By a News Reporter-Staff News Editor at Pain & Central Nervous System Week -- Current study results on Central Nervous System have been published. According to news originating from London, Canada, by NewsRx correspondents, research stated, "Opiate reward memories are powerful triggers for compulsive opiate-seeking behaviors. The basolateral amygdala (BLA) is an important structure for the processing of opiate-related associative memories and is functionally linked to the mesolimbic dopamine (DA) pathway."
Our news journalists obtained a quote from the research from the University of Western Ontario, "Transmission through intra-BLA DA D1-like and D2-like receptors independently modulates the formation of opiate reward memories as a function of opiate-exposure state. Thus, in the opiate-naive state, intra-BLA D1 transmission is required for opiate-related memory formation. Once opiate dependence and withdrawal has developed, a functional switch to a DA D2-mediated memory mechanism takes place. However, the downstream molecular signaling events that control this functional switch between intra-BLA DA D1 versus D2 receptor transmission are not currently understood. Using an unbiased place conditioning procedure in rats combined with molecular analyses, we report that opiate reward memory acquisition requires intra-BLA ERK1/2 signaling only in the previously opiate-naive state. However, following chronic opiate exposure and withdrawal, intra-BLA reward memory processing switches to a CaMKII alpha-dependent memory substrate. Furthermore, the ability of intra-BLA DA D1 or D2 receptor transmission to modulate the motivational salience of opiates similarly operates through a D1-mediated ERK-dependent mechanism in the opiate-naive state, but switches to a D2-mediated CaMKII alpha-dependent mechanism in the dependent/withdrawn state."
According to the news editors, the research concluded: "Protein analysis of BLA tissue revealed a downregulation of ERK1/2 phosphorylation and a dramatic reduction in both total and phosphorylated CaMKII alpha signaling, specifically in the opiate-dependent/withdrawn state, demonstrating functional control of ERK1/2-dependent versus CaMKII alpha-dependent memory mechanisms within the BLA, controlled by opiate-exposure state."
For more information on this research see: Opiate Exposure and Withdrawal Induces a Molecular Memory Switch in the Basolateral Amygdala between ERK1/2 and CaMKII alpha-Dependent Signaling Substrates. Journal of Neuroscience, 2013;33(37):14693-14704. Journal of Neuroscience can be contacted at: Soc Neuroscience, 11 Dupont Circle, NW, Ste 500, Washington, DC 20036, USA. (Society for Neuroscience - www.sfn.org/; Journal of Neuroscience - www.sfn.org/index.aspx?pagename=JournalOfNeuroscience)
The news correspondents report that additional information may be obtained from D. Lyons, University of Western Ontario, Dept. of Psychol, Schulich Sch Med & Dental, London, ON N6A 5C1, Canada. Additional authors for this research include X. de Jaeger, L.G. Rosen, T. Ahmad, N.M. Lauzon, J. Zunder, L.M. Coolen, W. Rushlow and S.R. Laviolette (see also Central Nervous System).
Keywords for this news article include: Brain, London, Canada, Ontario, Amygdala, Basal Ganglia, Limbic System, Telencephalon, Nanotechnology, Prosencephalon, Molecular Memory, Emerging Technologies, Central Nervous System, North and Central America
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