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Antipsychotic dopamine glutamate

Nao Chuhma, Susana Mingote, Abigail Kalmbach, Leora Yetnikoff, Stephen Rayport
Brain imaging has revealed alterations in dopamine uptake, release, and receptor levels in patients with schizophrenia that have been resolved on the scale of striatal subregions. However, the underlying synaptic mechanisms are on a finer scale. Dopamine neuron synaptic actions vary across the striatum, involving variations not only in dopamine release but also in dopamine neuron connectivity, cotransmission, modulation, and activity. Optogenetic studies have revealed that dopamine neurons release dopamine in a synaptic signal mode, and that the neurons also release glutamate and gamma-aminobutyric acid as cotransmitters, with striking regional variation...
July 12, 2016: Biological Psychiatry
Diane Grillault Laroche, Adeline Gaillard
The prevalence of OCS and OCD is higher in schizophrenic patients than in the general population. These disorders are sometimes induced by AAPs. There is higher frequency of OCS and greater severity in patients treated with antipsychotics with predominant anti-serotoninergic profiles opposed to those with predominant dopaminergic blockade. Induced OCS may be due to complex neuromodulation involving many serotonin, dopamine and glutamate receptors and several subtypes. Concerning connectivity, AAPs differentially influence the BOLD signal, depending on the intensity of D2 receptor blockade...
September 21, 2016: Psychiatry Research
Nadja P Maric, Milica J Jovicic, Marina Mihaljevic, Cedo Miljevic
Preclinical Research After the identification of the schizophrenia as an illness over a century ago, treatment of affected individuals included unspecific, mostly very robust methods including deep insulin coma and lobectomy/leucotomy. The first relatively specific treatment of schizophrenia started about 60 years ago with the antipsychotic chlorpromazine. All currently approved antipsychotic drugs block dopamine receptors, indicating that manipulation of dopaminergic function is fundamental to a therapeutic response in psychosis...
September 16, 2016: Drug Development Research
Kirsten E Schoonover, Lesley A McCollum, Rosalinda C Roberts
The substantia nigra (SN) provides the largest dopaminergic input to the brain, projects to the striatum (the primary locus of action for antipsychotic medication), and receives GABAergic and glutamatergic inputs. This study used Western blot analysis to compare protein levels of tyrosine hydroxylase (TH), glutamate decarboxylase (GAD67), and vesicular glutamate transporters (vGLUT1 and vGLUT2) in postmortem human SN in schizophrenia subjects (n=13) and matched controls (n=12). As a preliminary analysis, the schizophrenia group was subdivided by 1) treatment status: off- (n=4) or on-medication (n=9); or 2) treatment response: treatment resistant (n=5) or treatment responsive (n=4)...
August 23, 2016: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
Nora Wa van de Kerkhof, Durk Fekkes, Frank Mma van der Heijden, Witte Jg Hoogendijk, Gerald Stöber, Jos Im Egger, Willem Ma Verhoeven
Cycloid psychoses (CP) differ from schizophrenia regarding symptom profile, course, and prognosis and over many decades they were thought to be a separate entity within the psychosis spectrum. As to schizophrenia, research into the pathophysiology has focused on dopamine, brain-derived neurotrophic factor, and glutamate signaling in which, concerning the latter, the N-methyl-d-aspartate receptor plays a crucial role. The present study aims to determine whether CP can biochemically be delineated from schizophrenia...
2016: Neuropsychiatric Disease and Treatment
Rachel K Lanning, Clement C Zai, Daniel J Müller
Tardive dyskinesia (TD) is a serious and potentially irreversible side effect of long-term exposure to antipsychotic medication characterized by involuntary trunk, limb and orofacial muscle movements. Various mechanisms have been proposed for the etiopathophysiology of antipsychotic-induced TD in schizophrenia patients with genetic factors playing a prominent role. Earlier association studies have focused on polymorphisms in CYP2D6, dopamine-, serotonin-, GABA- and glutamate genes. This review highlights recent advances in the genetic investigation of TD...
August 2016: Pharmacogenomics
Monika Woźniak, Krystyna Gołembiowska, Karolina Noworyta-Sokołowska, Francine Acher, Paulina Cieślik, Magdalena Kusek, Krzysztof Tokarski, Andrzej Pilc, Joanna M Wierońska
LSP4-2022 is a novel, orthosteric agonist of mGlu4 receptor that induces antipsychotic-like activity in animal studies. In the present study, the involvement of 5-HT1A receptors in LSP4-2022-induced antipsychotic actions and the neurochemical background of that interaction were investigated. In several behavioral tests the actions of effective doses of the compound (0.5-2 mg/kg) were antagonized via the administration of the 5-HT1A antagonist WAY100635 (0.1 mg/kg). The co-administration of sub-effective dose of the 5-HT1A agonist (R)-(S)-8-OH+DPAT (0...
July 24, 2016: Neuropharmacology
S Mas, P Gassó, A Lafuente, M Bioque, A Lobo, A Gonzàlez-Pinto, M S Olmeda, I Corripio, A Llerena, B Cabrera, J Saiz-Ruiz, M Bernardo
This study investigated whether the risk of presenting antipsychotic (AP)-induced extrapyramidal symptoms (EPS) could be related to single-nucleotide polymorphisms (SNPs) in a naturalistic cohort of first episode psychosis (FEP) patients. Two hundred and two SNPs in 31 candidate genes (involved in dopamine, serotonin and glutamate pathways) were analyzed in the present study. One hundred and thirteen FEP patients (43 presenting EPS and 70 non-presenting EPS) treated with high-potency AP (amisulpride, paliperidone, risperidone and ziprasidone) were included in the analysis...
October 2016: Pharmacogenomics Journal
Arijana Turčin, Vita Dolžan, Stefano Porcelli, Alessandro Serretti, Blanka Kores Plesničar
The existing antipsychotic therapy is based on dopamine hyperfunction and glutamate hypofunction hypotheses of schizophrenia. Adenosine receptors (ADORA) have a neuromodulatory role and can control dopaminergic and glutamatergic systems. To elucidate the effect of ADORA polymorphisms on psychopathological symptoms and adverse effects in patients with schizophrenia on long-term antipsychotic treatment, we examined 127 nonacute schizophrenia outpatients in a cross-sectional study using the Positive and Negative Symptoms Scale, Simpson-Angus Scale, Barnes Akathisia Rating Scale, and Abnormal Involuntary Movement Scale...
May 2016: Omics: a Journal of Integrative Biology
Andrea de Bartolomeis, Federica Marmo, Elisabetta F Buonaguro, Gianmarco Latte, Carmine Tomasetti, Felice Iasevoli
The postsynaptic density (PSD) has been regarded as a functional switchboard at the crossroads of a dopamine-glutamate interaction, and it is putatively involved in the pathophysiology of psychosis. Indeed, it has been demonstrated that antipsychotics may modulate several PSD transcripts, such as PSD-95, Shank, and Homer. Despite switching antipsychotics is a frequent strategy to counteract lack of efficacy and/or side effect onset in clinical practice, no information is available on the effects of sequential treatments with different antipsychotics on PSD molecules...
October 3, 2016: Progress in Neuro-psychopharmacology & Biological Psychiatry
Dasiel O Borroto-Escuela, Julia Pintsuk, Thorsten Schäfer, Kristina Friedland, Luca Ferraro, Sergio Tanganelli, Fang Liu, Kjell Fuxe
The dopamine (DA) neuron system most relevant for schizophrenia is the meso-limbic-cortical DA system inter alia densely innervating subcortical limbic regions. The field of dopamine D2 receptors and schizophrenia changed markedly with the discovery of many types of D2 heteroreceptor complexes in subcortical limbic areas as well as the dorsal striatum. The results indicate that the D2 is a hub receptor which interacts not only with many other G protein-coupled receptors (GPCRs) including DA isoreceptors but also with ion-channel receptors, receptor tyrosine kinases, scaffolding proteins and DA transporters...
April 2016: Therapeutic Advances in Psychopharmacology
Robert E Davis, Christoph U Correll
ITI-007 is an investigational drug being developed for schizophrenia and other neuropsychiatric/neurodegenerative diseases. ITI-007 has a unique pharmacological profile, combining potent 5-HT2a receptor antagonism with cell-type-specific dopamine and glutamate receptor modulation, plus serotonin reuptake inhibition. At dopamine-D2 receptors, ITI-007 acts as a post-synaptic antagonist and pre-synaptic partial agonist. Additionally, ITI-007 stimulates phosphorylation of glutamatergic NMDA-NR2B receptors, downstream of dopamine-D1 receptor intracellular signaling...
June 2016: Expert Review of Neurotherapeutics
Rama M Kamal, Martijn S van Noorden, Ernst Franzek, Boukje A G Dijkstra, Anton J M Loonen, Cornelius A J De Jong
OBJECTIVE: x03B3;-Hydroxybutyrate (GHB) has gained popularity as a drug of abuse. In the Netherlands the number of patients in treatment for GHB dependence has increased sharply. Clinical presentation of GHB withdrawal can be life threatening. We aim, through this overview, to explore the neurobiological pathways causing GHB dependency and withdrawal, and their implications for treatment choices. METHODS: In this work we review the literature discussing the findings from animal models to clinical studies focused on the neurobiological pathways of endogenous but mainly exogenous GHB...
2016: Neuropsychobiology
Mohamed Sherif, Rajiv Radhakrishnan, Deepak Cyril D'Souza, Mohini Ranganathan
Some of the most compelling evidence supporting an association between cannabinoid agonists and psychosis comes from controlled laboratory studies in humans. Randomized, double-blind, placebo-controlled, crossover laboratory studies demonstrate that cannabinoid agonists, including phytocannabinoids and synthetic cannabinoids, produce a wide range of positive, negative, and cognitive symptoms and psychophysiologic deficits in healthy human subjects that resemble the phenomenology of schizophrenia. These effects are time locked to drug administration, are dose related, and are transient and rarely necessitate intervention...
April 1, 2016: Biological Psychiatry
Felix-Martin Werner, Rafael Covenas
BACKGROUND: Alzheimer's disease is a neurodegenerative disease showing alterations in classical neurotransmitters, above all in the hippocampus and prefrontal/temporal cortices. In this disease, acetylcholine shows hypoactivity, noradrenaline first shows hyperactivity, and during the course of the disease an increasing hypoactivity, glutamate shows hyperactivity and excitotoxicity and GABA shows hypoactivity. In post-mortem studies, serotonin levels and the number of specific serotonergic subreceptors, for example 5-HT1B receptors, decreased...
2016: Current Pharmaceutical Design
Elias Mouchlianitis, Michael A P Bloomfield, Vincent Law, Katherine Beck, Sudhakar Selvaraj, Naresh Rasquinha, Adam Waldman, Federico E Turkheimer, Alice Egerton, James Stone, Oliver D Howes
INTRODUCTION: Resistance to antipsychotic treatment is a significant clinical problem in patients with schizophrenia with approximately 1 in 3 showing limited or no response to repeated treatments with antipsychotic medication. The neurobiological basis for treatment resistance is unknown but recent evidence implicates glutamatergic function in the anterior cingulate cortex. We examined glutamate levels of chronically ill treatment-resistant patients directly compared to treatment-responsive patients...
May 2016: Schizophrenia Bulletin
H Javelot
Pharmacological treatment of acute anxiety still relies on benzodiazepines, while chronic anxiety disorders and depression are treated with different antidepressants, according to specific indications. The monoaminergic axis is represented by two families which are being developed: (i) serotonin-norepinephrine-dopamine reuptake inhibitors (SNDRI), also called triple reuptake inhibitors (TRI), for the treatment of depression (amitifadine), (ii) multimodal antidepressants for depression and anxiety disorders (generalized anxiety disorder mainly) (tedatioxetine, vortioxetine and vilazodone)...
March 2016: Annales Pharmaceutiques Françaises
Marina Šagud
Despite pharmacological advances in the treatment of schizophrenia, significant number of patients continue to be treatment-resistant. Poor control of symptoms could be related to low concentration of antipsychotics because of non-adherence or pharmacokinetic issues. However, there is growing evidence that "true" treatment-resistance might be associated with biological changes, i.e. alterations in dopaminergic and glutaminergic systems, genetics, neurodegeneration and neuroinflamation. Clozapine is recommended as first-line treatment for treatment-resistant schizophrenia (TRS) in all guidelines...
September 2015: Psychiatria Danubina
Peter H Hutson, Helen L Rowley, James Gosden, Rajiv S Kulkarni, Nigel Slater, Patrick L Love, Yiyun Wang, David Heal
The etiology of schizophrenia is poorly understood and two principle hypotheses have dominated the field. Firstly, that subcortical dopamine function is enhanced while cortical dopamine function is reduced and secondly, that cortical glutamate systems are dysfunctional. It is also widely accepted that currently used antipsychotics have essentially no impact on cognitive deficits and persistent negative symptoms in schizophrenia. Reduced dopamine transmission via dopamine D1 receptors in the prefrontal cortex has been hypothesized to be involved in the aetiology of these symptom domains and enhancing cortical dopamine transmission within an optimal window has been suggested to be potentially beneficial...
February 2016: Neuropharmacology
Yasuto Kunii, Wenyu Zhang, Qing Xu, Thomas M Hyde, Whitney McFadden, Joo Heon Shin, Amy Deep-Soboslay, Tianzhang Ye, Chao Li, Joel E Kleinman, Kuan Hong Wang, Barbara K Lipska
OBJECTIVE: CHRNA7, coding α-7 nicotinic acetylcholine receptor (α7 nAChR), is involved in cognition through interneuron modulation of dopamine and glutamate signaling. CHRNA7 and its partially duplicated chimeric gene CHRFAM7A have been implicated in schizophrenia through linkage and association studies. METHOD: Expression of CHRNA7 and CHRFAM7A mRNA was measured in the postmortem prefrontal cortex in more than 700 subjects, including patients with schizophrenia, bipolar disorder, major depression, and normal comparison subjects...
November 1, 2015: American Journal of Psychiatry
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