Monoacylglycerol lipase inhibition-induced changes in plasma corticosterone levels, anxiety and locomotor activity in male CD1 mice

Aliczki, Manó; Zelena, Dóra; Mikics, Éva; Varga, Zoltán; Pintér, Ottó; Bakos, Nikoletta; Várga, J.; Haller, József

doi:10.1016/j.yhbeh.2013.03.017

Cited by 42 publications

(31 citation statements)

References 42 publications

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“…Although plasma corticosterone concentrations resulting from corticosterone administration were significantly higher than those resulting from forced swim (t 23 = 5.70; Po0.001; two-tailed t-test), they were within previously reported stress-induced ranges (Aliczki et al, 2013;Gong et al, 2015;Malisch et al, 2007).…”

Section: Effects Of Corticosterone On Cocaine-primed Reinstatementsupporting

confidence: 73%

Corticosterone Potentiation of Cocaine-Induced Reinstatement of Conditioned Place Preference in Mice is Mediated by Blockade of the Organic Cation Transporter 3

McReynolds

Taylor

Vranjkovic

et al. 2016

Neuropsychopharmacol

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The mechanisms by which stressful life events increase the risk of relapse in recovering cocaine addicts are not well understood. We previously reported that stress, via elevated corticosterone, potentiates cocaine-primed reinstatement of cocaine seeking following selfadministration in rats and that this potentiation appears to involve corticosterone-induced blockade of dopamine clearance via the organic cation transporter 3 (OCT3). In the present study, we use a conditioned place preference/reinstatement paradigm in mice to directly test the hypothesis that corticosterone potentiates cocaine-primed reinstatement by blockade of OCT3. Consistent with our findings following self-administration in rats, pretreatment of male C57/BL6 mice with corticosterone (using a dose that reproduced stress-level plasma concentrations) potentiated cocaine-primed reinstatement of extinguished cocaine-induced conditioned place preference. Corticosterone failed to re-establish extinguished preference alone but produced a leftward shift in the dose-response curve for cocaineprimed reinstatement. A similar potentiating effect was observed upon pretreatment of mice with the non-glucocorticoid OCT3 blocker, normetanephrine. To determine the role of OCT3 blockade in these effects, we examined the abilities of corticosterone and normetanephrine to potentiate cocaine-primed reinstatement in OCT3-deficient and wild-type mice. Conditioned place preference, extinction and reinstatement of extinguished preference in response to low-dose cocaine administration did not differ between genotypes. However, corticosterone and normetanephrine failed to potentiate cocaine-primed reinstatement in OCT3-deficient mice. Together, these data provide the first direct evidence that the interaction of corticosterone with OCT3 mediates corticosterone effects on drugseeking behavior and establish OCT3 function as an important determinant of susceptibility to cocaine use.

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Section: Effects Of Corticosterone On Cocaine-primed Reinstatementsupporting

confidence: 73%

Corticosterone Potentiation of Cocaine-Induced Reinstatement of Conditioned Place Preference in Mice is Mediated by Blockade of the Organic Cation Transporter 3

McReynolds

Taylor

Vranjkovic

et al. 2016

Neuropsychopharmacol

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“…Intriguingly, aggressionrelated glucocorticoid production was increased by JZL184 neither in the residents studied here nor in the same strain of mice submitted to forced swimming stress as reported earlier (Aliczki et al 2013 ). One can assume that the endocrine effects of JZL184 emerge in especially critical situations only, but the phenomenon certainly needs further studies.…”

Section: Discussionsupporting

confidence: 42%

“…The corticosterone synthesis blocker metyrapone (2Methyl 1,2di3pyridyl1propanone) (Sigma Aldrich, Saint Louis, MO) was dissolved in saline containing 5 % Tween 80 and administered in doses 0 (Vehicle) and 30 mg/kg intraperitoneally in a volume of 5 ml/kg body weight. The selection of the metyrapone dose was based on previous studies (Aliczki et al 2013 ). When drugs were coadministered, they were delivered in two separate injections in rapid succession.…”

Section: Drugsmentioning

confidence: 99%

“…The JZL184 dose employed was 16 mg/kg; metyrapone was co administered in the dose 0 (vehicle) and 30 mg/kg. Doses were based on previous experience with the compound (Aliczki et al 2013 ). Subjects were studied 40 min later in the resident/intruder test as intruders.…”

Section: Experimental Designmentioning

confidence: 99%

“…As the blockade of 2AG degradation by JZL184 increases corticosterone secretion (Aliczki et al 2013 ), which may per se affect aggressiveness (Mikics et al 2004 ), we also studied glucocorticoid responses to the resident/intruder test and the impact of the corticosterone synthesis inhibitor metyrapone. In nonsocial tests, the behavioral effects of enhanced 2AG signaling depended largely on context (Aliczki et al 2013; BusquetsGarcia et al 2011; Sciolino et al 2011 ); therefore, we studied the effects of the compound in both residents and intruders, for which the very same resident/intruder test is contextually highly different. Finally, we investigated molecular mechanisms by employing the CB1 receptor blocker AM251.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of 2-arachidonoylglycerol signaling in social challenge responding of male CD1 mice

et al. 2014

Self Cite

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RationaleEndocannabinoids are strong modulators of emotionality and present a novel target for psychotropic drug development. Increasing evidence suggests that endocannabinoids anandamide and 2arachidonoylglycerol (2AG) affect behavior differentially. While the roles of anandamide have been investigated extensively, studies regarding the specific roles of 2AG became possible only recently, and its involvement in social behaviors has not yet been studied. ObjectiveWe studied the impact of 2AG signaling on aggression as a first attempt to characterize the role of this endocannabinoid in social behaviors. ResultsJZL184 near completely abolished aggressiveness in residents and increased victimization (i.e., attacks by the opponent). Interestingly, the level of defensiveness remained unaltered, despite the large increase in bites received. The CB1 receptor blocker AM251 (0.5 mg/kg) did not influence the effects of JZL184. In intruders, JZL184 near completely suppressed bites and offensive behavior in a fashion similar to residents, but it also increased agitation and defensiveness during, and the corticosterone response to, aggressive encounters. Experiments involving the corticosterone synthesis inhibitor metyrapone (30 mg/kg) suggest that the suppression of biting and offensive behavior is directly influenced by JZL184, whereas increased agitation and defensiveness (seen in intruders only) are a secondary development of the stress endocrine effects of JZL184. Conclusions2AG signaling emerges as a surprisingly strong negative modulator of aggressiveness, which warrants further studies into its general role in social behavior and the target receptors involved.

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Molecular basis underlying default mode network functional abnormalities in postpartum depression with and without anxiety

Chen,

Yang,

et al. 2024

Human Brain Mapping

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Although Postpartum depression (PPD) and PPD with anxiety (PPD‐A) have been well characterized as functional disruptions within or between multiple brain systems, however, how to quantitatively delineate brain functional system irregularity and the molecular basis of functional abnormalities in PPD and PPD‐A remains unclear. Here, brain sample entropy (SampEn), resting‐state functional connectivity (RSFC), transcriptomic and neurotransmitter density data were used to investigate brain functional system irregularity, functional connectivity abnormalities and associated molecular basis for PPD and PPD‐A. PPD‐A exhibited higher SampEn in medial prefrontal cortex (MPFC) and posterior cingulate cortex (PPC) than healthy postnatal women (HPW) and PPD while PPD showed lower SampEn in PPC compared to HPW and PPD‐A. The functional connectivity analysis with MPFC and PPC as seed areas revealed decreased functional couplings between PCC and paracentral lobule and between MPFC and angular gyrus in PPD compared to both PPD‐A and HPW. Moreover, abnormal SampEn and functional connectivity were associated with estrogenic level and clinical symptoms load. Importantly, spatial association analyses between functional changes and transcriptome and neurotransmitter density maps revealed that these functional changes were primarily associated with synaptic signaling, neuron projection, neurotransmitter level regulation, amino acid metabolism, cyclic adenosine monophosphate (cAMP) signaling pathways, and neurotransmitters of 5‐hydroxytryptamine (5‐HT), norepinephrine, glutamate, dopamine and so on. These results reveal abnormal brain entropy and functional connectivities primarily in default mode network (DMN) and link these changes to transcriptome and neurotransmitters to establish the molecular basis for PPD and PPD‐A for the first time. Our findings highlight the important role of DMN in neuropathology of PPD and PPD‐A.

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Monoacylglycerol lipase inhibition-induced changes in plasma corticosterone levels, anxiety and locomotor activity in male CD1 mice

Cited by 42 publications

References 42 publications

Corticosterone Potentiation of Cocaine-Induced Reinstatement of Conditioned Place Preference in Mice is Mediated by Blockade of the Organic Cation Transporter 3

Corticosterone Potentiation of Cocaine-Induced Reinstatement of Conditioned Place Preference in Mice is Mediated by Blockade of the Organic Cation Transporter 3

Involvement of 2-arachidonoylglycerol signaling in social challenge responding of male CD1 mice

Molecular basis underlying default mode network functional abnormalities in postpartum depression with and without anxiety

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