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glutamic acid decarboxylase/епилептични припадъци
Линкът е запазен в клипборда
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Developmental PCB Exposure Increases Audiogenic Seizures and Decreases Glutamic Acid Decarboxylase in the Inferior Colliculus.
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Previously, we observed that developmental polychlorinated biphenyl (PCB) exposure resulted in an increase in audiogenic seizures (AGSs) in rats. However, the rats were exposed to loud noise in adulthood, and were not tested for AGS until after 1 year of age, either of which could have interacted
Convulsions induced by methylmalonic acid are associated with glutamic acid decarboxylase inhibition in rats: a role for GABA in the seizures presented by methylmalonic acidemic patients?
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Methylmalonic acid (MMA) is an endogenous convulsing compound that accumulates in methylmalonic acidemia, an inborn error of the metabolism characterized by severe neurological dysfunction, including seizures. The mechanisms by which MMA causes seizures involves the activation of the
MDMA decreases glutamic acid decarboxylase (GAD) 67-immunoreactive neurons in the hippocampus and increases seizure susceptibility: Role for glutamate.
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3,4-Methylenedioxy-methamphetamine (MDMA) is a unique psychostimulant that continues to be a popular drug of abuse. It has been well documented that MDMA reduces markers of 5-HT axon terminals in rodents, as well as humans. A loss of parvalbumin-immunoreactive (IR) interneurons in the hippocampus
Hippocampal granule cells express glutamic acid decarboxylase-67 after limbic seizures in the rat.
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Temporal lobe epilepsy is the most common form of epilepsy. Decreased GABA-ergic inhibition has been suggested as one cause of hyperexcitability. On the other hand, increased expression of glutamic acid decarboxylase, the rate-limiting enzyme of GABA synthesis, has been found in interneurons of the
Genetic variability in glutamic acid decarboxylase genes: associations with post-traumatic seizures after severe TBI.
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Post traumatic seizures (PTS) occur frequently after traumatic brain injury (TBI). Since gamma-amino butyric acid (GABA) neurotransmission is central to excitotoxicity and seizure development across multiple models, we investigated how genetic variability for glutamic acid decarboxylase (GAD)
Cerebral glutamic acid decarboxylase activity and gamma-aminobutyric acid concentrations in mice susceptible or resistant to audiogenic seizures.
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DBA/2 mice between 21 and 28 days of age are highly susceptible to sound-induced seizures. Drug studies suggest a possible deficit of gamma-aminobutyric acid (GABA)-mediated neurotransmission may be involved. We have measured the whole brain GABA concentration and glutamic acid decarboxylase
The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures.
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The intracerebroventricular administration of Zn2+ (0.3 mumol/10 microliters) causes epileptic seizures characterized by running fits, jumping, vocalization, fasiculation of facial muscles, myoclonic movements of the limbs and tonic-clonic convulsions. These episodes are blocked or reversed by
Selective resistance of taurine-fed mice to isoniazide-potentiated seizures: in vivo functional test for the activity of glutamic acid decarboxylase.
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Taurine, 2-aminoethanesulfonic acid, is one of the most abundant free amino acids especially in excitable tissues, with wide physiological actions. We have previously reported that in mice, supplementation of the drinking water with taurine induces alterations in the inhibitory GABAergic system. In
Mice lacking the 65 kDa isoform of glutamic acid decarboxylase (GAD65) maintain normal levels of GAD67 and GABA in their brains but are susceptible to seizures.
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The gene encoding of the 65 kDa isoform of the gamma-aminobutyric acid (GABA)-synthesizing enzyme, glutamic acid decarboxylase (GAD), GAD65, was targeted in mice by homologous recombination. Viable GAD65 -/- mice were obtained with the expected mendelian frequency and displayed no gross
Seizures induced by allylglycine, 3-mercaptopropionic acid and 4-deoxypyridoxine in mice and photosensitive baboons, and different modes of inhibition of cerebral glutamic acid decarboxylase.
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1. DL-C-Allyglycine, 4-deoxypyridoxine hydrochloride and 3-mercaptopropionic acid have been studied with reference to their convulsant effects in mice and in baboons (Papio papio) with photosensitive epilepsy, and their action on the cerebral enzyme synthesizing gamma-aminobutyric acid
Vitamin B 6 -dependency of glutamic acid decarboxylase in the kidney from a patient with vitamin B 6 dependent convulsion.
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Anti-Glutamic Acid Decarboxylase Encephalitis Presenting With Choreo-Dystonic Movements and Coexisting Electrographic Seizures.
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Glutamic acid decarboxylase (GAD) in mammalian tissue outside the central nervous system, and its possible relevance to hereditary vitamin B6 dependency with seizures.
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A comparison of the effects of allylglycine and 2-keto-4-pentenoic acid on cerebral glutamic acid decarboxylase activity and convulsions in mice [proceedings].
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Glutamic acid decarboxylase autoimmunity with brainstem, extrapyramidal, and spinal cord dysfunction.
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OBJECTIVE
To describe novel neurological manifestations associated with glutamic acid decarboxylase (GAD65) autoimmunity.
METHODS
This retrospective study (1987-2003) describes 62 patients Incidentally found to have a serum autoantibody that bound selectively to synapse-rich central nervous system
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