cholera/seizures

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Cholera toxin B decreases bicuculline seizures in prenatally morphine- and saline-exposed male rats.

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Prenatal morphine exposure on gestation days 11-18 alters bicuculline-induced seizures in rats during development and in adulthood. Adult, morphine-exposed male progeny exhibit an increased latency to bicuculline seizures, which can be reversed by administration of the opioid receptor antagonist

Epilepsy-like convulsive seizures induced by cholera toxin administration into amygdaloid complex and lateral ventricle.

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Epilepsy-like convulsive seizures have been induced by cholera toxin administration into the rat amygdaloid complex and lateral ventricle. Between the 8th and 48th h following the administration, rhythmic spike discharges (1-3 spikes/s) were electroencephalographically observed bilaterally in the

Ganglioside alterations of the rat brain in cholera toxin-induced convulsion.

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[Cholera in children. A report of 8 cases].

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Cholera is an acute intestinal infection caused by Vibrio cholerae 01. When an infected person presents severe dehydration and is not adequately treated, he or she will develop hypovolemic shock and eventually could died. There is scarce information concerning this disease in the Pediatric group.

Effect of pertussis and cholera toxins administered supraspinally on CA3 hippocampal neuronal cell death and the blood glucose level induced by kainic acid in mice.

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The effect of cholera toxin (CTX) or pertussis toxin (PTX) administered supraspinally on hippocampal neuronal cell death in CA3 region induced by kainic acid (KA) was examined in mice. After the pretreatment with either PTX or CTX intracerebroventricularly (i.c.v.), mice were administered i.c.v.

Epileptic focus induced in rat by intrahippocampal cholera toxin: neuronal properties in vitro.

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Injecting 0.5-1.0 microgram of cholera toxin into rat hippocampus induces a chronic epileptic focus which generates interictal discharges and brief epileptic seizures intermittently over the following seven to 10 days. Here we examined the electrophysiological properties of hippocampal slices

[Cholera toxin induced epileptogenic focus--special reference to cyclic AMP metabolism and epileptogenic focus (author's transl)].

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Epilepsy-like convulsive seizures have been induced by cholera toxin administration into the rat amygdaloid complex. Between the 8th and 48th hr after the administration, rhythmic spike discharges (1--3 spikes/sec) were electroencephalographically observed bilaterally in the amygdaloid complexes,

Epileptic focus induced by intrahippocampal cholera toxin in rat: time course and properties in vivo and in vitro.

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A small dose (0.5-1.0 micrograms) of cholera toxin injected into rat hippocampus induced an epileptic focus which discharged intermittently for 7-10 days. Epileptic discharges lasting from 70 ms to 2 min were recorded in vivo through implanted electrodes. The longer bursts could generalize to the

Aspirin attenuates spontaneous recurrent seizures in the chronically epileptic mice.

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OBJECTIVE Neuroinflammatory processes are pathologic hallmarks of both experimental and human epilepsy, and could be implicated in the neuronal hyperexcitability. Aspirin represents one of the non-selective nonsteroidal anti-inflammatory drugs with fewer side effects in long-term application. This

Measles-associated diarrhoea in northeastern Thailand.

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A significant proportion of the illness and death of diarrhoeal diseases in the developing world is estimated to be due to the diarrhoea associated with measles. During February 1983-January 1984 a prospective study of measles in a hospital in Northeastern Thailand was conducted. A total of 550

Intracranial V. cholerae sialidase protects against excitotoxic neurodegeneration.

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Converging evidence shows that GD3 ganglioside is a critical effector in a number of apoptotic pathways, and GM1 ganglioside has neuroprotective and noötropic properties. Targeted deletion of GD3 synthase (GD3S) eliminates GD3 and increases GM1 levels. Primary neurons from GD3S-/- mice are resistant

Folate interactions with cerebral G proteins.

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Intracerebral folate injections produce convulsions and brain lesions, folic acid itself and tetrahydrofolate being more potent toxins than 5-methyltetrahydrofolate, the primary folate of mammalian extracellular fluids. Folates are known to excite neurons, by unknown mechanisms Folates stimulate GTP

Possible regulation of high-affinity glutamate uptake in synaptosomes of normal and epileptic mice.

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Glutamate (Glu) uptake is the primary mechanism for its removal from the synapse. In genetic audiogenic seizures (AGS), Glu uptake is elevated prior to the appearance of seizures. Increased Glu uptake is also observed in synaptosomes from normal mice preincubated with lithium or nitroarginine, an NO

Glutamatergic drugs exacerbate symptomatic behavior in a transgenic model of comorbid Tourette's syndrome and obsessive-compulsive disorder.

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We previously created a transgenic mouse model of comorbid Tourette's syndrome and obsessive-compulsive disorder (TS+OCD), by expressing a neuropotentiating cholera toxin (CT) transgene in a subset of dopamine D1 receptor-expressing (D1+) neurons thought to induce cortical and amygdalar glutamate

Interactions of lithium and drugs that affect signal transduction on behaviour in rats.

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The therapeutic mechanism of the action of lithium in the treatment of bipolar affective disorder is not known, in spite of a burgeoning number of biochemical studies linking lithium to signal transduction processes. This article reviews a decade of studies examining the behavioural manifestations

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