Editorial: structural plasticity induced by drugs of abuse

Citation: Olive MF and Gass JT (2015) Editorial: structural plasticity induced by drugs of abuse. Front. Pharmacol. 6:88. The roots of addiction are often attributed to the ability of repeated drug use to compromise proper functioning of the central nervous system. Drug-induced functional changes in the brain occur on many levels, including altered expression of specific genes via genomic and epigenetic mechanisms, induction of synaptic plasticity and other cellular adaptations, and volumetric changes in discrete brain regions (Luscher and Malenka, 2011). These alterations can be drug class-specific and occur in both neuronal and non-neuronal cell populations. Drug-induced plasticity, or " rewiring " of the brain contributes to the development, maintenance, and persistence of the addicted state (Kalivas and O'Brien, 2008). The goal of this Research Topic is to assimilate recent findings related to plasticity and structural alterations produced by drug of abuse in neurons, glia, and other cell types of the brain. The mesolimbic dopamine system, originating in the ventral tegmental area (VTA) of the midbrain and projecting rostrally to the nucleus accumbens (NAc) and prefrontal cortex (PFC), mediates the acute reinforcing and incentive salience of abused drugs, as well as their aversive properties. As reviewed by Vashchinkina et al. (2014) mesolimbic dopamine neurons are highly regulated by intrinsic and extrinsic inhibitory GABAergic neurons. Vashchinkina et al. (2014) hypothesize that abused drugs induce structural and functional mesolimbic adaptations differentially via endogenous (e.g., THIP and neurosteroids) vs. exogenous (e.g., benzodiazepines and alcohol) modulators of GABA A receptors, as well as via synaptic vs. extrasynaptic GABA A receptors in the VTA. Collo et al. (2014) review evidence that drug-induced plasticity in mesolimbic dopaminergic neurons is mediated by common dopamine and brain-derived neurotrophic factor (BDNF) signaling pathways, specifically those recruiting MEK-ERK1/2, and PI3K-Akt-mTOR. Cadet and Bisagno (2014) review evidence for substantial plasticity in non-neuronal cell types in brain reward circuitry, including changes in astrocytic glutamate transporter expression, increases in pro-inflammatory cytokine production by microglia, and dysregulated oligodendrocytic myelin production. This latter topic is further elaborated on by Somkuwar et al. (2014) in their review of the proteoglycan neuron-glial antigen 2 (NG2), its expression by oligodendrocyte progenitor cells in the brain reward circuitry, and its interaction with stress-related neuromodulators. In addition, Bajo et al. (2015) provide evidence that interleukin-1β alters both basal and ethanol-facilitated GABAergic transmission in the central nucleus of the amygdala, part of the extended amygdala circuitry which is implicated in ethanol's …