scholarly journals Mechanism of Action of Atypical Antipsychotic Drugs in Mood Disorders

2020 ◽  
Vol 21 (24) ◽  
pp. 9532
Author(s):  
Daniil Grinchii ◽  
Eliyahu Dremencov
Keyword(s):  
Mood Disorders ◽  
Atypical Antipsychotic ◽  
Mechanism Of Action ◽  
Atypical Antipsychotics ◽  
Antipsychotic Drugs ◽  
Therapeutic Potential ◽  
Antidepressant Drugs ◽  
Atypical Antipsychotic Drugs ◽  
Experimental Drugs ◽  
Typical Antipsychotics

Atypical antipsychotic drugs were introduced in the early 1990s. Unlike typical antipsychotics, which are effective only against positive symptoms of schizophrenia, atypical antipsychotics are effective against negative and cognitive symptoms as well. Furthermore, they are effective not only in psychotic but also in affective disorders, on their own or as adjuncts to antidepressant drugs. This review presents the neural mechanisms of currently existing atypical antipsychotics and putative antipsychotics currently being investigated in preclinical and clinical studies and how these relate to their effectiveness in mood disorders such as depression, anxiety, and post-traumatic stress disorder (PTSD). Typical antipsychotics act almost exclusively on the dopamine system. Atypical drugs, however, modulate serotonin (5-HT), norepinephrine, and/or histamine neurotransmission as well. This multimodal mechanism of action putatively underlies the beneficial effect of atypical antipsychotics in mood and anxiety disorders. Interestingly, novel experimental drugs having dual antipsychotic and antidepressant therapeutic potential, such as histamine, adenosine, and trace amine-associated receptors (TAAR) ligand, are also characterized by a multimodal stimulatory effect on central 5-HT, norepinephrine, and/or histamine transmission. The multimodal stimulatory effect on central monoamine neurotransmission may be thus primarily responsible for the combined antidepressant and antipsychotic therapeutic potential of certain central nervous system (CNS) drugs.

scholarly journals Mechanism of Action of Atypical Antipsychotic Drugs in Mood Disorders

2020 ◽  
Author(s):  
Daniil Grinchii ◽  
Eliyahu Dremencov
Keyword(s):  
Mood Disorders ◽  
Atypical Antipsychotic ◽  
Atypical Antipsychotics ◽  
Antipsychotic Drugs ◽  
Antidepressant Drugs ◽  
Dopamine Neurons ◽  
Atypical Antipsychotic Drugs ◽  
Experimental Drugs ◽  
Catecholamine Neurons ◽  
Typical Antipsychotics

Atypical antipsychotic drugs were introduced in the early 1990th. Unlike typical antipsychotics, which are effective only against positive symptoms of schizophrenia, atypical antipsychotics show effectiveness against negative and cognitive symptoms as well. Furthermore, they are effective not only in psychotic, but also in affective disorders, by their own or as adjuncts to antidepressant drugs. While typical antipsychotics act, almost exclusively, via dopamine-2 (D2) receptors, atypical target serotonin-1A/1B/2A/2C (5-HT1A/1B/2A/2C), α1/2-adrenergic, and/or histamine-1 (H1) receptors as well. Blocking of 5-HT1A/1B autoreceptors, inducing their early desensitization, and/or activation of α1-adrenoceptors, allow some atypical drugs to enhance 5-HT transmission. Blocking of 5-HT2A/2C and/or α2-adrenoceptors enable some atypical antipsychotics to stimulate catecholamine transmission and/or diminish the inhibition of catecholamine neurons induced by some antidepressants. It is possible, that the activation of H1 and/or blocking of H3 boost monoamine transmission as well, via a mechanism involving stimulation of firing activity of dopamine neurons. The experimental drugs with antipsychotic potential, acting on adenosine and trace amino associated (TAAR) receptors, might be effective in mood disorders as well, because of the ability to modulate the excitability of monoamine-secreting neurons and to potentiate extracellular concentrations of monoamines in the limbic areas of the brain.

The Importance of Serotonin-Dopamine Interactions in the Action of Clozapine

1992 ◽  
Vol 160 (S17) ◽  
pp. 22-29 ◽  
Author(s):  
Herbert Y. Meltzer
Keyword(s):  
Atypical Antipsychotic ◽  
Atypical Antipsychotics ◽  
Antipsychotic Drugs ◽  
Typical Antipsychotic ◽  
Atypical Antipsychotic Drugs ◽  
Clinical Dose ◽  
High Affinity ◽  
The Relationship

Clozapine has an affinity for the dopamine (DA) D2 receptor which is relatively weak but is in line with its average clinical dose when compared with typical neuroleptic drugs. A few atypical antipsychotic drugs may have high absolute affinities for the D2 receptor, but most are weak D2 blockers. The atypical antipsychotic drugs also differ from the typical antipsychotic drugs by a relatively high affinity for the serotonin (5-HT2) receptor. This is evident on both in vitro and in vivo binding to cortical 5-HT2 receptors. The atypical antipsychotics are best distinguished from the typical antipsychotics on the basis of the relationship between strong 5-HT2 and weak D2 affinities. High D1 receptor binding is not characteristic of the group of atypical drugs. A new group of putative atypical antipsychotic drugs with high affinities for 5-HT2 compared to D2 receptors is under study.

Mechanism of Action of Atypical Antipsychotic Drugs and the Neurobiology of Schizophrenia

CNS Drugs ◽  
2006 ◽  
Vol 20 (5) ◽  
pp. 389-409 ◽  
Author(s):  
Jiri Horacek ◽  
Vera Bubenikova-Valesova ◽  
Milan Kopecek ◽  
Tomas Palenicek ◽  
Colleen Dockery ◽  
...  
Keyword(s):  
Atypical Antipsychotic ◽  
Mechanism Of Action ◽  
Antipsychotic Drugs ◽  
Atypical Antipsychotic Drugs

Atypical Antipsychotic Drugs and the Risk of Sudden Cardiac Death

2018 ◽  
Author(s):  
Hamilton Hicks ◽  
Cenk Tek
Keyword(s):  
Sudden Cardiac Death ◽  
Atypical Antipsychotic ◽  
Cardiac Death ◽  
Atypical Antipsychotics ◽  
Antipsychotic Drugs ◽  
Atypical Antipsychotic Drugs ◽  
Source Study ◽  
Study Intervention ◽  
Landmark Study

This chapter provides a summary of a landmark study on schizophrenia. The study authors sought to compare the safety of typical and atypical antipsychotics with regard to a fatal adverse event. Are atypical antipsychotic drugs associated with a lower risk of sudden cardiac death compared to typical antipsychotics? Starting with that question, this chapter describes the basics of the study, including the funding source, study location, who was studied, how many patients, study design, study intervention, follow-up, study endpoints, results, as well as criticism and limitations. The chapter briefly reviews other relevant studies and information, discusses implications, and concludes with a relevant clinical case.

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