Experimental elimination of macrophages by an anti-CD115 antibody significantly attenuated the features of status epilepticus, likely through suppressing activation of NF-κB signaling.
Status epilepticus (a prolonged seizure activity, SE) differently affects vasogenic edema formation and dystrophin-aquaporin 4 (AQP4) expressions between the rat hippocampus and the piriform cortex (PC).
Most of the GRIM-19-positive cells induced by SE in the stratum radiatum and stratum lacunosum-moleculare were glial fibrillary acidic protein-expressing reactive astrocytes.
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.
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.
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.
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.
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 rats, repetitive seizures or status epilepticus induced high expression of P-gp and loss Kir expression in the brain and heart, and promoted membrane depolarization, malignant bradycardia, and the high rate of mortality.
We employed conditional doublecortin-dependent expression of the green fluorescent protein (GFP) to label adult-born cells committed to neuronal lineage either one month before (mature DGCs) or seven days after (immature DGCs) SE.
TRPC6-Mediated ERK1/2 Activation Increases Dentate Granule Cell Resistance to Status Epilepticus Via Regulating Lon Protease-1 Expression and Mitochondrial Dynamics.