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veratridine/atrophy

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Ca2+-mediated neuronal death in rat brain neuronal cultures by veratridine: protection by flunarizine.

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Neuronal cell degeneration was studied in vitro in primary rat brain neuronal cultures grown in serum-free, chemically defined, CDM R12 medium, by measuring lactate dehydrogenase (LDH) released in the culture medium. A Ca2+-dependent neuronal cell degeneration was observed after prolonged and

The role of potassium channels in Schwann cell proliferation in Wallerian degeneration of explant rabbit sciatic nerves.

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1. Patch clamp studies of whole-cell ionic currents and biochemical studies of proliferation were carried out on Schwann cells of myelinated axons in explant segments of sciatic nerves of adult rabbit maintained in culture for 0-10 days. 2. Schwann cell proliferation, as assayed by [3H]thymidine
The effect of various Ca++ antagonists and local anesthetics on neuronal cell degeneration induced by veratridine was studied in primary rat brain neuronal cultures. Cell death was quantified by measuring lactate dehydrogenase (LDH) released in the culture medium. The neuronal cell degeneration was
Previous studies have shown that dopamine, bicuculline, or d-amphetamine reduce the electrical and dye-coupling between the axon terminals of the horizontal cells of the turtle retina (see Piccolino et al., 1984). In the present study we observed similar effects following the application of

The role of striatal metabotropic glutamate receptors in degeneration of dopamine neurons: review article.

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Degeneration of dopaminergic nigrostriatal neurons is a primary cause of Parkinson's disease. Oxidative stress, excitotoxicity and mitochondrial failure are thought to be key mechanisms responsible for degeneration of dopaminergic cells. We found that the selective antagonist of the mGluR5 subtype

Generating and influencing Torsades de Pointes--like polymorphic ventricular tachycardia in isolated guinea pig hearts.

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Torsades de Pointes (TdP) is a polymorphic ventricular arrhythmia which can degenerate into ventricular fibrillation. The most typical symptom of TdP is the ECG morphology where QRS complexes seem to rotate around the isoelectric baseline. Bradycardia and delayed repolarization are regarded as

Sodium dependence of the nerve growth factor--regulated hexose uptake in chick embryo ganglionic cells.

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Embryonic dorsal root ganglionic cells, when incubated in vitro in the absence of nerve growth factor (NGF) undergo a general metabolic degeneration which is preceded by certain changes in permeation properties. Previous studies demonstrated that NGF can rapidly modulate permeation properties which

The effects of excitatory amino acids on intracellular calcium in single mouse striatal neurons in vitro.

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Using microspectrofluorimetry and the calcium-sensitive dye fura-2, we examined the effect of excitatory amino acids on [Ca2+]i in single striatal neurons in vitro. N-methyl-D-aspartic acid (NMDA) produced rapid increases in [Ca2+]i. These were blocked by DL-2-amino-5-phosphonovaleric acid (AP5), by
Sodium channels in Drosophila embryonic neurons were characterized pharmacologically in the primary culture of individual gastrulae. In normal cultures, presence of sodium channels was demonstrated by neuronal degeneration in the presence of veratridine and ouabain, which was inhibited by

Glutamate cytotoxicity in a neuronal cell line is blocked by membrane depolarization.

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To understand better the proximate mechanism involved in the excitotoxic response to L-glutamate (Glu), we have exploited the Glu receptor present in the N18-RE-105 neuroblastoma-embryonic retinal hybrid cell line. These cells undergo lysis dependent on extracellular Ca2+ when exposed to Glu. We now

Does thyroid hormone influence the maturation of cerebellar granule neurones?

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The following hypotheses were tested: is the degeneration of differentiating granule cells in the internal granular layer of the thyroid deficient cerebellum due to a direct requirement of these cells for thyroid hormone, or is it mediated through the failure of some of these cells to make synaptic

Amyloid beta-peptide inhibits high-affinity choline uptake and acetylcholine release in rat hippocampal slices.

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The characteristic pathological features of the postmortem brain of Alzheimer's disease (AD) patients include, among other features, the presence of neuritic plaques composed of amyloid beta-peptide (A beta) and the loss of basal forebrain cholinergic neurons, which innervate the hippocampus and the

Rescue of mesencephalic dopaminergic neurons in culture by low-level stimulation of voltage-gated sodium channels.

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We used a model system in which dopaminergic (DA) neurons from embryonic rat mesencephalon undergo spontaneous and selective degeneration as they develop in culture. Here, we show that DA cell loss can be prevented efficiently by low concentrations of the Na+ channel agonist veratridine. The

L-alpha-aminoadipic acid as a regulator of kynurenic acid production in the hippocampus: a microdialysis study in freely moving rats.

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L-alpha-Aminoadipic acid is a lysine metabolite with neuroexcitatory properties, and has previously been shown to inhibit the production of the broad spectrum excitatory amino acid receptor antagonist kynurenic acid in brain tissue slices. The effects of L-alpha-aminoadipic acid on the levels of
Spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats were fed a diet containing 10% rapeseed (canola) oil or soybean oil as dietary fat, and given drinking water containing 1% NaCl for 26 weeks. From the 10th week and later, systolic blood pressure in the canola oil group became higher
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