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tyrosine/epileptischer anfall
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Lamotrigine inhibits the in situ activity of tyrosine hydroxylase in striatum of audiogenic seizure-prone and audiogenic seizure-resistant Balb/c mice.
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Lamotrigine (LTG), an anticonvulsive drug, was tested for its effects on striatal content of DA and its metabolites, DOPAC and HVA, in audiogenic seizure-resistant (ER) and audiogenic seizure-prone (EP) lines of Balb/c mice. A single dose of LTG (20 mg/kg) prevented audiogenic seizures in
Receptor tyrosine kinase gene amplification is predictive of intraoperative seizures during glioma resection with functional mapping.
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OBJECTIVEIntraoperative seizures during craniotomy with functional mapping is a common complication that impedes optimal tumor resection and results in significant morbidity. The relationship between genetic mutations in gliomas and the incidence of intraoperative seizures has not been well
Differential effects of alpha-methyl-p-tyrosine and 6-hydroxydopamine on pentylenetetrazol seizures in mice.
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An intraperitoneal injection of the tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine, did not alter the incidence of seizures induced by pentylenetetrazol, but increased the severity and duration of the tonic and clonic phases which resulted in death of some animals. By contrast,
Central action of a catechol-amide seizure-inducing agent: opposing effect on tyrosine and tryptophan hydroxylase activity in vivo.
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The audiogenic seizure-inducing drug H13/04 was found to elicit opposing effects on the in vivo accumulation of 5-HTP (5-hydroxytryptophan) and DOPA (3,4-dihydroxyphenylalanine) in the brain following inhibition of L-amino acid decarboxylase. In strains of mice that normally do not exhibit
Reduced immunoreactivity of tyrosine hydroxylase in the hypothalamic paraventricular nucleus of the seizure sensitive gerbil.
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We compared the immunoreactivity and numbers of tyrosine hydroxylase (TH) immunoreactive neurons and neuropil in the paraventricular nucleus (PVN) of the hypothalamus between the seizure sensitive (SS) and seizure resistant (SR) gerbils. The distributional pattern of TH immunoreactivity was similar
Kainic acid-induced seizures: potentiation by alpha-methyl-p-tyrosine.
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We have investigated the influence of central noradrenergic and dopaminergic systems on the susceptibility of rats to seizures in the kainic acid (KA)-model of epilepsy. In the dose range of 0.75 to 10 mg/kg s.c., KA dose-dependently induced characteristic behavioural changes. Partial depletion of
Effect of tyrosine on the potentiation by aspartame and phenylalanine of metrazol-induced convulsions in rats.
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Male rats were treated by oral intubation with tyrosine (Tyr), at doses of 0.5 and 1.0 g/kg body weight, alone or together with 1 g aspartame (APM)/kg body weight, or an equivalent dose of phenylalanine (Phe; 0.5 g/kg body weight); the effects on seizures induced by an effective dose of metrazol
Halogenated aromatic amino acid 3,5-dibromo-D: -tyrosine produces beneficial effects in experimental stroke and seizures.
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The effects of the halogenated aromatic amino acid 3,5-dibromo-D: -tyrosine (3,5-DBr-D: -Tyr) were studied in rat models of stroke and epileptic seizures caused by middle cerebral artery occlusion (MCAo) through respective intracerebral injection of endothelin-1 (ET-1) and intraperitoneal (i.p.)
Effect of repeated seizure experiences on tyrosine hydroxylase immunoreactivities in the brain of genetically epilepsy-prone rats.
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The genetically epilepsy-prone rat (GEPR) is a model of generalized tonic/clonic epilepsy, and has functional noradrenergic deficiencies that act as partial determinants for the seizure predisposition and expression. The present study investigated the effect of repeated seizure experiences by
Regulation of norepinephrine transporter and tyrosine hydroxylase mRNAs after kainic acid-induced seizures.
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Noradrenergic locus coeruleus (LC) efferents to the forebrain suppress seizures in several models of epilepsy. Using in situ hybridization, we demonstrate that tyrosine hydroxylase (TH) and norepinephrine transporter (NET) but not vesicular monoamine transporter 2 (VMAT2) mRNA levels are transiently
Regionally selective stimulation of mitogen activated protein (MAP) kinase tyrosine phosphorylation after generalized seizures in the rat brain.
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Immunoblot analysis using a phosphotyrosine-specific antibody was performed to investigate tyrosine phosphorylation of the mitogen activated protein (MAP) kinase in the rat brain. Epileptic seizures induced by systemic injection of bicuculline caused a rapid and transient stimulation of MAP kinase
Seizure-induced protein tyrosine phosphorylation in rat brain regions.
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Phosphorylation of protein tyrosines is an important modulatory process for cell signaling and other cellular functions. Rat brain regions were examined for altered protein phosphotyrosines, using Western blot analysis and microwave irradiation to limit postmortem alterations, after administration
Tyrosine hydroxylase-immunoreactive neurons in the temporal lobe in complex partial seizures.
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The anterior mesial portion of the temporal lobe removed from 16 patients who underwent surgery for the treatment of complex partial seizures was found to contain tyrosine hydroxylase-immunoreactive neurons. The distribution of these neurons was correlated with the underlying neuropathological
Seizure activity results in increased tyrosine phosphorylation of the N-methyl-D-aspartate receptor in the hippocampus.
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Systemic administration of kainic acid (KA) induces status epilepticus (SE) that causes neurodegeneration and may subsequently lead to spontaneous recurrent seizures. We investigated the effects of KA-induced SE on tyrosine phosphorylation and solubility properties of the NMDA receptor. Following 1
Repetitive febrile seizures in rat pups cause long-lasting deficits in synaptic plasticity and NR2A tyrosine phosphorylation.
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Adult rats with early-life frequently repetitive febrile seizures (FRFS), but not single febrile seizure (SFS), exhibited impaired performance in inhibitory avoidance tasks but without significant hippocampal neuronal loss. The mechanisms of long-term memory impairment in the hippocampus of adult
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