uridine/seizures

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Effect of electrical convulsions on uridine labeling and activity pattern in nerve cells in mice.

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Male white mice were exposed to electroshock and then injected intravenously with 5-[3H]uridine immediately after the shock. After 5, 30, or 60 min or 6, 12, or 24 h, the mice were killed, microautoradiographs were prepared, and grains were counted in the cortex, hippocampus, and basal ganglia. The

Study of Uridine Effect on the Development of Audiogenic Tonic Seizures in Krushinsky-Molodkina Strain Rats.

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The latency of tonic seizure in response to loud sound (in rats of the Krushinsky-Molodkina strain with audiogenic epilepsy) had been slightly (although statistically significantly) longer after chronic uridine injections (100 mg/kg, i.p., three times a day during 9 or 12 days). The recovery time

Effects of uridine in models of epileptogenesis and seizures.

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Due to the limited efficacy and side effects of current antiepileptic drugs (AEDs), the search for new therapeutic agents is critical. Uridine, a possible endogenous antiepileptic modulator, has been demonstrated to have anticonvulsant effects in some models of epilepsy, but not others. In this

[Role of uridine and pathogenesis of epileptic seizures].

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Patterns of seizures, hippocampal injury and neurogenesis in three models of status epilepticus in galanin receptor type 1 (GalR1) knockout mice.

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The neuropeptide galanin exhibits anticonvulsant effects in experimental epilepsy. Two galanin receptor subtypes, GalR1 and GalR2, are present in the brain. We examined the role of GalR1 in seizures by studying the susceptibility of GalR1 knockout (KO) mice to status epilepticus (SE) and

Alteration of RNA synthesis in vitro in intact cerebral cortex nuclei induced by convulsions in seizure-susceptible El mice.

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We examined the effects of convulsive seizures on in vitro RNA synthesis by cerebral cortex nuclei in El mice. The rate of incorporation of [3H]uridine-5'-triphosphate by intact nuclei during seizures was decreased to 47.4% compared with the rate during the interictal period, but gradually

Alterations in polyadenylic acid-containing messenger RNA synthesis of brain polysomes after seizures of seizure-susceptible E1 mice.

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The effect of seizures on synthesis of the polyadenylic acid (poly(A]-containing messenger RNA (mRNA) isolated from brain polysomes in a genetically seizure-susceptible E1 mouse was studied in vivo. The seizure in the E1 mice was induced by tossed-up stimulation. Immediately after the seizure

Cerebrospinal fluid nucleotide metabolites following short febrile convulsions.

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Cerebrospinal fluid (CSF) markers of cerebral energy depletion were measured in 32 infants and children following short (less than 10 minutes) febrile convulsions, and in 19 controls. Specific and sensitive indices of high-energy phosphate compound depletion (hypoxanthine, xanthine and uridine)

Pharmacokinetic and pharmacodynamic considerations for the clinical efficacy of perampanel in focal onset seizures.

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Medical therapy is the mainstay of management of epilepsy. Despite the increasing number of available antiepileptic drugs (AEDs), approximately one-third of epileptic patients do not have adequate control of seizures. There is still a need for the development of new AEDs with enhanced

Uridine release during aminopyridine-induced epilepsy.

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Uridine, like adenosine, is released under sustained depolarization and it can inhibit hippocampal neuronal activity, suggesting that uridine may be released during seizures and can be involved in epileptic mechanisms. In an in vivo microdialysis study, we measured the extracellular changes of

Interaction between uridine and GABA-mediated inhibitory transmission: studies in vivo and in vitro.

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Na+-independent [3H]gamma-aminobutyric acid (GABA) binding to membrane preparations from frontal cortex, hippocampus, and thalamus is competitively inhibited by the in vitro addition of a naturally occurring pyrimidinic compound, uridine. Moreover, the intraperitoneal injection of uridine produces a

Functional disruption of pyrimidine nucleoside transporter CNT1 results in a novel inborn error of metabolism with high excretion of uridine and cytidine.

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Genetic defects in the pyrimidine nucleoside transporters of the CNT transporter family have not yet been reported. Metabolic investigations in a patient with infantile afebrile tonic-clonic seizures revealed increased urinary uridine and cytidine excretion. Segregation of this metabolic trait in

Non-adenosine nucleoside inosine, guanosine and uridine as promising antiepileptic drugs: a summary of current literature.

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Adenosine (Ado) and some non-adenosine (non-Ado) nucleosides including inosine (Ino), guanosine (Guo) and uridine (Urd) are modulatory molecules in the central nervous system (CNS), regulating different physiological and pathophysiological processes in the brain such as sleep and epilepsy. Indeed,

A Patient With CAD Deficiency Responsive to Uridine and Literature Review.

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CAD encodes a multifunctional enzyme involved in de novo pyrimidine biosynthesis, and pyrimidine can be alternatively recycled from uridine. Trio whole-exome sequencing identified CAD compound heterozygous mutations in a new male patient with global developmental delay (DD), refractory

CAD mutations and uridine-responsive epileptic encephalopathy.

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Unexplained global developmental delay and epilepsy in childhood pose a major socioeconomic burden. Progress in defining the molecular bases does not often translate into effective treatment. Notable exceptions include certain inborn errors of metabolism amenable to dietary intervention. CAD encodes

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