Rottlerin impairs the formation and maintenance of psychostimulant-supported memory

Liao, Tien You; Tzeng, Wen Yu; Wu, Hsin Hua; Cherng, Chianfang G.; Wang, Ching Yi; Hu, Sherry Shu Jung; Yu, Lung

doi:10.1007/s00213-016-4251-8

Cited by 10 publications

(3 citation statements)

References 34 publications

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“…To assess the impact of stressor and behavioral control on tight and adherens junction components and autophagic flux in VH, mice were euthanized and their brains were removed and placed on the dorsal surface on a glass dish sitting on crushed ice. Hippocampal tissues were dissected as previously described [ 31 ] and dorsal and ventral hippocampal samples were obtained from the top and bottom halves of bilateral hippocampal tissues. These tissue samples were homogenized in ice-cold lysis buffer containing protease inhibitor cocktail (Roche, Basel, Switzerland).…”

Section: Methodsmentioning

confidence: 99%

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

et al. 2022

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Section: Methodsmentioning

confidence: 99%

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

et al. 2022

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“…The number of mice in each group is summarized in Table 1 . The dose of rottlerin was determined based on previous studies [ 38 , 43 ]. The experimental design is shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Effect of rottlerin on astrocyte phenotype polarization after trimethyltin insult in the dentate gyrus of mice

Hwang

Kim

Shin

2022

J Neuroinflammation

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Background It has been demonstrated that reactive astrocytes can be polarized into pro-inflammatory A1 phenotype or anti-inflammatory A2 phenotype under neurotoxic and neurodegenerative conditions. Microglia have been suggested to play a critical role in astrocyte phenotype polarization by releasing pro- and anti-inflammatory mediators. In this study, we examined whether trimethyltin (TMT) insult can induce astrocyte polarization in the dentate gyrus of mice, and whether protein kinase Cδ (PKCδ) plays a role in TMT-induced astrocyte phenotype polarization. Methods Male C57BL/6 N mice received TMT (2.6 mg/kg, i.p.), and temporal changes in the mRNA expression of A1 and A2 phenotype markers were evaluated in the hippocampus. In addition, temporal and spatial changes in the protein expression of C3, S100A10, Iba-1, and p-PKCδ were examined in the dentate gyrus. Rottlerin (5 mg/kg, i.p. × 5 at 12-h intervals) was administered 3–5 days after TMT treatment, and the expression of A1 and A2 transcripts, p-PKCδ, Iba-1, C3, S100A10, and C1q was evaluated 6 days after TMT treatment. Results TMT treatment significantly increased the mRNA expression of A1 and A2 phenotype markers, and the increased expression of A1 markers remained longer than that of A2 markers. The immunoreactivity of the representative A1 phenotype marker, C3 and A2 phenotype marker, S100A10 peaked 6 days after TMT insult in the dentate gyrus. While C3 was expressed evenly throughout the dentate gyrus, S100A10 was highly expressed in the hilus and inner molecular layer. In addition, TMT insult induced microglial p-PKCδ expression. Treatment with rottlerin, a PKCδ inhibitor, decreased Iba-1 and C3 expression, but did not affect S100A10 expression, suggesting that PKCδ inhibition attenuates microglial activation and A1 astrocyte phenotype polarization. Consistently, rottlerin significantly reduced the expression of C1q and tumor necrosis factor-α (TNFα), which has been suggested to be released by activated microglia and induce A1 astrocyte polarization. Conclusion We demonstrated the temporal and spatial profiles of astrocyte polarization after TMT insult in the dentate gyrus of mice. Taken together, our results suggest that PKCδ plays a role in inducing A1 astrocyte polarization by promoting microglial activation and consequently increasing the expression of pro-inflammatory mediators after TMT insult.

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“…All drugs were injected at a volume of 1 mL/100 mg of body weight. We chose doses of methamphetamine that produce CPP in mice according to previous research. , The dose of CP94253 and the interval between administration for conditioning/testing (30 min) were selected based on previous studies reporting effects on locomotor activity, as well as other behavioral tasks. , …”

Section: Methodsmentioning

confidence: 99%

Neural Circuits Associated with 5-HT_1B Receptor Agonist Inhibition of Methamphetamine Seeking in the Conditioned Place Preference Model

Der-Ghazarian

Charmchi

Noudali

et al. 2019

ACS Chem. Neurosci.

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5-HT1B receptors (5-HT1BRs) modulate psychostimulant reward and incentive motivation in rodents. Here we investigated the effects of the 5-HT1BR agonist CP94253 (10 mg/kg, IP) on the acquisition and expression of methamphetamine (Meth) conditioned place preference (CPP) in C57BL/6 male mice. We subsequently examined the potential brain regions involved in CP94253 effects using FOS as a marker of neural activity. In the acquisition experiment, mice received the agonist 30 min before each of the Meth injections given during conditioning. In the expression experiment, mice that had acquired Meth-CPP were given either saline or CP94253 and were tested for CPP 30 min later. We found that CP94253 attenuated the expression of Meth-CPP, but had no effect on acquisition. Mice expressing Meth-CPP had elevated numbers of FOS+ cells in the ventral tegmental area (VTA) and basolateral amygdala (BlA) and reduced FOS+ cells in the central amygdala (CeA) compared to saline controls. CP94253 given before the expression test, but not acutely in drug-naive mice, enhanced FOS+ cells in the VTA, the nucleus accumbens (NAc) shell and core, and the dorsomedial striatum and reversed the Meth-conditioned changes in FOS in the BlA and CeA. Approximately 50–70% of FOS+ cells in the NAc and VTA were GABAergic regardless of group. By contrast, we did not observe FOS-labeling in dopamine neurons in the VTA. The findings suggest that CP94253 attenuates the motivational effects of the Meth-associated environment and highlight the amygdala, VTA, NAc, and dorsomedial striatum as potential regions involved in this effect.

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Rottlerin impairs the formation and maintenance of psychostimulant-supported memory

Cited by 10 publications

References 34 publications

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

Effect of rottlerin on astrocyte phenotype polarization after trimethyltin insult in the dentate gyrus of mice

Neural Circuits Associated with 5-HT_1B Receptor Agonist Inhibition of Methamphetamine Seeking in the Conditioned Place Preference Model

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Rottlerin impairs the formation and maintenance of psychostimulant-supported memory

Cited by 10 publications

References 34 publications

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

Stress while lacking of control induces ventral hippocampal autophagic flux hyperactivity and a depression-like behavior

Effect of rottlerin on astrocyte phenotype polarization after trimethyltin insult in the dentate gyrus of mice

Neural Circuits Associated with 5-HT1B Receptor Agonist Inhibition of Methamphetamine Seeking in the Conditioned Place Preference Model

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Neural Circuits Associated with 5-HT_1B Receptor Agonist Inhibition of Methamphetamine Seeking in the Conditioned Place Preference Model