Neuroplasticity transcript profile of the ventral striatum in the extinction of opioid-induced conditioned place preference.

Autor: Martínez-Rivera FJ; Department of Anatomy and Neurobiology, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA., Martínez NA; Department of Physiology and Biophysics, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA; Molecular Sciences Building, University of Puerto Rico, San Juan, PR 00926, USA., Martínez M; Department of Physiology and Biophysics, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA; Molecular Sciences Building, University of Puerto Rico, San Juan, PR 00926, USA., Ayala-Pagán RN; Department of Anatomy and Neurobiology, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA., Silva WI; Department of Physiology and Biophysics, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA; Molecular Sciences Building, University of Puerto Rico, San Juan, PR 00926, USA., Barreto-Estrada JL; Department of Anatomy and Neurobiology, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, PR 00936, USA. Electronic address: jennifer.barreto1@upr.edu.
Jazyk: angličtina
Zdroj: Neurobiology of learning and memory [Neurobiol Learn Mem] 2019 Sep; Vol. 163, pp. 107031. Date of Electronic Publication: 2019 Jun 04.
DOI: 10.1016/j.nlm.2019.107031
Abstrakt: Persistent drug-seeking behavior has been associated with deficits in neural circuits that regulate the extinction of addictive behaviors. Although there is extensive data that associates addiction phases with neuroplasticity changes in the reward circuit, little is known about the underlying mechanisms of extinction learning of opioid associated cues. Here, we combined morphine-conditioned place preference (CPP) with real-time polymerase chain reaction (RT-PCR) to identify the effects of extinction training on the expression of genes (mRNAs) associated with synaptic plasticity and opioid receptors in the ventral striatum/nucleus accumbens (VS/NAc). Following morphine extinction training, we identified two animal subgroups showing either extinction (low CPP) or extinction-resistance (high CPP). A third group were conditioned to morphine but did not receive extinction training (sham-extinction; high CPP). RT-PCR results showed that brain derived neurotrophic factor (Bdnf) was upregulated in rats showing successful extinction. Conversely, the lack of extinction training (sham-extinction) upregulated genes associated with kinases (Camk2g), neurotrophins (Ngfr), synaptic connectivity factors (Ephb2), glutamate neurotransmission (Grm8) and opioid receptors (μ1, Δ1). To further identify genes modulated by morphine itself, comparisons with their saline-counterparts were performed. Results revealed that Bdnf was consistently upregulated in the extinction group. Alternatively, widespread gene modulation was observed in the group with lack of extinction training (i.e. Drd2, Cnr1, Creb, μ1, Δ1) and the group showing extinction resistance (i.e. Crem, Rheb, Tnfa). Together, our study builds on the identification of putative genetic markers for the extinction learning of drug-associated cues.
(Published by Elsevier Inc.)
Databáze: MEDLINE
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