Sensitization to the conditioned rewarding effects of morphine modulates gene expression in rat hippocampus

Marie-Claire, Cynthia; Courtin, Cindie; Robert, Amélie; Gidrol, Xavier; Roques, Bernárd P.; Noble, Florence

doi:10.1016/j.neuropharm.2006.08.012

Cited by 16 publications

(10 citation statements)

References 37 publications

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“…Considering the critical role of SNAP25 in exocytosis and regulating neural plasticity (60 -62), SIP30 is likely involved in mediating long term pain plasticity and LTP. This hypothesis is in agreement with a recent paper in which SIP30 was identified as a long term memory consolidation associated gene in opiate addiction (63). Furthermore, SIP30 would be probably located in spinal excitatory interneurons to enhance neuron excitability, as hippocampal GABAergic inhibitory synapses lack SNAP-25 (64, 65).…”

Section: Discussionsupporting

confidence: 91%

SIP30 Is Regulated by ERK in Peripheral Nerve Injury-induced Neuropathic Pain

Peng

Han

et al. 2009

Journal of Biological Chemistry

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ERK plays an important role in chronic neuropathic pain. However, the underlying mechanism is largely unknown. Here we show that in chronic constriction injury-treated rat spinal cords, up-regulation of SIP30 (SNAP25-interacting protein 30), which is involved in the development and maintenance of chronic constriction injury-induced neuropathic pain, correlates with ERK activation and that the up-regulation of SIP30 is suppressed by intrathecal delivery of the MEK inhibitor U0126. In PC12 cells, up-regulation of SIP30 by nerve growth factor is also dependent on ERK activation. We found that there is an ERK-responsive region in the rat sip30 promoter. Activation of ERK promotes the recruitment of the transcription factor cyclic AMP-response element-binding protein to the sip30 gene promoter. Taken together, our results provide a potential downstream target of ERK activation-mediated neuropathic pain.Neuropathic pain is a chronic painful condition due to nerve injury caused by trauma, disease, or surgical accidents. This kind of chronic pain brings severe distress, which disrupts the quality of life. There is a lack of effective treatment for neuropathic pain, and the underlying mechanism is poorly understood. Recently, attention has been focused on the central sensitization of spinal dorsal horn neurons, which are responsible for the modulation of neuropathic pain transmission. Central sensitization is a consequence of increased neuron excitability (1, 2). It has been shown that MAPKs 4 play a critical role in this sensitization and are responsible for the transduction of nociceptive signals (3). MAPKs are activated in the damaged neurons, and their inhibition can suppress or reverse neuropathic pain (4 -9). In various pain models, ERK, a member of the MAPK family, is specifically activated in the superficial dorsal horn neurons by noxious but not innocuous stimulation. Inhibition of ERK activation alleviates pain hypersensitivity, indicating that ERK may play an important role in neuropathic pain (10 -17). ERK appears to regulate pain hypersensitivity in various aspects. It produces not only short term functional changes by post-translational processes, such as phosphorylation of membrane receptors and channels, but also long term adaptive alterations by changing gene expression (10,12,18,19). Neuropathic pain is a chronic painful situation. It is believed that the long term gene expression regulated by ERK in the spinal cord plays a central role in the development of the disease (14). Thus, understanding of the molecular mechanism by which ERK regulates neuropathic pain is important to understand the pathology of central sensitization.SIP30 (SNAP25-interacting protein 30) was first reported as a SNAP25-interacting protein of 30 kDa that functioned in vesicle trafficking (20). Through a differential screening of a rat brain cDNA library, we found that sip30 was among the genes that were differentially expressed in the spinal cord CCI rats (21). We further showed that sip30 mRNA and protein levels were up-regulate...

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Section: Discussionsupporting

confidence: 91%

SIP30 Is Regulated by ERK in Peripheral Nerve Injury-induced Neuropathic Pain

Peng

Han

et al. 2009

Journal of Biological Chemistry

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“…Similarly, training in conditioned place preference for amphetamine increased c-fos expression in the hippocampus of rats [207]. Furthermore, extended training in a morphine-conditioned place preference paradigm altered gene expression in the hippocampus of rats [208]. Changes in gene expression are not limited to laboratory animals.…”

Section: Nicotine Contextual Learning and Addictionmentioning

confidence: 99%

Modulation of Hippocampus-Dependent Learning and Synaptic Plasticity by Nicotine

2008

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A long-standing relationship between nicotinic acetylcholine receptors (nAChRs) and cognition exists. Drugs that act at nAChRs can have cognitive-enhancing effects and diseases that disrupt cognition such as Alzheimer's disease and schizophrenia are associated with altered nAChR function. Specifically, hippocampus-dependent learning is particularly sensitive to the effects of nicotine. However, the effects of nicotine on hippocampus-dependent learning vary not only with the doses of nicotine used and whether nicotine is administered acutely, chronically, or withdrawn after chronic nicotine treatment but also vary across different hippocampus-dependent tasks such as the Morris water maze, the radial arm maze, and contextual fear conditioning. In addition, nicotine has variable effects across different types of hippocampal long-term potentiation (LTP). Because different types of hippocampus-dependent learning and LTP involve different neural and molecular substrates, comparing the effects of nicotine across these paradigms can yield insights into the mechanisms that may underlie the effects of nicotine on learning and memory and aid in understanding the variable effects of nicotine on cognitive processes. This review compares and contrasts the effects of nicotine on hippocampus-dependent learning and LTP and briefly discusses how the effects of nicotine on learning could contribute to nicotine addiction.

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“…One such study, which involved morphine-induced conditioned place preference, showed changes in the expression of genes in the hippocampus involved in vesicular transport, neurotransmitter release, and receptor trafficking (Marie-Claire et al, 2007). However, there are few studies detailing the effects of prescription opioids on changes in gene expression in the adolescent brain (Ellgren et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Self administration of oxycodone alters synaptic plasticity gene expression in the hippocampus differentially in male adolescent and adult mice

et al. 2015

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Abuse and addiction to prescription opioids such as oxycodone (a short-acting Mu opioid receptor (MOP-r) agonist) in adolescence is a pressing public health issue. We have previously shown differences in oxycodone self-administration behaviors between adolescent and adult C57BL/6J mice and expression of striatal neurotransmitter receptor genes, in areas involved in reward. In this study, we aimed to determine whether oxycodone self-administration differentially affects genes regulating synaptic plasticity in the hippocampus of adolescent compared to adult mice, since the hippocampus may be involved in learning aspects associated with chronic drug self administration. Hippocampus was isolated for mRNA analysis from mice that had self administered oxycodone (0.25 mg/kg/infusion) 2 h/day for 14 consecutive days or from yoked saline controls. Gene expression was analyzed with real-time polymerase chain reaction (PCR) using a commercially available “synaptic plasticity” PCR array containing 84 genes. We found that adolescent and adult control mice significantly differed in the expression of several genes in the absence of oxycodone exposure, including those coding for mitogen-activated protein kinase, calcium/calmodulin-dependent protein kinase II gamma subunit, glutamate receptor, ionotropic AMPA2 and metabotropic 5. Chronic oxycodone self administration increased proviral integration site 1 (Pim1) and thymoma viral proto-oncogene 1 mRNA levels compared to controls in both age groups. Both Pim1 and cadherin 2 mRNAs showed a significant combined effect of Drug Condition and Age × Drug Condition. Furthermore, the mRNA levels of both cadherin 2 and cAMP response element modulators showed an experiment-wise significant difference between oxycodone and saline control in adult but not in adolescent mice. Overall, this study demonstrates for the first time that chronic oxycodone self-administration differentially alters synaptic plasticity gene expression in the hippocampus of adolescent and adult mice.

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Sensitization to the conditioned rewarding effects of morphine modulates gene expression in rat hippocampus

Cited by 16 publications

References 37 publications

SIP30 Is Regulated by ERK in Peripheral Nerve Injury-induced Neuropathic Pain

SIP30 Is Regulated by ERK in Peripheral Nerve Injury-induced Neuropathic Pain

Modulation of Hippocampus-Dependent Learning and Synaptic Plasticity by Nicotine

Self administration of oxycodone alters synaptic plasticity gene expression in the hippocampus differentially in male adolescent and adult mice

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