ribose/seizures

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The combination of ribose and adenine promotes adenosine release and attenuates the intensity and frequency of epileptiform activity in hippocampal slices: Evidence for the rapid depletion of cellular ATP during electrographic seizures.

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In addition to being the universal cellular energy source, ATP is the primary reservoir for the neuromodulator adenosine. Consequently, adenosine is produced during ATP-depleting conditions, such as epileptic seizures, during which adenosine acts as an anticonvulsant to terminate seizure activity

Poly(ADP-ribose) signal in seizures-induced neuron death.

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Poly(ADP-ribose) is found to be involved in many physiological or pathological processes. It is mainly modulated by poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG). Either PARP or PARG is associated with the neuronal death in a variety of neurodegenerative diseases.

Inhibition of CD38/Cyclic ADP-ribose Pathway Protects Rats against Ropivacaine-induced Convulsion.

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BACKGROUND The CD38/cyclic ADP-ribose (cADPR) pathway plays a role in various central nervous system diseases and in morphine tolerance, but its role in local anesthetic intoxication is unknown. The aim of this study was to determine the role of the CD38/cADPR pathway in ropivacaine-induced

Bok Is Not Pro-Apoptotic But Suppresses Poly ADP-Ribose Polymerase-Dependent Cell Death Pathways and Protects against Excitotoxic and Seizure-Induced Neuronal Injury.

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Bok (Bcl-2-related ovarian killer) is a Bcl-2 family member that, because of its predicted structural homology to Bax and Bak, has been proposed to be a pro-apoptotic protein. In this study, we demonstrate that Bok is highly expressed in neurons of the mouse brain but that bok was not required for

Benzamide, a poly(ADP-ribose) polymerase inhibitor, is neuroprotective against soman-induced seizure-related brain damage.

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Effect of D-ribose on purine synthesis and neurological symptoms in a patient with adenylosuccinase deficiency.

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Oral supplementation of 10 mmol/kg/day of D-ribose to a patient with an inherited deficit of adenylosuccinase, severe psychomotor retardation, and epilepsy caused a marked increase in plasma concentration and urinary excretion of urate, while minor changes in succinylpurine levels were observed.

D-ribose therapy in four Polish patients with adenylosuccinate lyase deficiency: absence of positive effect.

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Deficiency of adenylosuccinate lyase (ADSL) (OMIM 103050) is an autosomal recessive disorder of the purine de novo synthesis pathway and purine nucleotide cycle, diagnosed so far in approximately 50 patients. The clinical presentation is characterized by severe neurological involvement including

Zinc inhibits astrocyte glutamate uptake by activation of poly(ADP-ribose) polymerase-1.

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Several processes by which astrocytes protect neurons during ischemia are now well established. However, less is known about how neurons themselves may influence these processes. Neurons release zinc (Zn2+) from presynaptic terminals during ischemia, seizure, head trauma, and hypoglycemia, and

Poly(ADP-ribose) polymerase inhibition protects epileptic hippocampal neurons from apoptosis via suppressing Akt-mediated apoptosis-inducing factor translocation in vitro.

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Inhibition of poly(ADP-ribose) polymerase (PARP) has been proposed to have a neuroprotective effect on hippocampal neurons in animal models of epilepsy. However, the mechanisms of PARP-mediated epileptic neuron apoptosis in vitro are still not thoroughly understood. Therefore, we investigated the

Progressive neurologic deterioration and renal failure due to storage of glutamyl ribose-5-phosphate.

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A six-year-old boy presented with a history of seizures, progressive neurologic deterioration, and proteinuria. Physical examination revealed mildly coarse facies, failure to thrive, generalized hypotonia with muscle wasting, and optic atrophy; there was no organomegaly. The family history suggested

Maternal seizures can affect the brain developing of offspring.

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To elucidate the impact of maternal seizures in the developing rat brain, pregnant Wistar rats were subjected to the pilocarpine-induced seizures and pups from different litters were studied at different ages. In the first 24 h of life, blood glucose and blood gases were analyzed. (14)C-leucine

Repeated electroconvulsive seizure induces c-Myc down-regulation and Bad inactivation in the rat frontal cortex.

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Repeated electroconvulsive seizure (ECS), a model for electroconvulsive therapy (ECT), exerts neuroprotective and proliferative effects in the brain. This trophic action of ECS requires inhibition of apoptotic activity, in addition to activation of survival signals. c-Myc plays an important role in

Poly(ADP-ribose) polymerase inhibitor is neuroprotective in epileptic rat via apoptosis-inducing factor and Akt signaling.

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3-Aminobenzamide (3-AB), an inhibitor of poly(ADP-ribose) polymerase (PARP), has been proved to have neuroprotective properties. In this study, we examined the role of 3-AB in rat hippocampal neuron death induced by seizures. Our data showed that the seizures resulted in PARP activation and

PARP1 activation/expression modulates regional-specific neuronal and glial responses to seizure in a hemodynamic-independent manner.

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Poly(ADP-ribose) polymerase-1 (PARP1) plays a regulatory role in apoptosis, necrosis and other cellular processes after injury. Status epilepticus (SE) induces neuronal and astroglial death that show regional-specific patterns in the rat hippocampus and piriform cortex (PC). Thus, we investigated

Prolonged seizures and cellular injury: understanding the connection.

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Status epilepticus (SE)-induced neuronal death is morphologically necrotic and is initiated by excessive glutamate release, which activates postsynaptic N-methyl-D-aspartate (NMDA) receptors and triggers receptor-mediated calcium influx (excitotoxicity). This results in activation of intracellular

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