The authors make a short presentation of antipsychotics mechanisms consecutive to the interaction with receptors of the neurotransmission systems, respectively the meso-cortico-limbic dopaminergic system, the serotoninergic, glutamatergic, cholinergic systems and so on. Hence, a brief review is performed by means of the pharmacological proofs of schizophrenia pathogenic theories. Another of the regarded domains addresses the etio-pathogenic aspects of schizophrenia as background for potential pharmacologic targets - the genetic component and the impact of factors which disrupt the neurodevelopment and / or initiated neurodegeneration processes in favorable contexts. The authors analyze the eff ects of antipsychotics correlated on various receptor levels with the complex therapeutic eff ects on schizophrenia. Existing data show that these eff ects can either be: 1) the direct consequence of action on receptor or the indirect outcome of counter-regulations determined in other neuromediation systems, or 2) these eff ects can be relatively immediate (a matter of hours - days) or slowly instated (weeks) or, these eff ects can not appear at all (resistance to treatment, non-responders etc.). In this regard, two concepts are brought into discussion: the therapeutic eff ects with immediate onset and defi nition after 2-3 weeks and the slow eff ects, sharpened up after around one month and either defi ned or not after a few months. Another type of reasonings are also brought into discussion: the slow and late eff ects of antidepressants, the onset of the addiction phenomenon as a complex neuroadaptive process, and also the experimental and clinical proof that antipsychotics induce complex phenomena on cerebral structures. In fact, in the context of chronic antipsychotic treatment, the brain behave according to the acknowledged rules: it launches short latency, rapid processes with homeostatic destiny, thus initiating a series of other, slower reactions, implying protein and receptor synthesis, synaptic plasticity, neuroplasticity, neurogenesis etc. These processes, which entail changes in the expression of certain genes, are approached as epigenetic phenomena which confer to the organism, on one hand, fl exibility and adaptability and, on the other hand, genomic stability. Given this context, the authors deem that there are convincing arguments (either direct or indirect) towards admitting that throughout the interaction antipsychotic - pathogenic psychotic processes, two successive interdependent and correlated phases are envisaged: 1) the pharmacodynamic phase where the active compound determines the known eff ects consecutive to antagonizing or activating the receptors for which it has affi nity and 2) the pharmacotherapeutic phase implying slower, more complex processes. The rapid counter-regulations of the interconnected neurotransmission systems are part of the phenomena which probably initiate slower and more complex reactions entailing compensatory phenomena in a positive or negative sense (up or downregulation) at receptor level, neuromediator synthesis, synaptic connections or even the emergence of new neurons in certain cerebral regions. This second phase will outline the fi nal therapeutic response which will install in weeks, months. In connection with the rearrangement, modulation and resetting between diff erent neurotransmission systems (aff ected in the schizophrenia context), on the basis of the presented epigenetic processes, we might either report or not an individual therapeutic eff ect as hinted end-point.read more..