: Midazolam; veh: vehicle; furo: furosemide; bic: bicuculline.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308778&req=5

Figure 2: Cell Counting Kit 8 cell proliferation test.(A) Dose response studies indicated that mid significantly decreased the proliferation of neural stem cells at a concentration of 30 μM and 90 μM.The repeated administration of 30 μM mid decreased the proliferation of neural stem cells. Pretreatment with 300 μM furo (B) or 10 μM bic (C) partly reversed this repressed proliferation.Data are expressed as mean ± SEM (n = 5 wells/group in A; n = 8 wells/group in B and C). aP < 0.05, vs. veh group; bP < 0.05, vs. mid group using one-way analysis of variance followed by Newman-Keuls multiple comparison test.mid: Midazolam; veh: vehicle; furo: furosemide; bic: bicuculline.
Mentions: Repeated administration of 30 μM midazolam significantly decreased the proliferation of neural stem cells, as revealed by the CCK8 proliferation assay. Pretreatment with the gamma-aminobutyric acid A receptor receptor antagonist bicuculline (10 μM; P < 0.05) or the Na-K-2Cl cotransport (NKCC1) inhibitor furosemide (300 μM; P < 0.05) partly rescued the depressed proliferation (Figure 2).

Bottom Line: Pretreatment with the gamma-aminobutyric acid A receptor antagonist bicuculline or Na-K-2Cl cotransport inhibitor furosemide partially rescued this inhibition.In addition, midazolam triggered a calcium influx into neural stem cells.The calcium influx triggered by midazolam may be a trigger factor leading to further downstream events.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, the General Hospital of Chinese PLA, Beijing 100853, China.

ABSTRACT
In many recent studies, the inhibitory transmitter gamma-aminobutyric acid has been shown to modulate the proliferation, differentiation and survival of neural stem cells. Most general anesthetics are partial or allosteric gamma-aminobutyric acid A receptor agonists, suggesting that general anesthetics could alter the behavior of neural stem cells. The neuroprotective efficacy of general anesthetics has been recognized for decades, but their effects on the proliferation of neural stem cells have received little attention. This study investigated the potential effect of midazolam, an extensively used general anesthetic and allosteric gamma-aminobutyric acid A receptor agonist, on the proliferation of neural stem cells in vitro and preliminarily explored the underlying mechanism. The proliferation of neural stem cells was tested using both Cell Counting Kit 8 and bromodeoxyuridine incorporation experiments. Cell distribution analysis was performed to describe changes in the cell cycle distribution in response to midazolam. Calcium imaging was employed to explore the molecular signaling pathways activated by midazolam. Midazolam (30-90 μM) decreased the proliferation of neural stem cells in vitro. Pretreatment with the gamma-aminobutyric acid A receptor antagonist bicuculline or Na-K-2Cl cotransport inhibitor furosemide partially rescued this inhibition. In addition, midazolam triggered a calcium influx into neural stem cells. The suppressive effect of midazolam on the proliferation of neural stem cells can be partly attributed to the activation of gamma-aminobutyric acid A receptor. The calcium influx triggered by midazolam may be a trigger factor leading to further downstream events.

No MeSH data available.


Related in: MedlinePlus