Disease relevance of Corazol

• Blockade of tonic hindlimb extension in the maximal electroshock test and blockade of tonic and clonic seizures produced by pentylenetetrazole and bicuculline were obtained by elevating GABA in the ventral midbrain tegmentum [1].
• GalKO mice showed increased propensity to develop status epilepticus after perforant path stimulation or systemic kainic acid, as well as greater severity of pentylenetetrazol-induced convulsions [2].
• Ganaxolone was assessed in the low-dose pentylenetetrazol (PTZ) and the gamma-hydroxybutyric acid (GHB) model of absence seizures in rats [3].
• During ischemia in so-called slow heart-rate hearts, there is a marked inhibition of the mitochondrial ATPase mediated by inhibitor protein binding to the enzyme (Rouslin, W., and Pullman, M. E. (1987) J. Mol. Cell. Cardiol. 19, 661-668) [4].
• The protection against Metrazol and the toxicity of PB are both potentiated by PEMA at low concentrations [5].

Psychiatry related information on Corazol

• Seizures induced in the rat by electroshock or by injections of pentylenetetrazol increase the specific binding of diazepam to putative receptor sites in cerebral cortical membranes [6].
• The pentylenetetrazole and peptide treatments also improved reversal learning [7].
• Sedation was assessed by measuring spontaneous locomotor activity and beam walking performance, and anticonvulsant efficacy was determined by pentylenetetrazole (PTZ) and amygdala kindling-induced seizures [8].
• Pentylenetetrazol-induced amnesia: a case for overt seizures [9].
• Do the reductions in social interaction produced by picrotoxin and pentylenetetrazole indicate anxiogenic actions [10]?

High impact information on Corazol

• While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory [11].
• Interruption of the connection between the mammillary bodies and the anterior nucleus of the thalamus in guinea pigs, by discrete bilateral electrolytic lesions of the mammillothalamic tract, resulted in essentially complete protection from the behavioral and electroencephalographic convulsant action and lethal effect of pentylenetetrazol [12].
• Compounds that antagonize neuronal excitation induced by dicarboxylic amino acids were tested in two animal models of epilepsy, namely sound-induced seizures in DBA/2 mice and threshold pentylenetetrazol seizures in Swiss mice [13].
• The calcium content of the cell membrane area increased during pentylenetetrazole-induced bursting activity [14].
• In the neurons of Aplysia californica pentylenetetrazole (2 millimolar) greatly reduced chloride-dependent responses to the iontophoresis of putative transmitters [15].

Chemical compound and disease context of Corazol

• Acetone suppressed seizures in all of the models, with the following ED(50)'s (expressed in mmol/kg): maximal electroshock, 6.6; pentylenetetrazole, 9.7; generalized kindled seizures, 13.1; focal kindled seizures, 26.5; AY-9944, 4 [16].
• Neurotoxicity and protection against maximal electroshock and Metrazol seizures from primidone (PRM), phenobarbital (PB), and phenylethylmalonamide (PEMA) were determined in mice for each drug separately and expressed in terms of brain concentrations [17].
• 2-Ethylcyclohexanone was very effective against pentylenetetrazol seizures but did not prevent maximal electroshock seizures [18].
• In the 2-piperidinone series, 3,3-diethyl compound 7b is the most effective anticonvulsant against pentylenetetrazole-induced seizures (ED50, 37 mg/kg; PI (TD50/ED50), 4.46), and 3-benzyl compound 4c (ED50, 41 mg/kg; PI, 7.05) is the most effective anticonvulsant against seizures induced by maximal electroshock [19].
• The hypotension produced by leptazol was mainly due to inhibition of sympathetic vasomotor tone since it was little affected by section of the vagi and by atropine given intravenously [20].

Biological context of Corazol

• The M1 muscarinic receptor antagonist pirenzepine in low doses decreases resting heart rate; this effect declines with age (Poller, U., G. Nedelka, J. Radke, K. Pönicke, and O.-E. Brodde. 1997. J. Am. Coll. Cardiol. 29:187-193) [21].
• Conversely, the convulsant agents pentylenetetrazol and picrotoxin each caused an increase in the state of phosphorylation of these proteins [22].
• The mice show a reduction in the duration and severity of seizures induced by kainate or pentylenetetrazole, and both necrosis and apoptosis of hippocampal neurons are prevented [23].
• To discriminate between events that are products of the seizures elicited by KA and those that are specifically associated with its neurotoxic actions, we have examined the expression of cellular immediate-early genes (cIEGs) following KA or pentylenetetrazol (PTZ) treatment in c-fos-lacZ transgenic rats [24].
• This phenotype is maintained on two different strain backgrounds, is rescued by transgenic expression of Thy-1 and by administration of the GABA(A) receptor antagonist pentylenetetrazole [25].

Anatomical context of Corazol

• Administration of the convulsants pentylenetetrazole (Metrazole) or picrotoxin to rats caused a dramatic increase in mRNAs of four putative transcription factor genes, zif/268, c-jun, jun-B, and c-fos, in neurons of the hippocampus and dentate gyrus, as well as other areas of the cerebral cortex, including pyriform cortex and cingulate cortex [26].
• We found that nur77 and nurr-1 are induced in the adrenal gland upon treatment with pentylene tetrazole (Ptz; Metrazole) [27].
• RNA blot analysis demonstrates that NGFI-C mRNA is induced within minutes of stimulation of PC12 cells by nerve growth factor and is similarly activated in brain after a Metrazol-induced seizure [28].
• Microvessels were isolated by albumin flotation and glass bead filtration from cerebral cortices of gerbils decapitated during pentylenetetrazol (PTZ)-induced seizures and ischemia-induced seizures [29].
• Metrazole-stimulated seizure activity triggers rapid (<1 h) but transient up-regulation of MKP-3 mRNA in the cortex, piriform cortex, and some amygdala nuclei [30].

Associations of Corazol with other chemical compounds

• Intracerebroventricular administration of equimolar doses of 2'-deoxyinosine, which is more potent than inosine in inhibiting the binding of [3H]diazepam in vitro, significantly increased pentylenetetrazole-evoked seizure latency [31].
• In contrast, both 7-methylinosine and thymidine were ineffective in inhibiting the in vitro binding of [3H]diazepam and increasing the latency to pentylenetetrazole-induced seizures in vivo [31].
• Convulsant doses of pentylenetetrazol (100 mg/kg) increase levels of both cyclic adenosine monophosphate (AMP) and cyclic guanosine monophosphate (GMP in mouse cerebral cortex and hippocampus [32].
• Hippocampal acetylcholine release was evaluated with the microdialysis technique in freely moving rats either after acute administration of isoniazid (an inhibitor of GABA synthesis) or pentylenetetrazole (PTZ) (a blocker of the GABAA receptor-associated Cl- channel) or after chronic administration of PTZ [33].
• Recent studies have shown marked increases in brain content of neuropeptide Y (NPY) after seizures induced by intraperitoneal injection of kainic acid and after pentylenetetrazole kindling in the rat [34].

Gene context of Corazol

• In contrast to these lasting phosphorylation patterns, transient seizure activity by pentylenetetrazole provoked only a brief c-Jun phosphorylation and JNK activation [35].
• Metrazole induces the sequential activation of c-fos, proenkephalin, and tyrosine hydroxylase gene expression in the rat adrenal gland: modulation by glucocorticoid and adrenocorticotropic hormone [36].
• Involvement of tumor necrosis factor alpha and interleukin-1beta in enhancement of pentylenetetrazole-induced seizures caused by Shigella dysenteriae [37].
• Administration of convulsant doses of Metrazole (pentylenetetrazol) and picrotoxin, as well as maximal electroshock, results in a rapid but transient increase in c-fos mRNA in mouse brain [38].
• An acute intraperitoneal injection of pentylenetetrazole (PTZ) at a convulsive dose significantly potentiated binding of the probe for AP1 in the cerebral cortex, hippocampus, striatum, hypothalamus and midbrain, without affecting that in the medulla-pons and cerebellum, 2 h after the administration [39].

Analytical, diagnostic and therapeutic context of Corazol

• Spiking was reactivated after 4 weeks by intramuscular injection of pentylenetetrazole [40].
• Truly simultaneous electroencephalogram (EEG) and functional magnetic resonance imaging (fMRI) were registered in curarized rats injected with convulsive doses of pentylenetetrazol (PTZ, 65 mg/kg, sc) [41].
• Seizures were induced in rats by intraperitoneal injection of pentylenetetrazole (PTZ, 70 mg/kg), followed, 30 min later, by injection of [1-13C]glucose and [1,2-13C]acetate [42].
• Synthesis of both enantiomers of 29 and 39 indicated that the R isomers 30 and 40 were the most active and showed very good protection against MES, pentylenetetrazole, and mercaptopropionic acid induced seizures after oral administration in mice [43].
• The new compounds were found to possess anticonvulsant effects against seizures induced both by means of auditory stimulation in DBA/2 mice and by pentylenetetrazole or maximal electroshock in Swiss mice [44].

References