Transcriptional profiling of C57 and DBA strains of mice in the absence and presence of morphine

Grice, Dorothy E.; Reenilä, Ilkka; Männistö, Pekka T.; Brooks, Andrew I.; Smith, George Gilbert; Golden, Greg; Buxbaum, Joseph D.; Berrettini, Wade H.

doi:10.1186/1471-2164-8-76

Cited by 40 publications

(43 citation statements)

References 47 publications

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“…(Albertson et al, 2006;Ishikawa et al, 2009;Mu et al, 2010;Wang et al, 2008;Supplementary Table 2). Chronic morphine treatment also altered KCNN1 transcript levels in the mouse NAc (Grice et al, 2007), although the authors did not report the direction of the change. The findings of the present study add to a growing literature showing that alcohol, nicotine, and illicit drugs significantly alter K Ca 2 channel expression and function in key regions within the addiction neurocircuitry.…”

Section: Figurementioning

confidence: 89%

KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction

Padula

Griffin

López

et al. 2015

Neuropsychopharmacol

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Small-conductance Ca(2+)-activated K(+) (KCa2) channels control neuronal excitability and synaptic plasticity, and have been implicated in substance abuse. However, it is unknown if genes that encode KCa2 channels (KCNN1-3) influence alcohol and drug addiction. In the present study, an integrative functional genomics approach shows that genetic datasets for alcohol, nicotine, and illicit drugs contain the family of KCNN genes. Alcohol preference and dependence QTLs contain KCNN2 and KCNN3, and Kcnn3 transcript levels in the nucleus accumbens (NAc) of genetically diverse BXD strains of mice predicted voluntary alcohol consumption. Transcript levels of Kcnn3 in the NAc negatively correlated with alcohol intake levels in BXD strains, and alcohol dependence enhanced the strength of this association. Microinjections of the KCa2 channel inhibitor apamin into the NAc increased alcohol intake in control C57BL/6J mice, while spontaneous seizures developed in alcohol-dependent mice following apamin injection. Consistent with this finding, alcohol dependence enhanced the intrinsic excitability of medium spiny neurons in the NAc core and reduced the function and protein expression of KCa2 channels in the NAc. Altogether, these data implicate the family of KCNN genes in alcohol, nicotine, and drug addiction, and identify KCNN3 as a mediator of voluntary and excessive alcohol consumption. KCa2.3 channels represent a promising novel target in the pharmacogenetic treatment of alcohol and drug addiction.

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Section: Figurementioning

confidence: 89%

KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction

Padula

Griffin

López

et al. 2015

Neuropsychopharmacol

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“…Several recent studies using different morphine-exposure paradigms and examining different brain regions have analyzed genes regulated by morphine using microarray technology (Loguinov et al, 2001, Ammon et al, 2003, Ammon-Treiber and Hollt, 2005, McClung et al, 2005, Grice et al, 2007, Korostynski et al, 2007). In the first published study, Loguinov et al showed that 45 genes/ESTs were down-regulated in the mouse striatum and/or the spinal cord after a single morphine injection, whereas only nine genes/ESTs up-regulated, without major differences between the two regions (Loguinov et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling following short-term and long-term morphine exposure in mice uncovers genes involved in food intake

et al. 2010

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Addictive drugs including opioids activate signal transduction pathways that regulate gene expression in the brain. However, changes in CNS gene expression following morphine exposure are poorly understood. We determined changes in gene expression following short-and long-term morphine treatment in the hypothalamus and pituitary using genome-wide DNA microarray analysis and confirmed those alterations in gene expression by real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis. In the hypothalamus, short-term morphine administration up-regulated (at least 2-fold) 39 genes and down-regulated six genes. Long-term morphine treatment up-regulated 35 genes and down-regulated 51 genes. In the pituitary, shortterm morphine administration up-regulated 110 genes and down-regulated 29 genes. Long-term morphine treatment up-regulated 85 genes and down-regulated 37 pituitary genes. Microarray analysis uncovered several genes involved in food intake (neuropeptide Y, agouti-related protein, and cocaine and amphetamine-regulated transcript) whose expression was strongly altered by morphine exposure in either the hypothalamus or pituitary. Subsequent RT-PCR analysis confirmed similar regulation in expression of these genes in the hypothalamus and pituitary. Finally, we found functional correlation between morphine-induced alterations in food intake and Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported NIH Public Access regulation of genes involved in this process. Changes in genes related to food intake may uncover new pathways related to some of the physiological effects of opioids.

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“…We applied a similar strategy to explore the molecular basis of the differences in trait and restraint-induced anxiety-like behavior between B6 and D2 by examining patterns of gene expression in three key regional loci of the corticolimbic circuit mediating stress responses and stress-induced changes in behavior-the mPFC, amygdala, and hippocampus. Consistent with previous studies (Kerns et al, 2005;Grice et al, 2007), our analysis detected substantial expression difference between B6 and D2 with several genes differentially expressed in all three regions.…”

Section: Discussionsupporting

confidence: 92%

Multiscale Genomic Analysis of the Corticolimbic System: Uncovering the Molecular and Anatomic Substrates of Anxiety-Related Behavior

Mozhui¹

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Transcriptional profiling of C57 and DBA strains of mice in the absence and presence of morphine

Cited by 40 publications

References 47 publications

KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction

KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction

Gene expression profiling following short-term and long-term morphine exposure in mice uncovers genes involved in food intake

Multiscale Genomic Analysis of the Corticolimbic System: Uncovering the Molecular and Anatomic Substrates of Anxiety-Related Behavior

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