The mouse neocortical slice: Preparation and responses to excitatory amino acids

Burton, N.R.; Smith, Dianna; Stone, T.W.

doi:10.1016/0742-8413(87)90045-4

Cited by 17 publications

(20 citation statements)

References 15 publications

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“…Several groups of investigators have recently observed that slices of rat or mouse neocortex maintained in a twin compartment, grease gap bath (Harrison & Simmonds, 1985) produce spontaneous depolarizing shifts often with rhythmic after potentials when the magnesium content of the superfusing medium is lowered from a normal content of 1 mm to omM (Horne et al, 1986, Burton et al, 1987. This phenomenon is also seen in human cortex (Avoli et al, 1987).…”

Section: Introductionmentioning

confidence: 74%

“…This phenomenon is also seen in human cortex (Avoli et al, 1987). These depolarizing shifts usually appear within 30-60min of superfusion with magnesiumfree ACSF and gradually increase in both size and frequency over the following 1 to 2 h (Burton et al, 1987). Not all slices exhibit this activity spontaneously although most can be induced into producing depolarizing shifts following depolarization with an NMDA receptor agonist.…”

Section: Introductionmentioning

confidence: 93%

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Effect of changing extracellular levels of magnesium on spontaneous activity and glutamate release in the mouse neocortical slice

Smith

Connick

Stone

1989

British J Pharmacology

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1 The mouse neocortical slice preparation, maintained in a two compartment, grease gap bath, exhibits spontaneous depolarizing activity (with or without rhythmic after potentials) after perfusion with magnesium-free artificial cerebrospinal fluid. 2 If the magnesium concentration is decrementally lowered over an extended time period, then incrementally raised following a similar time course, the spontaneous depolarizing shift activity shows a hysteresis (with regard to both frequency and amplitude), the depolarizing shifts being more resistant to magnesium during the the incremental period. 3 The amino acid content of the perfusing fluid was analysed by high performance liquid chromatography (h.p.l.c.). Although a basal efflux of 6 amino acids was quantifiable, only glutamate levels increased following superfusion of the preparation with magnesium-free, artificial cerebrospinal fluid. 4 Glutamate release increased to 266% of the resting release in the presence of magnesium within the first 12min of the change into magnesium-free artificial cerebrospinal fluid. This increase in release preceded the onset of spontaneous depolarising activity. The release of glutamate remained elevated at 182% of control up to 60min after perfusion with magnesium-free buffer, when depolarizing activity was well established. 5 A model is presented and discussed for the genesis and maintenance of the spontaneous depolarizing shifts. It is suggested that the maintenance of this spontaneous activity reflects a long term enhancement of neocortical neurone excitability which may be related to long term potentiation in the hippocampus.

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Section: Introductionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 93%

Effect of changing extracellular levels of magnesium on spontaneous activity and glutamate release in the mouse neocortical slice

Smith

Connick

Stone

1989

British J Pharmacology

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“…This necessarily limits observations to this kind of neurone; cells that do not project via the callosal fibres but bear a receptor subtype for example could not be detected. Indirect effects on projecting neurones in these wedges mediated by neurones using action potentials must be very small, since inclusion of tetrodotoxin (TTX) in the ACSF had no measurable effect on the responses evoked by a variety of excitatory amino acid agonists (Harrison & Simmonds, 1985;Burton et al, 1987); though the contribution if any of direct TTX resistant effects on presynaptic terminals cannot be assessed. These experiments also assume firstly that drug effects at receptors are well described by the single site model (see Barlow, 1980), and secondly that the data obtained (after logarithmic transformation) are normally distributed.…”

Section: Discussionmentioning

confidence: 99%

“…Full details of the mouse neocortex preparation and a qualitative description of its properties appears elsewhere (Burton et al, 1987).…”

Section: Methodsmentioning

confidence: 99%

“…Acceptable sections had as rostral and caudal limits the genu of the corpus callosum and the rostral region of the cerebral ventricles respectively. These were transferred to an incubation chamber containing a 95% 02, 5% CO2 atmosphere at room temperature (20-240C (Harrison & Simmonds, 1985;Burton et al, 1987) Data were accepted only if the dose-ratio of recovery/control (R/G) was less than two. Thereafter, the extent of the rightward shift of the log doseresponse curve relative to the control log doseresponse curve gave the log dose-ratio, and its antilog the estimated dose-ratio (DRE) for a given concentration of antagonist.…”

Section: Tissue Preparationmentioning

confidence: 99%

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A quantitative pharmacological analysis of some excitatory amino acid receptors in the mouse neocortex in vitro

Burton

Smith

Stone

1988

British J Pharmacology

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1The effects of 2-amino-5-phosphonovalerate and kynurenate, either alone or in combination, were tested on responses evoked by the excitatory amino acid agonists quinolinate, ibotenate, Nmethyl-D-aspartate and N-methyl-DL-aspartate by use of an in vitro preparation of mouse neocortex and artificial cerebrospinal fluid nominally free of magnesium. 2 Schild plots for 2-amino-5-phosphonovalerate, using each of the excitatory amino acids, were linear and had a slope not significantly different from one. The apparent pA2 values for 2-amino-5-phosphonovalerate using each of the excitatory amino acids were 4.98 (quinolinate), 5.00 (N-methyl-DL-aspartate), 4.92 (N-methyl-D-aspartate) and 5.05 (ibotenate). The apparent pA2 obtained using ibotenate was distinct from that of N-methyl-D-aspartate but there were no significant differences between pA2 estimates for quinolinate, N-methyl-D-aspartate or N-methyl-DL-aspartate. 3 Schild plots for kynurenate, using each of the excitatory amino acids, were linear and had a slope of 1.36 + 0.03, significantly greater than one. The estimated apparent pA2 values for kynurenate were 3.65 (quinolinate), 3.71 (N-methyl-DL-aspartate), 3.65 (N-methyl-D-aspartate) and 3.89 (ibotenate). The apparent pA2 obtained using ibotenate was distinct from that of the other agonists. 4 Experiments using combinations of 2-amino-5-phosphonovalerate and kynurenate indicated that both antagonists apparently acted competitively at receptors activated by ibotenate or by quinolinate. 5 These results indicate that ibotenate acts at a site distinct from that of quinolinate, N-methyl-Daspartate and N-methyl-DL-aspartate.

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Carbamazepine inhibits NMDA-induced depolarizations in cortical wedges prepared from DBA/2 mice

Lancaster

Davies

1992

Experientia

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There is some doubt as to the mechanism of action of the widely-used anticonvulsant drug, carbamazepine. In cortical wedges prepared from genetically epilepsy-prone DBA/2 mice, carbamazepine at therapeutic concentrations (1-10 microM) markedly reduced the depolarization produced by N-methyl-D-aspartate (NMDA). The NMDA sub-type of glutamate receptor has been implicated in the pathogenesis of epilepsy and the inhibitory action of carbamazepine on this response suggests that the anticonvulsant action of the drug may be due to its blockade of NMDA receptor-mediated events.

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The mouse neocortical slice: Preparation and responses to excitatory amino acids

Cited by 17 publications

References 15 publications

Effect of changing extracellular levels of magnesium on spontaneous activity and glutamate release in the mouse neocortical slice

Effect of changing extracellular levels of magnesium on spontaneous activity and glutamate release in the mouse neocortical slice

A quantitative pharmacological analysis of some excitatory amino acid receptors in the mouse neocortex in vitro

Carbamazepine inhibits NMDA-induced depolarizations in cortical wedges prepared from DBA/2 mice

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