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J Louvel

Publications and source records attributed to J Louvel.

At least 37 records · Page 2Linked to original sources
PubMed1994

Extracellular free potassium during synchronous activity induced by 4-aminopyridine in the juvenile rat hippocampus.

Field potential recordings and measurements of the extracellular concentration of free K+ ([K+]o) were made in the stratum radiatum of the CA3 subfield of hippocampal slices that were obtained from 12- to 17-day-old rats. Spontaneous, synchronous field potentials were recorded in the presence of the convulsant drug 4-aminopyridine (4AP, 50 microM). They consisted of interictal- (duration = 0.2-1.2 s; rate of occurrence = 0.3-1.3 Hz) and ictal-like epileptiform discharges (8-40 s; 4-38.10(-3) Hz), as well as large amplitude, negative-going potentials that preceded the onset of the ictal-like event. Such a temporal correlation suggested that the negative-going potential might facilitate the onset of ictal-like activity. Interictal- and ictal-like discharges were abolished by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), while the negative-going potential was selectively blocked by bicuculline methiodide (BMI, 10 microM). Hence it was presumably due to the activation of GABAA receptors. [K+]o increased up to 12.5 mM (7.9 +/- 2.7 mM, mean +/- S.D.) from a resting value of 3.25 mM during the BMI-sensitive potentials (which also corresponded to the onset of ictal-like events), and after a decline to approximately 5 mM it remained elevated throughout the ictal event. Small, transient increases in [K+]o (up to 3.7 mM) could be seen during each interictal-like event. Following blockade of interictal- and ictal-like discharges by CNQX increases in [K+]o (up to 11 mM; 7.3 +/- 2.1; half-width = 7.2 +/- 2.3 s) still accompanied the BMI-sensitive negative-going potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1992

Responses to N-methyl-D-aspartate are enhanced in rats with petit mal-like seizures.

The responses to the glutamate agonist N-methyl-D-aspartate (NMDA) were studied in the sensori-motor cortex of rats with petit mal-like seizures. In a first study, the changes in extracellular concentration of calcium elicited through ionophoretic application of NMDA at various depths in the cortex were measured in vivo. The results show that in the cortex of epileptic rats the NMDA responses are much more widely distributed than in the cortex of control rats. In a second study, a current-source density analysis of the responses elicited through electrical stimulation of the white matter was performed in slices of neocortex in vitro. These findings show that the NMDA-dependent component of the synaptic responses are more widely distributed and of longer duration in the cortex of epileptic rats than in that of control rats. Taken together, these results suggest that in this model of absence epilepsy NMDA-dependent mechanisms are important in the triggering and maintenance of epileptic activity.

Amino Acids↗
PubMed1991

Epileptiform activity induced by low extracellular magnesium in the human cortex maintained in vitro.

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 1.5 to 2 hours of perfusion with Mg(2+)-free ACSF. The epileptiform discharges consisted of negative field potential shifts (amplitude, 0.8-10 mV) that lasted 2.5 to 80 seconds and recurred at intervals ranging between 4 and 160 seconds. Both duration and frequency of occurrence of epileptiform events were not significantly different when measured in slices obtained from spiking tissue compared with those gathered from nonspiking neocortical areas. Transient increases in [K+]o of up to 10.5 mM were associated with each epileptiform discharge; these changes were maximal and fastest in the middle neocortical layers. Spreading depression episodes were characterized by 20 to 30-mV negative shifts that lasted up to 200 seconds and were accompanied by increases in [K+]o of approximately 100 mM. Epileptiform discharges and spreading depressions did not occur during perfusion with Mg(2+)-free ACSF that contained either competitive or noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) receptor subtype. In contrast, pharmacological blockade of non-NMDA receptors did not influence the epileptiform activity observed in Mg(2+)-free ACSF. These findings demonstrate that decreasing [Mg2+]o leads to the appearance of both spontaneous epileptiform discharges and spreading depression in the human epileptogenic neocortex.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1990

Effects of pentetrazol on neuronal activity and on extracellular calcium concentration in rat hippocampal slices.

Effects of pentetrazol (PTZ) were studied on neuronal responses in dentate granule cells and area CA1 hippocampal pyramidal cells with intra- and extracellular recording techniques. PTZ induced spontaneous epileptiform field potential transients in areas CA3 and CA1, but not in the dentate gyrus. The concentration optimum for induction of spontaneous epileptiform activity was 2 mM. The epileptiform activity compared in many respects to that induced by GABA antagonists such as picrotoxin, bicuculline and penicillin. Paired pulse stimulus induced responses were affected by concentrations of 0.5 mM. In the concentration range 0.5-2 mM mostly disinhibitory effects were noted. Stimulus induced Ca2+ concentration changes were found to be maximally augmented at concentrations of 2-5 mM. In this range, intracellular studies revealed a block of frequency habituation and an increase in input resistance. The convulsant action of PTZ decreased at concentrations above 5 mM, probably due to a decrease of inward currents. We suggest that the action of PTZ in screening studies for anticonvulsants is mostly due to a decrease of GABAA-receptor mediated IPSPs.

Action Potentials↗
PubMed1990

Epileptiform activity induced by low chloride medium in the CA1 subfield of the hippocampal slice.

1. Extracellular and intracellular recordings and measurements of the extracellular concentration of free K+ ([K+]o) were performed in the CA1 subfield of the rat hippocampal slice during perfusion with artificial cerebrospinal fluid (ACSF) in which NaCl had been replaced with equimolar Na-isethionate or Na-methylsulfate (hereafter called low Cl- ACSF). 2. CAl pyramidal cells perfused with low Cl- ACSF generated intracellular epileptiform potentials in response to orthodromic, single-shock stimuli delivered in stratum (S.) radiatum. Low-intensity stimuli evoked a short-lasting epileptiform burst (SB) of action potentials that lasted 40-150 ms and was followed by a prolonged hyperpolarization. When the stimulus strength was increased, a long-lasting epileptiform burst (LB) appeared; it had a duration of 4-15 s and consisted of an early discharge of action potentials similar to the SB, followed by a prolonged, large-amplitude depolarizing plateau. The refractory period of the LB was longer than 20 s. SB and LB were also seen after stimulation of the alveus. 3. Variations of the membrane potential with injection of steady. DC current modified the shape of SB and LB. When microelectrodes filled with the lidocaine derivative QX-314 were used, the amplitudes of both SB and LB increased in a linear fashion during changes of the baseline membrane potential in the hyperpolarizing direction. The membrane input resistance, as measured by injecting brief square pulses of hyperpolarizing current, decreased by 65-80% during the long-lasting depolarizing plateau of LB. 4. A synchronous field potential and a transient increase in [K+]o accompanied the epileptiform responses. The extracellular counterpart of the SB was a burst of three to six population spikes and a small increase in [K+]o (less than or equal to 2 mM from a resting value of approximately 2.5 mM). The LB was associated with a large-amplitude, biphasic, negative field potential and a large increase in [K+]o (up to 12.4 mM above the resting value). Changes in [K+]o during the LB were largest at the border between S. oriens and S. pyramidale. This was also the site where the field potentials measured 2-5 s after the stimulus attained their maximal amplitude. Conversely, field potentials associated with the early component of the LB or with the SB displayed a maximal amplitude in the S. radiatum. 5. Spontaneous SBs and LBs were at times recorded in the CA1 and in the CA3 subfield.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Seizure-like discharges induced by lowering [Mg2+]o in the human epileptogenic neocortex maintained in vitro.

Seizure-like discharges were observed in slices of human epileptogenic neocortex maintained in vitro when [Mg2+]o was lowered near to zero. This type of epileptiform activity: (1) could occur spontaneously or following extracellular focal stimuli; (2) resembled the electrographic pattern associated with tonic-clonic seizures; (3) was accompanied by increases in [K+]o (maximally 6.2 mM from a baseline of 3.25 mM) and decreases in [Ca2+]o (maximally 0.23 mM from a baseline of 1.8 mM). Application of the selective antagonist of N-methyl-D-aspartate (NMDA) receptors, DL-2-amino-5-phosphonovalerate, suppressed in a reversible manner both spontaneous and stimulus-induced seizure-like discharges, suggesting that NMDA-activated conductances are important for the genesis of prolonged epileptiform discharges generated by human epileptogenic neocortical slices.

Epilepsies, Partial↗
PubMed1987

Ionic changes induced by excitatory amino acids in the rat cerebral cortex.

The ionic mechanisms underlying the action of excitatory amino acids were investigated in the rat motor cortex. Ion-selective microelectrodes were attached to micropipettes such that their tips were very close and local changes in extracellular concentration of sodium, calcium, and potassium ions elicited through ionophoretic applications of glutamate (Glu) and of its agonists N-methyl-D-aspartate (NMDA), quisqualate (Quis), and kainate (Ka) were measured. These agents produced moderate increases in [K+]o (up to 13 mM) but, in contrast, substantial tetrodotoxin-insensitive decreases in [Na+]o (maximally of 60 mM). NMDA-induced sodium responses could be blocked by manganese, while the Quis- and Ka-induced responses were not. Quis and Ka produced increases in [Ca2+]o or biphasic responses while NMDA, even with small doses, induced each time drastic decreases in [Ca2+]o (maximally of 1.15 mM), which could be attenuated or blocked by manganese but not by organic calcium channel blockers. NMDA responses could be abolished by reduced doses of 2-amino-phosphonovalerate. The largest Glu- and NMDA-induced calcium responses were observed in the superficial cortical layers, but such maxima disappeared after selective degeneration of pyramidal tract neurons. All amino acids produced sizeable reductions in the extracellular space volume. The following can be concluded. (i) All the excitatory amino acids tested induce an increased permeability to sodium and potassium ions. (ii) In addition, the NMDA-operated channels have specifically a large permeability for calcium, although calcium ions contribute only by less than 10% to the NMDA-induced inward currents.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1986

Long-term alterations in amino acid-induced ionic conductances in chronic epilepsy.

Extracellular free sodium (Na+)o and calcium (Ca2+)o concentration changes were measured in the rat motor cortex, using ion-selective microelectrodes. During ionophoretic applications of excitatory amino acids, decreases in (Na2+)o and in (Ca2+)o were observed. Ca2+ signals were not or very little modified by applications of tetrodotoxin while Na+ signals were slightly depressed, up to 20%. Laminar profile analysis revealed that, while the magnitude of Na+ signals was rather constant throughout the cortex, Ca2+ signals were largest in upper cortical layers. Lesioning and pharmacological experiments indicated that the corresponding permeabilities were most probably located on apical dendrites of pyramidal tract neurons. The relative amplitude of Na+ and Ca2+ signals induced by the release of the glutamate agonists N-methyl-D-aspartate, quisqualate and kainate and the shape of the laminar profile of such responses indicated that different ionic permeabilities located on different neurons underlie such responses. Similar experiments performed on chronic epileptogenic motor foci in rats indicated that the amino acid-induced ionic responses were altered. The significance of such alterations for epileptogenesis is discussed.

Amino Acids↗
PubMed1985

Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio.

The spread and persistence of epileptic seizures have generally been attributed to chemical synaptic interactions. Using ion-sensitive microelectrodes, we showed that in the allylglycine-treated photosensitive baboon, prolonged light-induced generalized seizures were accompanied by abnormally large decreases in the concentration of extracellular calcium ions, reaching values at which chemical synaptic transmission was certainly very reduced or blocked. This feature was observed in all cortical layers. Measurements of the concentration of extracellular potassium ions in the course of such light-induced seizures indicated that the observed low values of the concentration of calcium ions could not be ascribed to the occurrence of spreading depressions. These findings showed that nonsynaptic mechanisms play a prominent role in the persistence of epileptic seizures.

Animals↗
PubMed1983

Fast extracellular calcium transients: involvement in epileptic processes.

Improved liquid ion-exchanger microelectrodes made possible the observation of large, rapid decreases in the concentration of extracellular calcium ions during single epileptic spikes. Moreover, in definite cortical layers the decreases regularly started shortly before the onset of each epileptic spike. In view of the prominent role played by extracellular calcium ions in neuronal processes, including transmitter release and membrane excitability, these alterations probably exert a profound influence on the cellular events underlying epileptiform activity.

Action Potentials↗
PubMed1983

Changes in [Ca2+]o and [K+]o during repetitive electrical stimulation and during pentetrazol induced seizure activity in the sensorimotor cortex of cats.

Changes in [Ca2+]o and [K+]o were measured in the sensorimotor cortex of cats during repetitive electrical stimulation and during pentetrazol induced epileptiform activity. Repetitive stimulation of the thalamic ventrobasal complex (VB) or of the cortical surface (CS) caused decreases in [Ca2+]o by up to 0.45 mM and increases in [K+]o by up to 7 mM. Maximum reductions of [Ca2+]o delta [Ca2+]o were found in depths of 100 to 300 micrometers below cortical surface, while rises in [K+]o were largest in depths of 600 to 1000 micrometers dependent on stimulation site. At depths below 700-900 micrometers increases in [K+]o were often accompanied by rises in [Ca2+]o of about 0.2 mM. Pentetrazol (PTZ) when injected at doses of 25 to 40 mg/kg body weight induced spontaneous seizure activity, which was in about 40% preceded by a slight fall of baseline [Ca2+]o. Repetitive stimulation and spontaneous seizures resulted in delta [Ca2+]o of up to 0.6 mM, whereas rises in [K+]o remained limited to a 'ceiling level' of about 10 mM. After PTZ application, peak delta [Ca2+]o were found at the same recording sites, but, in contrast to normal cortex, decreases in [Ca2+]o were observed in all cortical layers. The enhanced Ca2+-signals after PTZ application and the observed reduction of [Ca2+]o before seizure onset suggest that PTZ utilizes Ca2+-dependent mechanisms to initiate seizure activity.

Animals↗
PubMed1983

Changes in [Ca2+]0, [K+]0 and neuronal activity during oenanthotoxin-induced epilepsy in cat sensorimotor cortex.

Effects of the convulsant drug oenanthotoxin on field potentials, neuronal discharges and extracellular free Ca2+ and K+ concentrations were studied in the sensorimotor cortex of cats. Fifteen to 20 min after topical OETX application spike activity developed (surface negative, deeper layers positive) with a frequency of 0.5-1/sec. With the maturation of the focus spikes became multipeaked and the reversal point of field potential polarity shifted deeper into the cortex. Spontaneous seizures developed when the spike activity had become negative in polarity in recording depths of 1300 micron below the cortical surface. Spontaneous seizures were associated with large rises in [K+]0 and reductions in [Ca2+]0 (delta [K+]0, delta [Ca]0). The latter were often larger than maximum changes in normal cortex. The decay in [Ca2+]0 associated with spontaneous seizures tended to precede the onset of ictal activity. The findings suggest that OETX, like other epileptogenic drugs, uses Ca2+-dependent mechanisms for the initiation of epileptiform activity.

Alkynes↗
PubMed1982

Aspartate-induced changes in extracellular free calcium in 'in vitro' hippocampal slices of rats.

Extracellular free calcium ([Ca2+]0) and neuronal activity were measured with double-barreled Ca2+-selective/reference microelectrodes in the CA1 field of rat hippocampal slices during stimulation of Schaffer collaterals and during iontophoretic application of the excitatory amino acid aspartate (Asp). Baseline [Ca2+]0 was 1.5 mM. Repetitive stimulation and aspartate application caused decreases in [Ca2+]0 (delta Ca), which were largest in the pyramidal cell layer. During iontophoretic application of GABA, aspartate often failed to induce significant alterations in [Ca2+]0. Mg2+ (9 mM) and Ni2+ (3mM) when added to the perfusion medium reduced aspartate-dependent delta Ca by 15 and 70% respectively. In tetrodotoxin (10(-6) M) containing Ringer the aspartate-induced delta Ca were about 10% smaller. These findings suggest that the decreases in [Ca2+]0 are mainly due to a postsynaptic Ca2+ entry through selective Ca2+ conductances.

Animals↗
PubMed1981

A simple and effective low cost frequency modulation system for neurophysiological recording.

A frequency modulation system to be used for electrophysiological signal recording on a standard Hifi tape recorder is described. This system can be built using a few common, easy-to-use and cheap integrated circuits. Its performance allows reliable recording of either DC potentials or fast transients (action potentials for instance). Possible uses (EEG, intracellular recording ....) are illustrated. The main advantages of this system are simplicity and low cost.

Humans↗
PubMed1981

[Mode of action of pentetrazole at the cellular level (author's transl)].

The question of the origin of the paroxysmal depolarization shifts which can be recorded from neurones within an experimental epileptogenic focus is still controversial. In this paper, a special reference is made to data obtained in thin hippocampal slices in vitro during intra- and extracellular recordings from CA1 pyramidal cell somas before and after pentylenetetrazole (PTZ) application onto the slice surface. It is shown that PTZ can decrease inhibitory potentials, increase membrane input resistance and increase action potential duration. Using calcium-selective microelectrodes, it is shown that PTZ can enhance the lowering of calcium ion concentration in extracellular space, which is normally induced by repetitive stimulations. These data, as well as those from others, support the hypothesis that paroxysmal depolarization shifts seen in hippocampus could result from the facilitation of a slow depolarizing calcium current through the cell membrane uncovered by a depression of repolarizing potassium current produced by the convulsants. The observed depression of inhibitory potential would further facilitate the development of long-lasting depolarizing potentials.

Action Potentials↗
PubMed1980

[Diminution of the extracellular concentration of calcium ions during focal epileptic crisis induced by enanthotoxin in the cat cortex].

OEnanthotoxin applied locally onto the Cat cortex produced a long-lasting epileptic focus. The basic cortical level of extracellular calcium concentration ([Ca2+]e) was decreased before the actual onset of paroxysmal discharges. In the active focus the [Ca2+]e decrease induced by a cortical or a thalamic stimulation was larger than in normal cortex. Maximal decreases were found at a depth of 300 micrometer below cortical surface. It is suggested that at this cortical level calcium conductances are increased by oenanthotoxin. This increase may be one of the mechanisms of onset of epileptic seizures.

Alkynes↗