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      mRNA and microRNA analysis reveals modulation of biochemical pathways related to addiction in the ventral tegmental area of methamphetamine self-administering rats.

      1 , 2 , 3 , 4 , 5
      BMC neuroscience
      Springer Nature

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          Abstract

          Methamphetamine is a highly addictive central nervous system stimulant with increasing levels of abuse worldwide. Alterations to mRNA and miRNA expression within the mesolimbic system can affect addiction-like behaviors and thus play a role in the development of drug addiction. While many studies have investigated the effects of high-dose methamphetamine, and identified neurotoxic effects, few have looked at the role that persistent changes in gene regulation play following methamphetamine self-administration. Therefore, the aim of this study was to identify RNA changes in the ventral tegmental area following methamphetamine self-administration. We performed microarray analyses on RNA extracted from the ventral tegmental area of Sprague-Dawley rats following methamphetamine self-administration training (2 h/day) and 14 days of abstinence.

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          Most cited references55

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          A brain-specific microRNA regulates dendritic spine development.

          MicroRNAs are small, non-coding RNAs that control the translation of target messenger RNAs, thereby regulating critical aspects of plant and animal development. In the mammalian nervous system, the spatiotemporal control of mRNA translation has an important role in synaptic development and plasticity. Although a number of microRNAs have been isolated from the mammalian brain, neither the specific microRNAs that regulate synapse function nor their target mRNAs have been identified. Here we show that a brain-specific microRNA, miR-134, is localized to the synapto-dendritic compartment of rat hippocampal neurons and negatively regulates the size of dendritic spines--postsynaptic sites of excitatory synaptic transmission. This effect is mediated by miR-134 inhibition of the translation of an mRNA encoding a protein kinase, Limk1, that controls spine development. Exposure of neurons to extracellular stimuli such as brain-derived neurotrophic factor relieves miR-134 inhibition of Limk1 translation and in this way may contribute to synaptic development, maturation and/or plasticity.
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            A MicroRNA feedback circuit in midbrain dopamine neurons.

            MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.
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              • Abstract: found
              • Article: not found

              Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling.

              Addictive drugs have in common that they target the mesocorticolimbic dopamine (DA) system. This system originates in the ventral tegmental area (VTA) and projects mainly to the nucleus accumbens (NAc) and prefrontal cortex (PFC). Here, we review the effects that such drugs leave on glutamatergic and GABAergic synaptic transmission in these three brain areas. We refer to these changes as drug-evoked synaptic plasticity, which outlasts the presence of the drug in the brain and contributes to the reorganization of neural circuits. While in most cases these early changes are not sufficient to induce the disease, with repetitive drug exposure, they may add up and contribute to addictive behavior. Copyright © 2011 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                BMC Neurosci
                BMC neuroscience
                Springer Nature
                1471-2202
                1471-2202
                Jul 19 2015
                : 16
                Affiliations
                [1 ] Centre for Biodiscovery, School of Biological Sciences, Victoria University of Wellington, Kelburn Parade, PO Box 600, Wellington, 6140, New Zealand. peetyrbosch@gmail.com.
                [2 ] Institute of Environmental Science and Research, Wellington, New Zealand. miles.benton84@gmail.com.
                [3 ] Genomics Research Centre, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Australia. miles.benton84@gmail.com.
                [4 ] Institute of Environmental Science and Research, Wellington, New Zealand. donia.macartney@esr.cri.nz.
                [5 ] Centre for Biodiscovery, School of Biological Sciences, Victoria University of Wellington, Kelburn Parade, PO Box 600, Wellington, 6140, New Zealand. Bronwyn.kivell@vuw.ac.nz.
                Article
                10.1186/s12868-015-0186-y
                10.1186/s12868-015-0186-y
                4506769
                26188473
                85e141e8-a8c4-4143-af6a-83fae94aeca3
                History

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