Disease relevance of Clausenamide

• The effects of (-)clausenamide on functional recovery in transient focal cerebral ischemia [1].
• RESULTS: I.c.v. injection of naloxone 1 nmol, affecting neither the basal PS amplitude nor the LTP induced by tetanus, reduced the l-clausenamide-potentiated LTP only when it was administrated prior to clausenamide [2].

Psychiatry related information on Clausenamide

• (-)Clausenamide ameliorated anisodine-induced memory deficits in step-through test in mice [3].
• The protective action of (-)clausenamide against anisodine-induced amnesia is due to its ability to reverse the ACh reduction [3].

High impact information on Clausenamide

• The effect of clausenamide on synaptic transmission in the dentate gyrus of rats in vivo and its possible mechanism of action were investigated in this study [4].
• We also found that mitochondria were involved in (-)clausenamide triggered Ca2+ transient [5].
• Application of IP3 receptor inhibitor MgCl2 and PLC-gamma inhibitor U73122 suppressed (-)clausenamide induced Ca2+ transient, suggesting that the major source of (-)clausenamide induced Ca2+ transient was from IP3 receptor pathway [5].
• The mean amplitude of (-)clausenamide (1 microM) induced Ca2+ transient was similar in extracellular solution with or without calcium; and (-)clausenamide failed to trigger calcium transient after treatment with endoplasmic reticulum Ca2+ pumps inhibitor BHQ to exhaust intracellular Ca2+ stores [5].
• (-)Clausenamide improves long-term potentiation impairment and attenuates apoptosis after transient middle cerebral artery occlusion in rats [6].

Chemical compound and disease context of Clausenamide

• OBJECTIVES: To study the action mechanism of a new cognition enhancer clausenamide and the effect of clausenamide on regional acetylcholine (ACh) levels, and to examine anisodine-induced ACh decrease in mice of memory deficits, and to compare the effect of (-)clausenamide on ACh with that of (+)clausenamide [3].

Biological context of Clausenamide

• The effects of (-)clausenamide (clau) on spatial cognitive functions and hippocampal long-term potentiation (LTP) after transient focal cerebral ischemia in rats were investigated [1].
• The pharmacokinetics of clausenamide (CLA) enantiomers and their metabolites were investigated in Wistar rat [7].
• The effects of (-)clausenamide (clau) on long-term potentiation (LTP) and neuronal DNA damage were investigated in a rat model of middle cerebral artery (MCA) occlusion [6].

Anatomical context of Clausenamide

• To identify which cytochrome P450 (CYP) isoform(s) are responsible for the metabolism of clausenamide (CLA) enantiomers in rats, effects of various CYP isoform inducers and inhibitors on the formation of CLA metabolites were investigated in liver microsomes [8].
• Of nine clausenamides, only (+) and (+/-)clausenamide markedly increased liver cytosol GSH content [9].
• RESULTS: Single administration of (-)clausenamide or (+)clausenamide (10, 20, 50 mg/kg, i.g.) had no effect on the ACh level in the frontal cortex, hippocampus and striatum [3].
• RESULTS: (-)Clausenamide increased the activity of ChAT and protein content in cultured neurons, as well as stimulated proliferation of neuronal cells, support survival and neurite outgrowth of neurons [10].

Analytical, diagnostic and therapeutic context of Clausenamide

• At the present study, we investigated the clausenamide induced Ca2+ signaling in primary cultures of rat cortical neurons by using laser confocal microscopy [5].
• Stereoselective pharmacokinetics of clausenamide enantiomers and their major metabolites after single intravenous and oral administration to rats [7].

References