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• W1789415031 abstract "Abstract Since the discovery of chlorpromazine in 1953, the number of antipsychotic medications has increased tremendously. Most of these drugs affect the dopaminergic neurotransmission (primarily blocking dopamine D 2 receptors). Antipsychotics registered until 2008 could be classified into 3 groups based on receptor occupancy profile rather than using their chemical structure. Conventional (or first‐generation antipsychotics, like haloperidol and fluphenazine) with a predominant D 2 receptor affinity have benefits in the treatment of delusions and hallucinations (positive symptoms of schizophrenia), which are parallel with a characteristic side‐effect profile of extrapyramidal symptoms (EPS) and prolactin elevation. Atypical antipsychotics—which are characterized by a higher antagonist affinity to serotonin (5‐hydroxytryptamine, 5HT) 5HT 2 receptors than to dopamine D 2 receptors—are generally thought to be effective in alleviation of negative symptoms (such as anhedonia, and lack of motivation) beyond the positive symptoms domain of schizophrenia, with a reduced EPS burden (such as clozapine, olanzapine, risperidone). A third group of novel antipsychotics has a partial dopamine agonist profile (aripiprazole), with a lack of or minimal EPS. The nondopaminergic N ‐methyl‐ D ‐aspartate (NMDA) antagonist model of schizophrenia raised new gulatamatergic targets for treatment. NMDA antagonists ketamine and phencyclidine produce wide range of symptoms characteristic for schizophrenia, such as positive and negative symptoms as well as cognitive impairment. Compounds that blunt gulatamatergic activity (for example lamotrigine) or NMDA receptor glycine site allosteric agonists have both showed improvement of schizophrenic symptoms in combination with antipscychotics. The first compound that produced improvement in monotherapy for the treatment of schizophrenia is LY214023, which is a metabotropic Glutamate 2/3 (mGlu2/3) receptor agonist. This article reviews neurobiological background of treatments and clinical experiences proven in controlled clinical trials." @default.
• W1789415031 created "2016-06-24" @default.
• W1789415031 creator A5002320307 @default.
• W1789415031 date "2009-03-13" @default.
• W1789415031 modified "2023-10-10" @default.
• W1789415031 title "Small Molecules that Target Schizophrenia" @default.
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• W1789415031 doi "https://doi.org/10.1002/9780470048672.wecb685" @default.
• W1789415031 hasPublicationYear "2009" @default.
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