Serotonin in antipsychotic drugs action

Amato, Davide

doi:10.1016/j.bbr.2014.07.025

Cited by 45 publications

(37 citation statements)

References 160 publications

(160 reference statements)

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“…In 2003, BACE1-null mice were reported to display timid behavior and reduced serotonin and dopamine (DA) levels in the hippocampus and striatum, respectively (Harrison et al 2003); dopamine and serotonin dysfunctions are the basis for many antipsychotic drugs (typical or atypical) developed to ameliorate SCZ positive and negative symptoms (Guidotti et al 2005;Strange 2008;Amato 2015). However, the link between BACE1 and SCZ pathogenesis has gained recent attention due to the observed SCZ-like endophenotypes in BACE1-null mice and BACE1 cleavage of Nrg1.…”

Section: Nrg1 Expression In Schwann Cells Severely Impairs Remyelinatmentioning

confidence: 99%

Neurological dysfunctions associated with altered BACE1‐dependent Neuregulin‐1 signaling

Fan

Hou

et al. 2015

Journal of Neurochemistry

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Inhibition of BACE1 is being pursued as a therapeutic target to treat patients suffering from Alzheimer’s disease because BACE1 is the sole β-secretase that generates β-amyloid peptide. Knowledge regarding other cellular functions of BACE1 is therefore critical for the safe use of BACE1 inhibitors in human patients. Neuregulin-1 (Nrg1) is a BACE1 substrate and BACE1 cleavage of Nrg1 is critical for signaling functions in myelination, remyelination, synaptic plasticity, normal psychiatric behaviors and maintenance of muscle spindles. This review summarizes the most recent discoveries associated with BACE1-dependent Nrg1 signaling in these areas. This body of knowledge will help to provide guidance for preventing unwanted Nrg1-based side effects following BACE1 inhibition in humans.

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Section: Nrg1 Expression In Schwann Cells Severely Impairs Remyelinatmentioning

confidence: 99%

Neurological dysfunctions associated with altered BACE1‐dependent Neuregulin‐1 signaling

Fan

Hou

et al. 2015

Journal of Neurochemistry

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“…[8][9][10] T gondii infection and schizophrenia also both manifest significant neuroinflammation [11][12][13][14][15][16][17] and disregulation of neurotransmitters, particularly dopamine and serotonin. [18][19][20][21] Additionally, several reports have documented the ability of T gondii to alter rodent neural connectivity 22 and fear behavior, 23,24 and influence human behavior (reviewed in ref. 25 ).…”

Section: Introductionmentioning

confidence: 99%

Shared Immune and Repair Markers During ExperimentalToxoplasmaChronic Brain Infection and Schizophrenia

Tomasik

Schultz

Kluge

et al. 2015

SCHBUL

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Chronic neurologic infection with Toxoplasma gondii is relatively common in humans and is one of the strongest known risk factors for schizophrenia. Nevertheless, the exact neuropathological mechanisms linking T gondii infection and schizophrenia remain unclear. Here we utilize a mouse model of chronic T gondii infection to identify protein biomarkers that are altered in serum and brain samples at 2 time points during chronic infection. Furthermore, we compare the identified biomarkers to those differing between "postmortem" brain samples from 35 schizophrenia patients and 33 healthy controls. Our findings suggest that T gondii infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients. The overlapping changes include increases in C-reactive protein (CRP), interleukin-1 beta (IL-1β), interferon gamma (IFNγ), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1). Potential roles of these factors in the pathogenesis of schizophrenia and toxoplasmosis are discussed. Identifying a defined set of markers shared within the pathophysiological landscape of these diseases could be a key step towards understanding their specific contributions to pathogenesis.

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“…On the other hand, risperidone possesses a much higher affinity for the serotonin 2A (5-HT 2A ) receptors than haloperidol, thus the D 2 /5-HT 2A affinity ratio of risperidone is approximately 500 times higher than that of haloperidol [13,16,17]. In addition to 5-HT 2A inhibition, risperidone is known to stimulate cortical and subcortical serotonin output [18]. 5-HT is known to be involved in both the anxiety and the neural transmission in the reflex arcs, which are involved in the generation of hiccups [3,9].…”

Section: Resultsmentioning

confidence: 99%

Intractable hiccups (singultus) abolished by risperidone, but not by haloperidol

2015

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Hiccups or singulata are rhythmic involuntary movements of the diaphragm, caused by a variety of conditions that interfere with the functions of the nerve nuclei in the medulla and supra-spinal hiccup center. Although neurotransmitters and receptors involved in the pathophysiology of hiccups are not defined well, dopamine has been considered to play an important role. In some cases, chlorpromazine or other antipsychotics are used for the treatment of intractable hiccups but their efficacy is often limited. This report involves an 18-year-old patient who experienced two episodes of intractable hiccups triggered by stress, which lasted for weeks or even months. In both episodes, haloperidol was initially used, but there was no significant effect. In contrast, risperidone, the second-generation antipsychotic that possesses a dopamine-serotonin antagonist property, completely abolished the hiccups 6 hours after administration. This is one of few case reports in which two antipsychotics were challenged for a single patient with hiccups, and the effects of the drugs were obviously different. Our finding suggests that, in addition to dopaminergic system, the serotonergic systems may be involved in the pathophysiology of some hiccup cases and that the serotonin-acting antipsychotics such as risperidone should be considered as a choice in the drug treatment of intractable hiccups.

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Serotonin in antipsychotic drugs action

Cited by 45 publications

References 160 publications

Neurological dysfunctions associated with altered BACE1‐dependent Neuregulin‐1 signaling

Neurological dysfunctions associated with altered BACE1‐dependent Neuregulin‐1 signaling

Shared Immune and Repair Markers During ExperimentalToxoplasmaChronic Brain Infection and Schizophrenia

Intractable hiccups (singultus) abolished by risperidone, but not by haloperidol

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