colchicine/seizures

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Mechanisms of colchicine neurotoxicity in the dentate gyrus: dissociation of seizures and cell death.

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Extracellular field potentials and the EEG were studied in the dentate gyrus of the rat after intrahippocampal injections of colchicine, which is a relatively selective neurotoxin for dentate granule cells. Injection of colchicine (0.5 microliters of a 5-mg/ml solution of colchicine in deionized

Decreased seizure threshold after intrahippocampal colchicine injection in rats.

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Wet dog shaking elicited by perforant path stimulation is little affected by bilateral injection of colchicine into the dorsal hippocampal formation but virtually eliminated by bilateral injection into the ventral hippocampal formation. Injection of colchicine into either dorsal or ventral

Differential effects of colchicine lesions of dentate granule cells on wet dog shakes and seizures elicited by direct hippocampal stimulation.

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Direct electrical stimulation of either the dorsal or ventral hippocampal formation elicits wet dog shakes and overt seizures. Destruction of dentate granule cells in the dorsal hippocampal formation does not significantly reduce the number of wet dog shakes elicited by ventral hippocampal

The effects of colchicine in mammalian brain from rodents to rhesus monkeys.

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The injection of colchicine into rats and monkeys produced two different types of brain damage. At selected doses, intradentate colchicine preferentially destroyed DGC in rats, whereas damage was less selective and more severe in monkeys. Experiments were performed with different tubulin-binding

Anatomical and behavioral effects of colchicine administration to rats late in utero.

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Offspring from pregnant rats injected with 4mg/kg body weight colchicine on Embryonic Days 18, 19, and 20 were found to have isocortical and hippocampal structures greatly reduced in mass when examined at birth. Cells with pyknotic nuclei were found in Layers 5, 4, and 3 of the cerebral isocortex,

Cellular localization of neuropeptide-Y receptors in the rat hippocampus: long-term effects of limbic seizures.

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To clarify the cellular localization of neuropeptide-Y receptor subtypes in the dentate gyrus and CA3 sector of the rat dorsal hippocampus and their changes after kainic acid-induced seizures, we used receptor autoradiography to measure [125I]PYY binding to Y1 and Y2 receptors after colchicine

Administration of kainic acid and colchicine alters mu and lambda opiate binding in rat hippocampus.

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Quantitative in vitro autoradiography was used to assess the effects of kainic acid (KA) and colchicine (COL) on mu and lambda opiate binding in the rat hippocampus. Rats were treated with either systemic KA, a neurotoxin that damages CA3 pyramidal cells and causes seizures and wet-dog shakes, or

Ventral hippocampal dentate granule cell lesions enhance motor seizures but reduce wet dog shakes induced by mu opioid receptor agonist.

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The role of the ventral hippocampal dentate granule neurons in the mu opioid receptor agonist-induced motor seizures and wet dog shakes was examined in this study. [NMe-Phe3-D-Pro4]morphiceptin (9.4 nmol) was injected into the left ventral hippocampus of rats 14 days after unilateral or bilateral

Limbic seizures cause pronounced changes in the expression of neurokinin B in the hippocampus of the rat.

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Immunohistological and in situ hybridization techniques were used to study the influence of kainic acid-induced seizures and of pentylenetetrazol kindling on neurokinin B immunoreactivity and neurokinin B mRNA in the rat hippocampus. Pronounced increases in neurokinin B immunoreactivity were

Acute colchicine intoxication--possible role of erythromycin administration.

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A 29-year-old patient with familial Mediterranean fever and amyloidosis involving the kidney, liver, and gastrointestinal tract received longterm colchicine, 1 mg daily. In the last year she developed diarrhea and abdominal pain, that coincided with toxic colchicine blood levels. After 2 weeks of

Dentate granule cells are essential for kainic acid-induced wet dog shakes but not for seizures.

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The purpose of this study was to determine the role that dentate granule cells play in wet dog shakes (WDS), behavioral seizures, and hippocampal cell loss caused by systemic administration of kainic acid (KA). Rats were given bilateral injections of colchicine (COL) into the hippocampal formation

Protective effects of mossy fiber lesions against kainic acid-induced seizures and neuronal degeneration.

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The effects of a hippocampal mossy fiber lesion have been determined on neuronal degeneration and limbic seizures provoked by the subsequent intracerebroventricular administration of kainic acid to unanesthetized rats. Mossy fiber lesions were made either by transecting this pathway unilaterally or

Benzodiazepine receptor increases after repeated seizures: evidence for localization to dentate granule cells.

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Repeated seizures, whether induced by kindling or electroshock, result in increased numbers of benzodiazepine receptors in hippocampal formation membranes. We sought to determine the cellular constituents containing the receptor increases. Binding studies of microdissected samples localized the

Kindled seizure-induced reduction of muscarinic cholinergic receptors in rat hippocampal formation: evidence for localization to dentate granule cells.

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The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal formation was analyzed by membrane binding assay and in vitro autoradiography. The destruction of dentate granule cells, either by neonatal irradiation or colchicine

[Neuronal plasticity associated with learning and epileptic seizures: LTP and KIP].

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Long-term synaptic potentiation (LTP) and kindling-induced potentiation (KIP) are hypothesized to play an important role in spatial learning and kindling development, respectively, and the possible roles of LTP in spatial learning and KIP in kindling development are reviewed in this paper. Blockage

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