A study of the role of catecholamines in the response to various central stimulants.
The effect of nomifensine on the depletion of brain serotonin and catecholamines induced respectively by fenfluramine and 6-hydroxydopamine in rats. Interrelationships between electroshock, the blood-brain barrier, and catecholamines.
A clinical and biochemical study of a trial of iproniazid in the treatment of depression. 2-(2-ethoxyphenoxymethyl)tetrahydro-1,4-oxazine hydrochloride, a potential psychotropic agent.
Mallion KB, Todd AH, Turner RW, Bainbridge JG, Greenwood DT, Madinaveitia J, Somerville AR, Whittle BA.The treatment of depressive states with G 22355 (imipramine hydrochloride). Uber die Behandlung depressiver Zustände mit einem Iminodibenzylderivat (G 22355). Amphetamine and apomorphine responses in the rat following 6-OHDA lesions of the nucleus accumbens septi and corpus striatum.
Selective 6OHDA-induced destruction of mesolimbic dopamine neurons: abolition of psychostimulant-induced locomotor activity in rats. A cholinergic-adrenergic hypothesis of mania and depression. Janowsky DS, el-Yousef MK, Davis JM, Sekerke HJ.Nomifensine: a new potent inhibitor of dopamine uptake into synaptosomes from rat brain corpus striatum. Depression induced by Rauwolfia compounds. A COMPARISON OF IMIPRAMINE, CHLORPROMAZINE AND RELATED DRUGS IN VARIOUS TESTS INVOLVING AUTONOMIC FUNCTIONS AND ANTAGONISM OF RESERPINE. Effects of drugs on the disposition of H-3-norepinephrine in the rat brain. Effect of nomifensine on motor activity, dopamine turnover rate and cyclic 3',5 -adenosine monophosphate concentrations of rat striatum. Chlorpromazine in the treatment of mental illness. Nomifensine: a potent dopaminergic agonist of antiparkinson potential. Effects of amphetamine on the turnover rate of brain catecholamines and motor activity. Potentiation of the antidepressive effect of a monoamine-oxidase inhibitor by tryptophan. The "switch process" in manic-depressive illness. Biogenic amines in normal and abnormal behavioral states.
Methylphenidate-like effects of the new antidepressant drug nomifensine (HOE 984). Noradrenaline, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid in hindbrains of suicidal patients.
This review explains (1) how TMDD happens (2) why large-molecule and small-molecule compounds exhibiting TMDD demonstrate substantially different nonlinear PK behaviors (3) what nonlinear PK profiles look like in large-molecule and small-molecule compounds exhibiting TMDD, using pegfilgrastim, erythropoietin, ABT-384, and linagliptin as case examples and (4) how to identify whether the nonlinear PK of a compound is because of TMDD. The goal of this review is to serve as a “primer” on TMDD. As the interaction between a drug and its pharmacologic target belongs to the process of pharmacodynamics (PD), TMDD can be viewed as a consequence of “PD affecting PK.” Although there are numerous TMDD-related articles in the literature, most of them focus on characterizing TMDD using various mathematical models, which may not be suitable for those readers who have little interest in mathematical modeling and only want to have an understanding of the basic concept. Target-mediated drug disposition (TMDD) is a term to describe a nonlinear pharmacokinetic (PK) phenomenon that is caused by high-affinity binding of a compound to its pharmacologic targets.