The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
Seizures were elicited by a GABA<sub>A</sub> antagonist pentylenetetrazol (PTZ) 3, 6, 9, and 13 days after SE (i.e., in P15, P18, P21, and P25 rats), and their possible potentiation by a GABA<sub>B</sub> receptor antagonist CGP46381 was studied.
These results indicate that expression of GRIM-19 in the hippocampus is mainly observed in neurons under normal conditions but is altered in the SE mouse model as evidenced by its increased expression in reactive astrocytes.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
These results suggest that the TSP-1-regulated TGF-β1/pSmad2/3 pathway plays a key role in KA-induced SE and astrogliosis, and that inhibiting this pathway may be a potential anti-seizure strategy.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
Seizures were elicited by a GABA<sub>A</sub> antagonist pentylenetetrazol (PTZ) 3, 6, 9, and 13 days after SE (i.e., in P15, P18, P21, and P25 rats), and their possible potentiation by a GABA<sub>B</sub> receptor antagonist CGP46381 was studied.
Seizures were elicited by a GABA<sub>A</sub> antagonist pentylenetetrazol (PTZ) 3, 6, 9, and 13 days after SE (i.e., in P15, P18, P21, and P25 rats), and their possible potentiation by a GABA<sub>B</sub> receptor antagonist CGP46381 was studied.
Seizures were elicited by a GABA<sub>A</sub> antagonist pentylenetetrazol (PTZ) 3, 6, 9, and 13 days after SE (i.e., in P15, P18, P21, and P25 rats), and their possible potentiation by a GABA<sub>B</sub> receptor antagonist CGP46381 was studied.
Seizures were elicited by a GABA<sub>A</sub> antagonist pentylenetetrazol (PTZ) 3, 6, 9, and 13 days after SE (i.e., in P15, P18, P21, and P25 rats), and their possible potentiation by a GABA<sub>B</sub> receptor antagonist CGP46381 was studied.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
In the pilocarpine-induced C57BL/6 mouse model, SHP-2 upregulation in the hippocampus began one day after status epilepticus, reached a peak at 21 days and then maintained a significantly high level until day 60.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
Here, we report that a single 20-min status epilepticus (SE) induces P-gp and EPO-R expression in cortical pyramidal neurons and only P-gp expression in astrocytes.
In the present study, rats were treated with vehicle or AST 1 h after SE onset and were injected once every other day for 2 weeks (total of seven times).
Roscovitine Attenuates Microglia Activation and Monocyte Infiltration via p38 MAPK Inhibition in the Rat Frontoparietal Cortex Following Status Epilepticus.
Two groups of male rats were subjected to 1 hr of SE with pilocarpine (280-300 mg/kg, i.p.), and treated with either C1-INH (SE+C1-INH, 20 U/kg, s.c.) or vehicle (SE+veh) at 4, 24, and 48 h after SE.Control rats were treated with saline.
In ex vivo experiments, post-SE microglia cells were isolated from the hippocampal CA1 area and subjected to lipopolysaccharide (LPS) stimulation followed by inflammatory cytokine IL-1β and IL-6 by qPCR and HMGB1, TLR2, TLR3 by Western blotting.
We show that BI1029539, an mPGES-1 inhibitor, prevented up-regulation of P-gp expression and transport activity in capillaries exposed to glutamate and in capillaries from humanized mPGES-1 mice after SE.
We also detected the expression of interleukin-1 receptor-associated protein kinases-1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) and nuclear factor-kappaB (NF-κB) p65 using Western blotting and immunohistochemistry, which indicated the expression of IRAK1, TRAF6 and NF-κB p-p65/p65 increased in the brain of SE rats, and overexpression of miR-146a-5p could downregulate the expression of IRAK1, TRAF6, NF-κB p-p65/p65 and P-gp.
We also detected the expression of interleukin-1 receptor-associated protein kinases-1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) and nuclear factor-kappaB (NF-κB) p65 using Western blotting and immunohistochemistry, which indicated the expression of IRAK1, TRAF6 and NF-κB p-p65/p65 increased in the brain of SE rats, and overexpression of miR-146a-5p could downregulate the expression of IRAK1, TRAF6, NF-κB p-p65/p65 and P-gp.