trimethylamine/епилептични припадъци

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Differential effects of trimethylamine and quinine on seizures induced by 4-aminopyridine administration in the entorhinal cortex of vigilant rats.

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In vivo and in vitro evidence from animals suggesting that gap junctions (GJs) play a role in the spreading of epileptiform activity. We have examined the influence of the gap junction opener trimethylamine (TMA) and the connexin 36 (Cx36) gap junctional blocker, quinine, on epileptiform activity

Intra-amygdala all-trans retinoic acid inhibits amygdala-kindled seizures in rats.

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Amygdala plays an important role in induction and control of limbic seizures. There is a network of gap junctional communications in basolateral amygdala (BLA) as well. We compared the effect of intra-BLA infusion of the typical gap junction (GJ) blocker carbenoxolone (CBX), with the effect of

Involvement of gap junctions in the manifestation and control of the duration of seizures in rats in vivo.

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OBJECTIVE The possible role of gap junctions in the manifestation and control of the duration of seizures was tested on the 4-aminopyridine-induced epilepsy model in rats in vivo, by using electrophysiologic, pharmacologic, and molecular biologic techniques. METHODS; In electrophysiologic

Functional contribution of specific brain areas to absence seizures: role of thalamic gap-junctional coupling.

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The synchronized discharges typical of seizures have a multifactorial origin at molecular, cellular and network levels. During recent years, the functional role of gap-junctional coupling has received increased attention as a mechanism that may participate in seizure generation. We have investigated

Thalamic modulation of cingulate seizure activity via the regulation of gap junctions in mice thalamocingulate slice.

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The thalamus is an important target for deep brain stimulation in the treatment of seizures. However, whether the modulatory effect of thalamic inputs on cortical seizures occurs through the modulation of gap junctions has not been previously studied. Therefore, we tested the effects of different

The inhibitory effect of trimethylamine on the anticonvulsant activities of quinine in the pentylenetetrazole model in rats.

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Quinine specifically blocks connexin 36 (Cx36), one of the proteins that form gap junction channels. Quinine suppressed ictal epileptiform activity in in vitro and in vivo studies without decreasing neuronal excitability. In this study, we considered the possible mechanism of anticonvulsant effects

Trimethylaminuria associated with seizures and behavioural disturbance: a case report.

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A 16-year-old left-handed male is presented with a history of seizures associated with a fish-like odour and behavioural disturbances thought to be related to trimethylaminuria. His seizures were complex-partial (cursive) seizures and started at the age of 18 months. They occurred in the context of

Postictal spectroscopy and imaging findings mimicking brain tumor recurrence.

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(1)H magnetic resonance spectroscopic imaging (MRSI) was performed on a patient with an admission diagnosis of recurrent astrocytoma. The patient had undergone surgical resection and radiation therapy for a left occipital astrocytoma WHO grade III 12 years previously, and presented with aphasia,

Longitudinal study of MRS metabolites in Rasmussen encephalitis.

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This study analyses the evolution of metabolite changes in an 8-year-old boy with focal Rasmussen encephalitis. Five MRI examinations, including magnetic resonance spectroscopy (MRS) were performed over 9 months. Following complex partial status, T2-weighted imaging showed transient dramatic signal

Epilepsy and trimethylaminuria: A new case report and literature review.

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Trimethylaminuria is a metabolic disorder characterized by the excessive excretion of trimethylamine in bodily secretions, which confers a very unpleasant odour resembling that of dead fish. Literature reports only two cases affected by trimethylaminuria and epilepsy. We describe a third patient

Connexin 43 Differentially Regulates Epileptiform Activity in Models of Convulsive and Non-convulsive Epilepsies.

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The influence of astrocytic cell networks on neuronal network activity is an emerging issue in epilepsy. Among the various mechanisms by which astrocytes modulate neuronal function, synchronization of astrocytes via gap junction channels is widely considered to be a crucial mechanism in epileptic

[Progress on formation and taste-masking technology of stench of animal medicines]

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Animal medicines have been called "medicine with affinity to flesh and blood" by doctors of all ages, which always act as an important branch of Chinese medicine. They have various types, extensive sources and long application history, with unique cli-nical effects in

Prolonged epileptiform bursting induced by 0-Mg(2+) in rat hippocampal slices depends on gap junctional coupling.

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The transition from brief interictal to prolonged seizure, or 'ictal', activity is a crucial event in epilepsy. In vitro slice models can mimic many phenomena observed in the electroencephalogram of patients, including transition from interictal to ictaform or seizure-like activity. In field

Unilateral microinjection of carbenoxolone into the pontis caudalis nucleus inhibits the pentylenetetrazole-induced epileptiform activity in rats.

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Pontine reticular formation (PRF) is involved in the generation and maintenance of generalized epileptic seizures. Carbenoxolone (CBX) is a gap junction blocker with anticonvulsant properties. Therefore, the present study was designed to explore the effects of CBX microinjected into the pontis

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