The Effects of Amfonelic Acid and Some Other Central Stimulants on Mouse Striatal Tyramine, Dopamine and Homovanillic Acid

Abstract

1 The concentrations of p-and m-tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous administration of amfonelic acid, (+)-amphetamine or nomifensine.2 The administration of 2.5-25 mg/kg of amfonelic acid produced a reduction in p-tyramine that lasted at least 8 h. m-Tyramine was significantly increased and this was observed between 2 and 24 h after drug treatment. The levels of homovanillic acid were increased within 4 h after amfonelic acid administration.3 (+)-Amphetamine treatment (5 mg/kg) produced a reduction in p-tyramine observed up to 4 h after its administration and no significant changes in m-tyramine. 4 The administration of 10 mg/kg of nomifensine produced no significant changes in p-tyramine, m-tyramine or homovanillic acid. By increasing the dose to 20 mg/kg, nomifensine produced an increase in p-tyramine and homovanillic acid. 5 The present results support the view that amfonelic acid and (+)-amphetamine would respectively release granular or newly synthesized dopamine, both actions being accompanied by an increase in tyrosine hydroxylase activity and dopamine turnover which in turn reduces p-tyramine but produces no change or an increase in m-tyramine.6 The effects of nomifensine were observed after the administration of a relatively high dose (20 mg/kg), that was lethal to some mice (about 20%, at 2 h), and more likely to possess unspecific actions.

Psychotoxic Effects of Ofloxacin

“…Amfonelic acid, which has structural analogies to ofloxacin, has been developed by Sterling-Winthrop as a psychostimulant ( Va/li and Bouyard, 1978). However, despite the chemical analogy, their effects -at least on monaminergic processes -do not seem to be identical (Juorio, 1982). It has been reported that a number of quinolones, especially ciprofloxacin (Ciprobay®), norfloxacin (Barazan®), enoxacin, pipemidic acid, and ofloxacin inhibit the binding of GABA in iso-Iated rat neurons (Hori et al, 1985(Hori et al, , 1986.…”

Dissolution Process and Thermodynamic Model Correlation of Homovanillic Acid in Different Solvents and Intermolecular Force Analysis

“…HVA has been recognized and utilized as a biomarker of various diseases and as a target molecule to measure the overall dopamine activity in the human body since the 1970s. 3,4 Therefore, the determination of HVA concentration in plasma, urine, or cerebrospinal fluid is related to diagnosis, disease progress monitoring, and drug dose optimization. 5,6 Cancer of adrenal medullary pheochromocytoma and neuroblastoma and neurological diseases such as post-traumatic stress disorder are related to the increase of HVA concentration in body fluid.…”

“…306-08-1, white crystalline powder, and its chemical structure is presented in Figure ) is a metabolite of catecholamine. , It is mainly derived from the whole grass and root of the dicotyledonous plant Paeoniaceae. HVA has been recognized and utilized as a biomarker of various diseases and as a target molecule to measure the overall dopamine activity in the human body since the 1970s. , Therefore, the determination of HVA concentration in plasma, urine, or cerebrospinal fluid is related to diagnosis, disease progress monitoring, and drug dose optimization. , Cancer of adrenal medullary pheochromocytoma and neuroblastoma and neurological diseases such as post-traumatic stress disorder are related to the increase of HVA concentration in body fluid. However, the decrease of HVA concentration is a typical symptom of depression and Parkinson’s disease. , …”