Publications by authors named "Avoli M"

Conventional intracellular recordings were made from neurons located in the superficial/middle layers of human temporal neocortical slices obtained from patients undergoing neurosurgical procedures for the treatment of epilepsy or brain tumour. In most of the neurons, inward membrane rectification was observed when the cell was depolarized or hyperpolarized from rest by intracellular injection of positive or negative current pulses. Bath application of tetrodotoxin abolished the depolarizing inward rectification, but not the "anomalous rectification" in the hyperpolarizing direction.

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A significant increase of A1 adenosine receptor binding (48% increase of mean) was detected in human neocortex obtained from patients suffering from temporal lobe epilepsy as compared to control neocortex from non-epileptic patients. Such increase was equally distributed in the six cortical layers and reached similar levels in each of the five specimens tested independently of age, sex and pharmacological treatment of the patient. Since adenosine exerts a depressant effect on neocortical neurons in slices obtained from epileptic patients, this upregulation of A1 receptor binding may constitute a protective mechanism against subsequent seizures, which is exerted by elevating the depressant response of the brain to endogenous adenosine.

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Whole-cell, patch-clamp recordings were used to study voltage-gated currents generated by cerebellar granule cells that were cultured in medium containing either 10% fetal calf serum (hereafter termed S + granules) or neurite outgrowth and adhesion complex (NOAC, hereafter called NOAC granules). NOAC is a protein complex found in rabbit serum that renders granules resistant to the excitotoxic action of excitatory amino acids. During depolarizing commands both S+ and NOAC granules generated Na+ and Ca2+ inward currents and an early and a late K+ outward currents.

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1. Conventional intracellular recordings were performed in rat hippocampal slices to investigate the electrophysiological properties of subicular neurons. These cells had a resting membrane potential (RMP) of -66 +/- 7.

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1. Extracellular field potential and intracellular recordings were made in the CA3 subfield of hippocampal slices obtained from 10- to 24-day-old rats during perfusion with artificial cerebrospinal fluid (ACSF) containing the convulsant 4-aminopyridine (4-AP, 50 microM). 2.

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Spontaneous spreading depression episodes were studied in CA1 and CA3 areas of immature hippocampal slices (two to 30 days postnatally) during 4-aminopyridine (50 microM) perfusion. Spreading depression occurred in the CA3 area of 34% of all slices tested (two to 30 days postnatally). The duration and frequency of the spreading depression field potentials changed with development.

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Extracellular field recordings were performed in guinea-pig and rat neocortical slice preparations maintained in vitro. Bath application of the convulsant drug 4-aminopyridine (4-AP, 100 microM) induced spontaneous epileptiform potentials in 80% of the guinea-pig neocortical slices and only in 6% of the neocortical slices from rat. In both species spontaneous epileptiform activity consisted of a 4-16 s long ictal-like discharge that recurred with a frequency range of 0.

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We analysed the effects induced by arachidonic acid on voltage-dependent outward currents generated by rat neocortical neurones in culture in the presence of Na+ and Ca2+ channel blockers. These currents, recorded with whole-cell voltage-clamping techniques, were presumably carried by K+ and were characterized by an early transient and a late persistent component. Extracellular application of arachidonic acid (50 microM) enhanced both components of the voltage-dependent K+ response by 15-29% (n > 20 cells).

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Extracellular field potential recordings were used to study the epileptiform activity evoked by tetraethylammonium (TEA) in the CA3 subfield of hippocampal slices obtained from young (12-18 day-old) and adult (> 60-day-old) rats. During TEA application (5-10 mM), young slices generated both ictal-like (duration: up to 28 s, rate of occurrence 1-3 x 10(-2) s-1) and interictal-like (duration: 1.5-2 s; rate of occurrence: 1-3 x 10(-1) s-1) activity.

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Field potential recordings were made in the CA3 and/or CA1 subfields of rat hippocampal slices maintained in vitro during perfusion with medium containing the convulsant drug 4-aminopyridine (4AP, 50 microM). In this experimental condition, spontaneous interictal epileptiform discharges caused by the activation of excitatory amino acid receptors and synchronous, GABA-mediated potentials occurred regularly in both areas. Interictal discharges and GABA-mediated potentials were reduced and eventually abolished in both subfields by bath application of baclofen (0.

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Intracellular recordings with K-acetate-filled microelectrodes were performed in slices of the adult rat hippocampus maintained in vitro at 35 - 36 degrees C to analyse the potentials associated with the orthodromic inhibitory sequence generated by CA1 pyramidal cells. In 43 of 72 cells, stimuli that were delivered in the stratum radiatum induced (i) an initial excitatory postsynaptic potential (EPSP), (ii) an early, hyperpolarizing inhibitory postsynaptic potential (IPSP) (peak latency from the stimulus artefact 20 ms), (iii) an intermediate depolarizing component (peak latency=60 - 120 ms; duration=60 - 150 ms, and (iv) a late, long-lasting hyperpolarizing IPSP (peak latency=120 - 160 ms, duration >400 ms). In the remaining cells the orthodromic inhibitory response lacked the intermediate depolarization.

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Extracellular field potential recordings were used to study the effects of the antiepileptic drugs (AEDs) carbamazepine (CBZ), phenytoin (PHT), phenobarbital (PhB) and valproic acid (VPA) on the epileptiform activity evoked by 4-aminopyridine (4-AP, 50 microM) in the CA3 subfield of rat hippocampal slices obtained from young (8-23-day-old) and adult (> 60-day-old) male rats. Ictal (duration: 3-20 s; rate of occurrence: 3-12 x 10(-3) s-1) and interictal (duration: 0.2-0.

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Conventional intracellular recordings were made from regular-spiking cells located in layers II-IV to examine the involvement of excitatory amino acid receptors in synaptic transmission in epileptogenic human neocortical slices maintained in vitro. Extracellular stimuli that were below the threshold for generating action potentials evoked an excitatory postsynaptic potential (EPSP) with short latency to onset (0.8-4 ms).

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Extracellular field potential recordings were performed in the CA1 subfield of hippocampal slices obtained from Wistar rats aged 2-38 days. When the brain tissue was maintained at 35 degrees-36 degrees C (values obtained in the tissue chamber well), single-shock orthodromic stimuli elicited a response in the stratum pyramidale that consisted of a single population spike. In contrast, when the temperature in the well was increased to levels greater than 38.

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1. Intracellular recording techniques were used to investigate the physiological and pharmacological properties of stimulus-induced excitatory postsynaptic potentials (EPSPs) recorded in regular-spiking cells located in layers II/III of rat sensorimotor cortical slices maintained in vitro. 2.

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Spontaneous episodes of spreading depression (SD) were observed in the CA3 subfield of immature or young (2-30 days postnatally) hippocampal slices perfused with medium containing 4-aminopyridine (4-AP, 50 microM). SD appeared in 34% of the hippocampal slices examined and was more frequently observed in slices obtained from 11 to 20-day-old animals. SD studied with extracellular field potential recordings consisted of large amplitude (18.

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Two types of spontaneous filed potentials were recorded in rat hippocampal slices after addition of 4-aminopyridine (4-AP; 50 microM). One consisted of brief, epileptiform discharges that occurred at 0.6 +/- 0.

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In this review we summarize a number of technical and methodological approaches that have been used in our laboratory to study human brain slices maintained in vitro. The findings obtained in the course of these studies appear to be relevant in establishing the mechanisms that underlie physiological phenomena of the human brain such as synaptic plasticity or responses to neuroactive drugs. Moreover, these data are important for understanding certain fundamental mechanisms of epilepsy.

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We report that extracellular application of cesium (Cs+, 3 mM) potentiated the epileptiform discharge evoked by GABAA-receptor antagonist bicuculline methiodide (BMI 50 microM) in rat neocortical slices maintained in vitro. Cs+ changed BMI-induced epileptiform burst of a few hundred milliseconds evoked by extracellular focal stimuli into epileptiform discharge only a few seconds long (1.8-7 s).

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Extracellular field potentials and [K+]o were recorded in slices of human epileptogenic neocortex maintained in vitro during perfusion with Mg(2+)-free artificial cerebrospinal fluid (ACSF). The human neocortex was obtained during neurosurgical procedures for the relief of seizures that were resistant to medical treatment. Spontaneous epileptiform activity and episodes of spreading depression appeared within 1.

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The effects induced by the antiepileptic drug valproic acid were studied in the CA3 subfield of in vitro hippocampal slices obtained from young (16- to 27-day-old) and adult (over 60-day-old) rats. Spontaneous epileptiform discharges were induced by the addition of the convulsant 4-aminopyridine to the medium. Valproic acid (0.

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1. Conventional intracellular and extracellular recording techniques were used to investigate the physiology and pharmacology of epileptiform bursts induced by 4-aminopyridine (4-AP, 50 microM) in the CA3 area of rat hippocampal slices maintained in vitro. 2.

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Intracellular recordings were performed in neurons located in layers II/III of rat neocortical slices maintained in vitro. High intensity negative current pulses elicited hyperpolarizing responses that were characterized by a sag of membrane potential towards the resting level. Graphically, this inward rectification was reflected as a break in the slope of the I-V plot at membrane level of around -98 mV.

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Conventional intracellular recording techniques were used to investigate the N-methyl-D-aspartate (NMDA) and non-NMDA mediated synaptic mechanisms underlying the stimulus-induced paroxysmal depolarization shift (PDS) generated by cells in rat neocortical slices treated with bicuculline methiodide (BMI). The NMDA receptor antagonists CPP or MK-801 were ineffective in abolishing the PDS. However, both drugs were able to attenuate the late phase of the PDS and delay its time of onset.

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