A5045520666- Neuroscience and Neuropharmacology Research
- Epilepsy research and treatment
- Cell death mechanisms and regulation
- Neuropeptides and Animal Physiology
- Infectious Encephalopathies and Encephalitis
- Neonatal and fetal brain pathology
- Pharmacological Effects and Toxicity Studies
- Mitochondrial Function and Pathology
- Memory and Neural Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Metabolism and Genetic Disorders
- S100 Proteins and Annexins
- Neuroinflammation and Neurodegeneration Mechanisms
- Anesthesia and Neurotoxicity Research
- Lipid Membrane Structure and Behavior
- Ion channel regulation and function
- Cell Adhesion Molecules Research
- Pesticide Exposure and Toxicity
- Cholinesterase and Neurodegenerative Diseases
- Autophagy in Disease and Therapy
- Receptor Mechanisms and Signaling
- Signaling Pathways in Disease
- Thermal Regulation in Medicine
- Cancer-related Molecular Pathways
- Axon Guidance and Neuronal Signaling
VA Greater Los Angeles Healthcare System
2010-2024
University of California, Los Angeles
2010-2023
UCLA Health
2021
West Los Angeles College
2004-2009
Neurology, Inc
2002
Universidad Nacional Autónoma de México
1999-2000
Inserm
1993-1996
Délégation Paris 5
1994-1996
Université Paris Cité
1994-1996
Maternité Port Royal
1995
Summary Objective Pharmacoresistance remains an unsolved therapeutic challenge in status epilepticus ( SE ) and cholinergic induced by nerve agent intoxication. triggers a rapid internalization of synaptic γ‐aminobutyric acid A GABA receptors externalization N ‐methyl‐ d ‐aspartate NMDA that may explain the loss potency standard antiepileptic drugs AED s). We hypothesized drug combination aimed at correcting consequences receptor trafficking would reduce severity its long‐term consequences....
Summary We used two models of status epilepticus ( SE ) to study trafficking N ‐methyl‐ d ‐aspartate NMDA receptors. is associated with increased surface expression NR 1 subunits receptors, and an increase synaptic extrasynaptic currents suggesting in number functional receptors on dentate granule cells. The therapeutic implications these results are discussed.
Status epilepticus is common in neonates and infants, associated with neuronal injury adverse developmental outcomes. γ-Aminobutyric acidergic (GABAergic) drugs, the standard treatment for neonatal seizures, can have excitatory effects brain, which may worsen seizures their effects. Using a recently developed model of status postnatal day 7 rat pups that results widespread injury, we found GABAA agonists phenobarbital midazolam significantly increased epilepticus-associated various brain...
Hypoxic necrosis of dentate gyrus neurons in primary culture required the activation an orderly cell death program independent protein synthesis. Early mitochondrial swelling and loss membrane potential were accompanied by release cytochrome c followed caspase-9-dependent caspase-3. Caspase-3 -9 inhibitors reduced neuronal necrosis. Calcium directly induced from isolated mitochondria. may be active process which direct effect hypoxia on mitochondria lead to final common pathway...
Summary During status epilepticus ( SE ), synaptic γ‐aminobutyric acid A receptors GABA R s) become internalized and inactive, whereas spare N ‐methyl‐ d ‐aspartate NMDAR assemble, move to the membrane, synaptically active. When treatment of is delayed, number s drastically reduced, a agonist cannot fully restore inhibition. We used combination low‐dose diazepam (to stimulate remaining s), ketamine mitigate effect increase), valproate enhance inhibition at nonbenzodiazepine site) treat...
The initiation and maintenance of cholinergic-induced status epilepticus (SE) are associated with decreased synaptic gamma-aminobutyric acid A receptors (GABA
Summary Objective To evaluate acute and long‐term effects of intravenous brivaracetam ( BRV ) + diazepam DZP combination treatment in a rat model self‐sustaining status epilepticus SSSE ). Methods Rats were treated with (10 mg/kg) 10 min after initiation perforant path stimulation PPS as early treatment; or (10–300 mg/kg), (1 (0.3–10 the end (established Seizure activity was recorded electrographically for 24 h posttreatment (acute effects), 1 week at 6–8 weeks 12 months' (long‐term...
During status epilepticus (SE), seizures become self-sustaining (Wasterlain, 1974), and pharmacoresistance to benzodiazepines develops progressively, can result in a 20-fold reduction of response diazepam after 30 min experimental (Kapur & Macdonald, 1997; Mazarati et al., 1998a,b). This time-dependent is not mediated by classical transporter mechanisms (Löscher, 2007), but may reflect seizure-induced internalization synaptic γ-aminobutyric acid (GABA)A receptors (GABAAR) containing the β2–3...
Summary Status epilepticus in the immature brain induces neuronal injury hippocampal formation, but mode and mechanism of death are poorly understood. Our laboratory has recently investigated role caspase‐3, ‐8, ‐9 injury, using a lithium–pilocarpine model status 2‐week‐old rat pups. results showed that dying neurons dentate gyrus CA1‐subiculum area do not share same death. In CA1‐subiculum, caspase‐8 upregulation preceded caspase‐3 activation morphologically necrotic neurons. The...
Abstract Objective Pharmacoresistance develops quickly during repetitive seizures, and refractory status epilepticus ( RSE ) remains a therapeutic challenge. The outcome of is poor, with high mortality morbidity. New treatments are needed. Deep hypothermia (20°C) used clinically reconstructive cardiac surgery neurosurgery, has proved safe effective in those indications. We tested the hypothesis that deep reduces its long‐term consequences. Methods model SE induced by lithium pilocarpine to...