Disease relevance of Flurothyl

• Thresholds for flurothyl-induced clonic and tonic-clonic seizures were determined [1].
• For animals experiencing multiple seizures, flurothyl seizure threshold was significantly lower than that of controls at 60 to 80 days, but not at 10 days, after hypoxia [2].
• A single, 2-hour episode of status epilepticus induced by flurothyl (1,500 mul) in 4-day-old rats irreversibly curtailed brain weight and brain DNA [3].
• High doses of each of the metals administered acutely caused a drop in body weight but had an inconsistent effect on flurothyl-induced seizure thresholds [4].
• Moderate systemic hypoglycemia had proconvulsant effects on flurothyl-induced clonic (forebrain) seizures [5].

Psychiatry related information on Flurothyl

• We previously demonstrated that there is a significant increase of interstitial dopamine of neuronal origin in the rat striatum after electroconvulsive shock (ECS) but not after chemically (flurothyl) induced seizures [6].
• Memory-enhancing low concentrations of flurothyl, applied after post-training amnesic treatment with carbon dioxide, reversed the carbon dioxide amnesia [7].
• Strong flurothyl treatment (1.7% v/v for 8 min) produces retrograde amnesia in chicks when administered as long as 24 hr after one-trial avoidance training with a strongly aversive stimulus [8].
• Flurothyl, a vapor with convulsive properties, had no pronounced effects on locomotor activity at subconvulsant concentrations [9].

High impact information on Flurothyl

• We investigated the effects of repeated early-life seizures induced by flurothyl inhalation on intrinsic membrane properties of hippocampal pyramidal neurons from young rats (postnatal day 15-20) [10].
• In CA1 pyramidal cells from flurothyl-treated rats, the spike frequency adaptation and afterhyperpolarizing potential following a spike train were markedly reduced when compared with controls [10].
• Intracellular recordings of CA1 and CA3 pyramidal neurons from flurothyl-treated and control rats revealed no significant differences in resting membrane potential, input resistance, membrane time constant, and action potential characteristics [10].
• Daily flurothyl-induced generalized clonic seizures resulted in a progressive decrease in both the generalized seizure threshold and the latency to the first myoclonic jerk [11].
• The substantia nigra pars reticulata (SNPR) has previously been shown to undergo tissue necrosis following status epilepticus induced by flurothyl in the rat [12].

Chemical compound and disease context of Flurothyl

• Carbamazepine and valproate each afforded protection against seizures induced by electroshock or by inhalation of hexafluorodiethyl ether (HFDE) [13].
• NET knockout (NET KO) mice essentially phenocopied the effects of reboxetine on flurothyl-induced seizures, and the trends were extended to pentylenetetrazole and maximal electroshock seizures (MES) [14].
• In rats, we used flurothyl to induce generalized seizures over a controlled time period and 2-deoxyglucose autoradiography mapping technique [15].
• Results indicate that thresholds for flurothyl-induced tonic-clonic seizures develop under the control of postnatal testosterone [16].
• The anticonvulsant effect was seizure-specific; thus, U50,488 protected against supramaximal electroshock seizures but failed to raise the threshold of flurothyl-induced convulsions [17].

Biological context of Flurothyl

• A seizure-producing chemical, flurothyl, was used to activate the neuron, thereby causing a demand for energy that could not be completely met by oxidative phosphorylation alone [18].
• In the present study, we investigated the effect of alterations in hippocampal mitotic activity on changes in seizure threshold and phenotype using flurothyl kindling [19].
• Selective impairment of GABAergic synaptic transmission in the flurothyl model of neonatal seizures [20].
• Flurothyl-induced convulsions delay the onset of sexual maturation in the female rat [21].
• Our data demonstrate that the BZD1 binding sites are involved in the SNR control of flurothyl seizures in adult and PN 15 male rats [22].

Anatomical context of Flurothyl

• The effect of convulsions induced by flurothyl on ribonucleic acid synthesis in rat cerebral cortex during the recovery phase [23].
• To investigate this relationship between hippocampal mitotic activity and epileptogenesis, mice were given brain irradiation, focused mainly on the hippocampus, bilaterally, and were exposed to the flurothyl kindling model of epileptogenesis [19].
• Increased mitotic activity in the dentate gyrus of the hippocampus of adult C57BL/6J mice exposed to the flurothyl kindling model of epileptogenesis [24].
• In each condition, generalized seizure behaviours were elicited in C57BL/6 mice using flurothyl and classified as either "forebrain" (face and forelimb clonus) or "brainstem" (running/bouncing, treading, tonic extension) [25].
• The lack of an effect of estradiol alone or estradiol followed by progesterone on flurothyl-induced seizures indicates that estradiol's effects on seizure susceptibility do not result from increased neuronal excitability throughout the brain, but rather involve action within the limbic system [26].

Associations of Flurothyl with other chemical compounds

• Seizures were induced by inhalation of the convulsant gas flurothyl, and terminated by withdrawal of flurothyl and a single injection of thiopental [27].
• Bilateral nigral infusions of muscimol markedly facilitated the development of flurothyl seizures in a dose-response manner and differed significantly from the vehicle controls or rats infused with muscimol dorsally to the substantia nigra [28].
• Desflurane (difluoromethyl 1-fluoro 2,2,2-trifluoroethyl ether: CF2-H-O-CFH-CF3) is a potent inhalation anesthetic agent being investigated for possible clinical use [29].
• The effects of flurothyl and iso-flurothyl were studied using the whole-cell patch-clamp technique on agonist-activated chloride currents in human GABA(A), glycine, and GABA(C) rho(1) receptors expressed in HEK 293 cells [30].
• 1. Effects of two volatile anesthetics [halothane (Hal) and enflurane (Enf)] and a volatile convulsant [hexafluorodiethyl ether (HFE)] on amino acid-induced membrane currents in neurons dissociated from the nucleus tractus solitarius of the rat were examined [31].

Gene context of Flurothyl

• Thus, we hypothesized that BDNF signaling pathways are altered by flurothyl-induced seizures [32].
• METHODS: Using flurothyl gas inhalation, we examined seizure-induction latencies in Cln3-/- mice and wildtype (wt) controls at time points that represent late neonatal, immature, mature, and aged time points [33].
• ZnT3-/- mice, which lack histochemically reactive zinc in synaptic vesicles, had slightly higher thresholds to seizures elicited by the GABA(A) antagonist, bicuculline, and no differences in seizure threshold were seen in response to pentylenetetrazol or flurothyl [34].
• Enhanced seizure susceptibility to flurothyl and increased seizure-induced c-fos mRNA expression were reversed by pretreatment with L-threo-3, 4-dihydroxyphenylserine, which partially restores the NE content in Dbh -/- mice [35].
• In flurothyl-induced seizures, CA deficient mice displayed longer latencies to the onset of both clonic and tonic-clonic seizures [36].

Analytical, diagnostic and therapeutic context of Flurothyl

• Oral administration of CBZ as an aqueous suspension every 8 h at a dose of 250 mg/kg was continuously protective against HFDE-induced seizures and was minimally toxic as measured by weight gain over 8 weeks of treatment [37].
• Here we studied the effects of moderate hypoglycemia on primarily generalized flurothyl-induced seizures in vivo and, using EEG recordings, we determined involvement of the hippocampus in hypoglycemic seizures [5].
• We conclude that hexafluorodiethyl ether-induced 20-min seizures lead to rapid, localized glial and neuronal changes in the rat brain as evidenced by GFA and NF immunohistochemistry, while the vascular network remains intact [38].
• Using a 4 day rat flurothyl kindling seizure model we found that the kindling rate was significantly decreased by intraventricular injection of CSF from depressed patients exposed to 1 Hz rTMS [39].
• Flurothyl-induced status epilepticus was studied by light and electron microscopy (LM, EM) to determine the time course and structural features of neuronal necrosis in the vulnerable brain regions in epilepsy [40].

References