Acute Cocaine Increases Interleukin-1β mRNA and Immunoreactive Cells in the Cortex and Nucleus Accumbens

Cearley, Cassia N.; Blindheim, Kelly; Sorg, Barbara A.; Krueger, James M.; Churchill, Lynn

doi:10.1007/s11064-011-0410-9

Cited by 33 publications

(31 citation statements)

References 43 publications

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“…In the brain, acute cocaine results in increased IL-1β mRNA in the NAc and cortex (Cearley et al, 2011), while methamphetamine leads to increased IL-6 and TNFα in hippocampus and frontal cortex (Gonçalves et al, 2008). Similarly, acute injections of cocaine results in elevated IL-1β mRNA in the VTA, an effect that is blocked with (+)-naloxone treatment (Northcutt et al, 2015).…”

Section: Psychostimulants Glia and Neuroimmune Signalingmentioning

confidence: 99%

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Lacagnina

Rivera

Bilbo

2016

Neuropsychopharmacol

223

170

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Drugs of abuse cause persistent alterations in synaptic plasticity that may underlie addiction behaviors. Evidence suggests glial cells have an essential and underappreciated role in the development and maintenance of drug abuse by influencing neuronal and synaptic functions in multifaceted ways. Microglia and astrocytes perform critical functions in synapse formation and refinement in the developing brain, and there is growing evidence that disruptions in glial function may be implicated in numerous neurological disorders throughout the lifespan. Linking evidence of function in health and under pathological conditions, this review will outline the glial and neuroimmune mechanisms that may contribute to drug-abuse liability, exploring evidence from opioids, alcohol, and psychostimulants. Drugs of abuse can activate microglia and astrocytes through signaling at innate immune receptors, which in turn influence neuronal function not only through secretion of soluble factors (eg, cytokines and chemokines) but also potentially through direct remodeling of the synapses. In sum, this review will argue that neural-glial interactions represent an important avenue for advancing our understanding of substance abuse disorders.

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Section: Psychostimulants Glia and Neuroimmune Signalingmentioning

confidence: 99%

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Lacagnina

Rivera

Bilbo

2016

Neuropsychopharmacol

223

170

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“…Here, high doses of methamphetamine promote NFκB-DNA binding and induce proinflammatory cytokine gene expression. More recent studies have identified that both cocaine and methamphetamine increase proinflammatory cytokines in the nucleus accumbens, hippocampus and prefrontal cortex (Cearley et al, 2011; Gonçalves et al, 2008). Interestingly, cocaine-induced increases in IL1β were inhibited by the low-affinity TLR4 antagonist, (+)-naloxone, suggesting the involvement of the TLR4 receptor (Northcutt et al, 2015).…”

Section: Drugs Of Abuse and Glial Cell Activitymentioning

confidence: 99%

Glial and neuroinflammatory targets for treating substance use disorders

Bachtell

Jones

Heinzerling

et al. 2017

Drug and Alcohol Dependence

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Background The plenary session at the 2016 Behavior, Biology and Chemistry: Translational Research in Addiction Conference focused on glia as potential players in the development, persistence and treatment of substance use disorders. Glia partake in various functions that are important for healthy brain activity. Drugs of abuse alter glial cell activity producing several perturbations in brain function that are thought to contribute to behavioral changes associated with substance use disorders. Consequently, drug-induced changes in glia-driven processes in the brain represent potential targets for pharmacotherapeutics treating substance use disorders. Methods Four speakers presented preclinical and clinical research illustrating the effects that glial modulators have on abuse-related behavioral effects of psychostimulants and opioids. This review highlights some of these findings and expands its focus to include other research focused on drug-induced glia abnormalities and glia-focused treatment approaches in substance use disorders. Results Preclinical findings show that drugs of abuse induce neuroinflammatory signals and disrupt glutamate homeostasis through their interaction with microglia and astrocytes. Preclinical and clinical studies testing the effects of glial modulators show general effectiveness in reducing behaviors associated with substance use disorders. Conclusions The contribution of drug-induced glial activity continues to emerge as an intriguing target for substance use disorder treatments. Clinical investigations of glial modulators have yielded promising results on substance use measures and indicate that they are generally safe and well-tolerated. However, results have not been entirely positive and more questions remain for continued exploration in the development and testing of glial-directed treatments for substance use disorders.

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“…100 However, the clinical relevance of these latter findings needs further investigation. Notably, in addition to its direct inflammatory responses at BBB endothelium, cocaine administration (5 mg/kg) in rats was also shown to stimulate induction and release of proinflammatory cytokines (such as TNFa and IL-1b) in reward regions of the brain 101 that would further aggravate regional BBB damage. 43,102 Brain microglial cells that secrete a plethora of cytokines, chemokines, and other neurotoxic factors upon activation are also shown to be critical cellular targets for cocaine-induced neuroinflammation and ensuing BBB disruption.…”

Section: Cocaine Abuse and Blood-brain Barrier Impairmentmentioning

confidence: 99%

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

Sajja

Rahman

Cucullo

2015

J Cereb Blood Flow Metab

119

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Psychostimulants and nicotine are the most widely abused drugs with a detrimental impact on public health globally. While the long-term neurobehavioral deficits and synaptic perturbations are well documented with chronic use of methamphetamine, cocaine, and nicotine, emerging human and experimental studies also suggest an increasing incidence of neurovascular complications associated with drug abuse. Short-or long-term administration of psychostimulants or nicotine is known to disrupt blood-brain barrier (BBB) integrity/function, thus leading to an increased risk of brain edema and neuroinflammation. Various pathophysiological mechanisms have been proposed to underlie drug abuse-induced BBB dysfunction suggesting a central and unifying role for oxidative stress in BBB endothelium and perivascular cells. This review discusses drug-specific effects of methamphetamine, cocaine, and tobacco smoking on brain microvascular crisis and provides critical assessment of oxidative stress-dependent molecular pathways focal to the global compromise of BBB. Additionally, given the increased risk of human immunodeficiency virus (HIV) encephalitis in drug abusers, we have summarized the synergistic pathological impact of psychostimulants and HIV infection on BBB integrity with an emphasis on unifying role of endothelial oxidative stress. This mechanistic framework would guide further investigations on specific molecular pathways to accelerate therapeutic approaches for the prevention of neurovascular deficits by drugs of abuse.

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Acute Cocaine Increases Interleukin-1β mRNA and Immunoreactive Cells in the Cortex and Nucleus Accumbens

Cited by 33 publications

References 43 publications

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Glial and neuroinflammatory targets for treating substance use disorders

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

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