Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.Reference of 695-53-4. In my other articles, you can also check out more blogs about 695-53-4
Reference of 695-53-4, Chemistry is the science of change. But why do chemical reactions take place? Why do chemicals react with each other? The answer is in thermodynamics and kinetics.In a document type is Article, and a compound is mentioned, 695-53-4, 5,5-Dimethyloxazolidine-2,4-dione, introducing its new discovery.
Effects of antiepileptic drugs on GABA responses and on reduction of GABA responses by PTZ and DMCM on mouse neurons in cell culture
The mechanisms of action of antiepileptic drugs effective against generalized absence seizures (antiabsence AEDs) remain uncertain. Antiabsence AEDs are generally effective against seizures induced in experimental animals by pentylenetetrazol (PTZ) and methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), drugs which reduce GABAergic inhibition. Thus, antiabsence AEDs have been suggested to enhance GABAergic inhibition. We studied the effects of several AEDs on GABA responses recorded from mouse spinal cord neurons grown in primary dissociated cell culture. Four antiabsence AEDs were included: ethosuximide (ESM), dimethadione (DMO), sodium valproate (VPA), and diazepam (DZP). Two experimental AEDs, CGS 9896 and ZK 91296, with anticonvulsant action against PTZ- or DMCM-induced seizures were also included. Possible effects of the antiabsence and experimental AEDs on PTZ- and DMCM-induced inhibition of GABA responses were also evaluated. PTZ and DMCM reversibly reduced GABA responses in a concentration-dependent manner. PTZ completely inhibited GABA responses at 10 mM (IC50 of 1.1 mM), whereas DMCM-induced inhibition of GABA responses reached a plateau level of 39% of control values at 1 muM (IC50 of 33 nM). ESM (1,200 muM), DMO (6 mM), VPA (200 muM), CGS 9896 (2 muM), and ZK 91296 (2 muM) did not alter GABA responses. DZP enhanced GABA responses in a concentration-dependent manner. The inhibition of GABA responses produced by PTZ 1 mM was unaltered by ESM (600 muM), DMO (6 mM), CGS 9896 (1 muM), or ZK 91296 (1 muM). Coapplication of VPA (200 muM) and PTZ (1 mM) slightly enhanced the PTZ effect. DZP (>10 nM), however, reversed the PTZ-induced reduction of GABA responses. The DMCM (250 nM) inhibition of GABA responses was unaltered by ESM (600 muM), DMO (2 mM), or VPA (200 muM). CGS 9896 (2 muM) and ZK 91296 (2 muM), however, antagonized the DMCM effect. DZP (>10 nM) significantly reversed the DMCM-induced inhibition of GABA responses. The lack of effect of VPA, ESM, and DMO on postsynaptic GABA responses suggests that direct enhancement of postsynaptic GABA action is not a common mechanism of action of antiabsence AEDs. The AEDs DZP, CGS 9896, and ZK 91296 all reversed DMCM, but not PTZ, reduction of GABA responses, suggesting that these AEDs blocked DMCM seizures by acting at benzodiazepine receptors. However, since only DZP enhanced GABA responses, it is unclear how CGS 9896 and ZK 91296 blocked PTZ seizures.
Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.Reference of 695-53-4. In my other articles, you can also check out more blogs about 695-53-4
Reference:
Oxazolidine – Wikipedia,
Oxazolidine | C3H1351NO – PubChem