A5102907637- Neuroscience and Neuropharmacology Research
- Epilepsy research and treatment
- Ion channel regulation and function
- Neural dynamics and brain function
- Memory and Neural Mechanisms
- Neuroscience and Neural Engineering
- Photoreceptor and optogenetics research
- Lipid Membrane Structure and Behavior
- Receptor Mechanisms and Signaling
- Genetics and Neurodevelopmental Disorders
- Mitochondrial Function and Pathology
- Nicotinic Acetylcholine Receptors Study
- Diet and metabolism studies
- EEG and Brain-Computer Interfaces
- Neurological disorders and treatments
- Cardiac electrophysiology and arrhythmias
- Pharmacological Effects and Toxicity Studies
- Neurobiology and Insect Physiology Research
- Electrochemical Analysis and Applications
- Neuroinflammation and Neurodegeneration Mechanisms
- Pharmacological Receptor Mechanisms and Effects
- Adenosine and Purinergic Signaling
- Genetic Neurodegenerative Diseases
- Neuropeptides and Animal Physiology
- Neurogenesis and neuroplasticity mechanisms
Montreal Neurological Institute and Hospital
2015-2024
McGill University
2015-2024
Sapienza University of Rome
2010-2021
University of Modena and Reggio Emilia
2002-2008
Istituto Neurologico Mediterraneo
2001-2005
University of Rome Tor Vergata
1989-2002
Inserm
1999-2002
Centre Paul Broca
2002
Université de Strasbourg
2001
Columbia University
1999
1. Conventional intracellular and extracellular recording techniques were used to investigate the physiology pharmacology of epileptiform bursts induced by 4-aminopyridine (4-AP, 50 microM) in CA3 area rat hippocampal slices maintained vitro. 2. 4-AP-induced bursts, consisting a 25-to 80-ms depolarizing shift neuronal membrane associated with three six fast action potentials, occurred at frequency 0.61 +/- 0.29 (SD)/s. The generated synchronously neurons triggered giant excitatory...
Continuous application of 4-aminopyridine (4-AP, 50 microM) to combined slices hippocampus-entorhinal cortex obtained from adult mice induces (1) interictal discharges that initiate in the CA3 area and propagate via hippocampal regions CA1 subiculum entorhinal return hippocampus through dentate gyrus; (2) ictal originate gyrus proper. Ictal disappear over time, whereas synchronous continue occur throughout experiment. Lesioning Schaffer collaterals abolishes CA1, cortex, discloses propagate,...
Application of 4-aminopyridine (4AP, 50 μ m ) to combined slices adult rat hippocampus–entorhinal cortex-induced ictal and interictal epileptiform discharges, as well slow field potentials that were abolished by the μ-opioid agonist [ d -Ala 2 ,N-Me-Phe 4 ,Gly-ol 5 ] enkephalin (DAGO, 10 or GABA A receptor antagonist bicuculline methiodide (BMI, ); hence, they represented synchronous GABA-mediated potentials. Ictal discharges originated in entorhinal cortex propagated hippocampus, whereas...
Two types of spontaneous filed potentials were recorded in rat hippocampal slices after addition 4-aminopyridine (4-AP; 50 microM). One consisted brief, epileptiform discharges that occurred at 0.6 +/- 0.2 sec-1 the CA3 and CA1 areas. The other type less frequently (0.036 0.013 sec-1) was CA1, CA3, dentate It corresponded all regions to an intracellular long-lasting depolarization (LLD; duration, 300-1200 msec; peak amplitude, 2-15 mV) abolished by bicuculline methiodide; therefore, it...
Abstract Extracellular field potentials and [K + ] o were recorded in slices of human epileptogenic neocortex maintained vitro during perfusion with Mg 2+ ‐free artificial cerebrospinal fluid (ACSF). The was obtained neurosurgical procedures for the relief seizures that resistant to medical treatment. Spontaneous epileptiform activity episodes spreading depression appeared within 1.5 2 hours ACSF. discharges consisted negative potential shifts (amplitude, 0.8–10 mV) lasted 2.5 80 seconds...
1. Neocortical slices of the first and second temporal gyrus frontal lobe, removed in human epileptic patients for relief intractable seizures, were maintained vitro at 35 +/- 1 degrees C. Electrophysiological properties neurons deep layers (1,800-2,600 micron below pial surface) studied with conventional intracellular recording stimulation techniques. Synaptic responses evoked by extracellular focal stimuli. Intracellular injections some cells fluorescent dye Lucifer yellow revealed large...
High-frequency oscillations (HFOs; 80-500 Hz) are thought to mirror the pathophysiological changes occurring in epileptic brains. However, distribution of HFOs during seizures remains undefined. Here, we recorded from hippocampal CA3 subfield, subiculum, entorhinal cortex, and dentate gyrus quantify occurrence ripples (80-200 fast (250-500 low-voltage fast-onset (LVF) hypersynchronous-onset (HYP) rat pilocarpine model temporal lobe epilepsy. We discovered LVF that (1) progression preictal...
Seizures in temporal lobe epilepsy can be classified as hypersynchronous and low-voltage fast according to their onset patterns. Experimental evidence suggests that fast-onset seizures mainly result from the synchronous activity of γ-aminobutyric acid-releasing cells. In this study, we tested hypothesis using optogenetic control parvalbumin-positive interneurons entorhinal cortex, vitro 4-aminopyridine model. We found both spontaneous optogenetically induced had similar addition, types...
Objective Ictal events occurring in temporal lobe epilepsy patients and experimental models mimicking this neurological disorder can be classified, based on their onset pattern, into low‐voltage, fast versus hypersynchronous seizures. It has been suggested that the pattern is mainly contributed by interneuronal (γ‐aminobutyric acidergic) signaling, whereas involves activation of principal (glutamatergic) cells. Methods Here, we tested hypothesis using optogenetic control parvalbumin‐positive...
Abstract Haploinsufficiency of the SYNGAP1 gene, which codes for a Ras GTPase-activating protein, impairs cognition both in humans and mice. Decrease Syngap1 mice has been previously shown to cause cognitive deficits at least part by inducing alterations glutamatergic neurotransmission premature maturation excitatory connections. Whether plays role development cortical GABAergic connectivity function remains unclear. Here, we show that haploinsufficiency significantly reduces formation...