Psychopharmacology

Journal: Psychopharmacology

Abbreviation

Psychopharm

Publisher

Springer

ISSN

0033-3158
1432-2072

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Publications 1 - 10 of 27

The glycine transporter 1 inhibitor SSR504734 enhances working memory performance in a continuous delayed alternation task in C57BL/6 mice
Singer, Philipp; Feldon, Joram; Yee, Benjamin K. (2009)
Psychopharmacology
Baseline prepulse inhibition expression predicts the propensity of developing sensitization to the motor stimulant effects of amphetamine in C57BL/6 mice
Peleg-Raibstein, Daria; Hauser, Jonas; Lopez, Luis H. L.; et al. (2013)
Psychopharmacology
The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
Sahlholm, Kristoffer; Ielacqua, Giovanna D.; Xu, Jinbin; et al. (2017)
Psychopharmacology
Rationale The dopamine D2 receptor (D2R) couples to inhibitory Gi/o proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied D2R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies D2R-dependent responses. Methods fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the D2R antagonist, eticlopride. Results Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions The prolonged striatal response decay rates in KO animals might reflect impaired D2R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of D2R.
Effects of the mGluR2/3 agonist LY354740 on computerized tasks of attention and working memory in marmoset monkeys
Spinelli, Simona; Ballard, Theresa; Gatti-McArthur, Silvia; et al. (2005)
Psychopharmacology
Prenatal exposure to infection: a primary mechanism for abnormal dopaminergic development in schizophrenia
Meyer, Urs; Feldon, Joram (2009)
Psychopharmacology
The postweaning social isolation in C57BL/6 mice
Pietropaolo, Susanna; Singer, Philipp; Feldon, Joram; et al. (2008)
Psychopharmacology
Prepulse inhibition during withdrawal from an escalating dosage schedule of amphetamine
Russig, Holger; Murphy, Carol A.; Feldon, Joram (2003)
Psychopharmacology
The developmental impact of prenatal stress, prenatal dexamethasone and postnatal social stress on physiology, behaviour and neuroanatomy of primate offspring: studies in rhesus macaque and common marmoset
Pryce, Christopher R.; Aubert, Yves; Maier, Claudia; et al. (2011)
Psychopharmacology
Rationale Exposure of the immature mammalian brain to stress factors, including stress levels of glucocorticoids, either prenatally or postnatally, is regarded as a major regulatory factor in short- and long-term brain function and, in human, as a major aetiological factor in neuropsychiatric disorders. Experimental human studies are not feasible and animal studies are required to demonstrate causality and elucidate mecha- nisms. A number of studies have been conducted and reviewed in rodents but there are relatively few studies in primates. Objectives Here we present an overview of our published studies and some original data on the effects of: (1) prenatal stress on hypothalamic–pituitary–adrenal (HPA) re/activity and hippocampus neuroanatomy in juvenile-adolescent rhesus macaques; (2) prenatal dexamethasone (DEX) on HPA activity, behaviour and prefrontal cortex neuroanatomy in infant-adolescent common marmosets; (3) postnatal daily parental separation stress on HPA re/activity, behaviour, sleep and hippocampus and prefrontal cortex neuroanatomy in infant-adolescent common marmoset. Results Prenatal stress increased basal cortisol levels and reduced neurogenesis in macaque. Prenatal DEX was without effect on HPA activity and reduced social play and skilled motor behaviour in marmoset. Postnatal social stress increased basal cortisol levels, reduced social play, increased awakening and reduced hippocampal glucocorticoid and mineralocorticoid receptor expression in marmoset. Conclusions Perinatal stress-related environmental events exert short- and long-term effects on HPA function, behaviour and brain status in rhesus macaque and common marmoset. The mechanisms mediating the enduring effects remain to be elucidated, with candidates including increased basal HPA function and epigenetic programming.
Effects of selective estrogen receptor alpha and beta modulators on prepulse inhibition in male mice
Labouesse, Marie A.; Langhans, Wolfgang; Meyer, Urs (2015)
Psychopharmacology
Rationale Multiple lines of evidence suggest that the sex steroid hormone 17-β estradiol (E2) plays a protective role in schizophrenia. Systemic E2 enhances prepulse inhibition (PPI) of the acoustic startle reflex, an operational measure of sensorimotor gating known to be impaired in schizophrenia and related disorders. However, the relative contribution of different estrogen-receptor (ER) isoforms in these associations still awaits examination. Objectives The present study explored the effects of ER-α and ER-β stimulation or blockade on PPI and their functional relevance in an amphetamine-induced PPI deficiency model in male mice. Methods Prior to the assessment of PPI, C57BL/6N male mice were injected with the ER-α agonist 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT), the ER-α antagonist 1,3-bis (4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy) phenol]-1N-pyrozole dihydrochloride (MPP), the ER-β agonist 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN), or the ER-β antagonist 4-[2-phenyl-5,7-bis (trifluoromethyl) pyrazolo [1,5-a] pyrimidin-3-yl] phenol (PHTPP), with or without concomitant amphetamine treatment. Results Acute pharmacological stimulation and blockade of ER-α, respectively, led to a dose-dependent increase and decrease in basal PPI. In contrast, acute treatment with preferential ER-β modulators spared PPI under basal conditions. Pretreatment with either ER-α or ER-β agonist was, however, effective in blocking amphetamine-induced PPI disruption. Conclusions Our study demonstrates that activation of either ER isoform is capable of modulating dopamine-dependent PPI levels. At the same time, our results suggest that endogenous ER-α signaling may be more relevant than ER-β in the regulation of sensorimotor gating under basal conditions.
Cognitive and socio-cognitive functioning of chronic non-medical prescription opioid users
Kroll, Sara L.; Nikolic, Emilija; Bieri, Franziska; et al. (2018)
Psychopharmacology

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