Effects of neuroleptic drugs, clonidine and lithium on the expression of conditioned behavioral excitation in rats

Poncelet, Marc; Dangoumau, Laure; Soubrié, P.; Simon, Patricia

doi:10.1007/bf00210850

Cited by 39 publications

(13 citation statements)

References 18 publications

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“…However, on each of the 6 days of conditioning, the respective groups were given 0 (saline), 10, 20 or 50 gg/ kg clonidine intraperitoneally (IP) 30 min prior to the conditioning heroin or saline injections. The highest dose has been shown to inhibit NA cell firing (Aghajanian and Vandermaelen 1982), and the two higher doses have been shown to disrupt conditioned hyperactivity in drug-free rats (Poncelet et al 1987) induced by amphetamine.…”

Section: Experiments 3: Effects Of Clonidine On the Acquisition And Exmentioning

confidence: 98%

Differential mechanisms in the acquisition and expression of heroin-induced place preference

1989

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These experiments examined the neurochemical mechanisms involved in the development and expression of place conditioning produced by heroin. Conditioned place preferences (CPP) lasting up to 8 weeks were obtained with doses of 50-1000 micrograms/kg heroin, using a regimen shown not to produce physical dependence. Naloxone pretreatment (50 micrograms/kg) during conditioning prevented the acquisition of heroin-induced CPP, but when given only on the test day, naloxone (50 or 1000 micrograms/kg) did not prevent the expression of heroin CPP. Clonidine disrupted the establishment of heroin CPP at 20 micrograms/kg, but disrupted its expression only at debilitating doses (100 and 200 micrograms/kg). Pimozide attenuated the acquisition (100 micrograms/kg) and expression (250 micrograms/kg) of heroin CPP. Together, these results support a role for opioid and catecholamine systems in the acquisition of heroin reinforcement, but they suggest that once heroin CPP is established, its expression in opiate-free subjects is not opiate receptor mediated and is relatively refractory to pharmacological treatments which disrupt acquisition. The data challenge the notion that the conditioned effects of opiates in drug-free animals are related to the release of endogenous opioids, and they also may help to explain why naloxone and clonidine are ineffective in the treatment of opiate addiction.

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Section: Experiments 3: Effects Of Clonidine On the Acquisition And Exmentioning

confidence: 98%

Differential mechanisms in the acquisition and expression of heroin-induced place preference

1989

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“…We further explored the role of VGF in bipolar disorder by testing its effect in amphetamine-induced hyperactivity, which has been used to phenocopy manic-like behavior and test novel lithium-mimetic compounds (Poncelet et al, 1987;Takigawa et al, 1994;Beaulieu et al, 2004;Frey et al, 2006;Gould et al, 2007;Shaldubina et al, 2007;Du et al, 2008;Shaltiel et al, 2008). Mice were acclimated to the open-field apparatus for 15 min and then injected with either amphetamine (2 mg/ kg) or saline intraperitoneally, followed immediately by a 40 min open-field test.…”

Section: Vgf Mimics the Effects Of Licl And Is Required In A Mouse Symentioning

confidence: 99%

The Neuropeptide VGF Is Reduced in Human Bipolar Postmortem Brain and Contributes to Some of the Behavioral and Molecular Effects of Lithium

Thakker‐Varia¹,

Jean²,

Parikh³

et al. 2010

Journal of Neuroscience

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Recent studies demonstrate that the neuropeptide VGF (nonacronymic) is regulated in the hippocampus by antidepressant therapies and animal models of depression and that acute VGF treatment has antidepressant-like activity in animal paradigms. However, the role of VGF in human psychiatric disorders is unknown. We now demonstrate using in situ hybridization that VGF is downregulated in bipolar disorder in the CA region of the hippocampus and Brodmann's area 9 of the prefrontal cortex. The mechanism of VGF in relation to LiCl was explored. Both LiCl intraperitoneally and VGF intracerebroventricularly reduced latency to drink in novelty-induced hypophagia, and LiCl was not effective in VGF ϩ/Ϫ mice, suggesting that VGF may contribute to the effects of LiCl in this behavioral procedure that responds to chronic antidepressant treatment. VGF by intrahippocampal injection also had novel activity in an amphetamine-induced hyperlocomotion assay, thus mimicking the actions of LiCl injected intraperitoneally in a system that phenocopies manic-like behavior. Moreover, VGF ϩ/Ϫ mice exhibited increased locomotion after amphetamine treatment and did not respond to LiCl, suggesting that VGF is required for the effects of LiCl in curbing the response to amphetamine. Finally, VGF delivered intracerebroventricularly in vivo activated the same signaling pathways as LiCl and is necessary for the induction of mitogen-activated protein kinase and Akt by LiCl, thus lending insight into the molecular mechanisms underlying the actions of VGF. The dysregulation of VGF in bipolar disorder as well as the behavioral effects of the neuropeptide similar to LiCl suggests that VGF may underlie the pathophysiology of bipolar disorder.

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“…The first behavior examined was amphetamineinduced hyperactivity. This test has been used as a model of mania, and lithium treatment has consistently been shown to inhibit amphetamine-induced hyperactivity (Poncelet et al, 1987;Takigawa et al, 1994;Beaulieu et al, 2004;Frey et al, 2006a,b;Shaldubina et al, 2007).…”

Section: Hippocampal Administration Of the Chemical Ampa Antagonist Gmentioning

confidence: 99%

“…Inhibition of synaptic AMPA receptor activity by GYKI 52466 or TAT-S845 in hippocampus attenuates amphetamineinduced manic behavior Previous studies have shown that lithium has an antimanic effect against amphetamine-induced hyperactivity (Poncelet et al, 1987;Takigawa et al, 1994;Beaulieu et al, 2004;Frey et al, 2006a,b;Shaldubina et al, 2007). In this study, we showed that three different experimental paradigms (treatment with lithium, treatment with AMPA antagonist GYKI 52466 infusion, or treatment with GluR1S845 phosphorylation inhibitory peptide TAT-S845 infusion) display a common effect; namely, they all attenuate hippocampal synaptic AMPA receptors and reduce amphetamine-induced hyperactivity.…”

Section: Regulation Of Ampa Receptor Trafficking By Antimanic Agents mentioning

confidence: 99%

The Role of Hippocampal GluR1 and GluR2 Receptors in Manic-Like Behavior

Du¹,

Creson²,

Ren³

et al. 2008

J. Neurosci.

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The cellular basis underlying the complex clinical symptomatology of bipolar disorder and the mechanisms underlying the actions of its effective treatments have not yet been fully elucidated. This study investigated the role of hippocampal synaptic AMPA receptors. We found that chronic administration of the antimanic agents lithium and valproate (VPA) reduced synaptic AMPA receptor GluR1/2 in hippocampal neurons in vitro and in vivo. Electrophysiological studies confirmed that the AMPA/NMDA ratio was reduced in CA1 regions of hippocampal slices from lithium-treated animals. Reduction in GluR1 phosphorylation at its cAMP-dependent protein kinase A site by the synthetic peptide TAT-S845, which mimics the effects of lithium or VPA, was sufficient to attenuate surface and synaptic GluR1/2 levels in hippocampal neurons in vitro and in vivo. Intrahippocampal infusion studies with the AMPA-specific inhibitor GYKI [4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodiazepin-5-yl)-benzenamine hydrochloride], a GluR1-specific TAT-S845 peptide, showed that GluR1/2 was essential for the development of manic/hedonic-like behaviors such as amphetamine-induced hyperactivity. These studies provide novel insights into the role of hippocampal GluR1/2 receptors in mediating facets of the manic syndrome and offer avenues for the development of novel therapeutics for these disorders.

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Effects of neuroleptic drugs, clonidine and lithium on the expression of conditioned behavioral excitation in rats

Cited by 39 publications

References 18 publications

Differential mechanisms in the acquisition and expression of heroin-induced place preference

Differential mechanisms in the acquisition and expression of heroin-induced place preference

The Neuropeptide VGF Is Reduced in Human Bipolar Postmortem Brain and Contributes to Some of the Behavioral and Molecular Effects of Lithium

The Role of Hippocampal GluR1 and GluR2 Receptors in Manic-Like Behavior

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