The Salted Food Addiction Hypothesis may explain overeating and the obesity epidemic DOI

James A. Cocores,

Mark S. Gold

Medical Hypotheses, Journal Year: 2009, Volume and Issue: 73(6), P. 892 - 899

Published: July 30, 2009

Language: Английский

Inhibitory control and emotional stress regulation: Neuroimaging evidence for frontal–limbic dysfunction in psycho-stimulant addiction DOI
Chiang‐Shan R. Li, Rajita Sinha

Neuroscience & Biobehavioral Reviews, Journal Year: 2007, Volume and Issue: 32(3), P. 581 - 597

Published: Dec. 5, 2007

Language: Английский

Citations

330

Social stress, therapeutics and drug abuse: Preclinical models of escalated and depressed intake DOI
Klaus A. Miczek,

Jasmine Yap,

H COVINGTONIII

et al.

Pharmacology & Therapeutics, Journal Year: 2008, Volume and Issue: 120(2), P. 102 - 128

Published: Aug. 16, 2008

Language: Английский

Citations

320

Natural rewards, neuroplasticity, and non-drug addictions DOI
Christopher M. Olsen

Neuropharmacology, Journal Year: 2011, Volume and Issue: 61(7), P. 1109 - 1122

Published: April 9, 2011

Language: Английский

Citations

320

Chronic dopaminergic stimulation in Parkinson's disease: from dyskinesias to impulse control disorders DOI
Valerie Voon, Pierre‐Olivier Fernagut, Jeffery R. Wickens

et al.

The Lancet Neurology, Journal Year: 2009, Volume and Issue: 8(12), P. 1140 - 1149

Published: Nov. 12, 2009

Language: Английский

Citations

288

Sex differences in the neurobiology of drug addiction DOI

Samara A.M. Bobzean,

Aliza K. De Nobrega, Linda I. Perrotti

et al.

Experimental Neurology, Journal Year: 2014, Volume and Issue: 259, P. 64 - 74

Published: Feb. 6, 2014

Language: Английский

Citations

241

The extracellular signal-regulated kinase 1/2 pathway in neurological diseases: A potential therapeutic target (Review) DOI Creative Commons
Jing Sun, Guangxian Nan

International Journal of Molecular Medicine, Journal Year: 2017, Volume and Issue: 39(6), P. 1338 - 1346

Published: April 21, 2017

Signaling pathways are critical modulators of a variety physiological and pathological processes, the abnormal activation some signaling can contribute to disease progression in various conditions. As result, have emerged as an important tool through which occurrence development diseases be studied, may then lead novel drugs. Accumulating evidence supports key role for extracellular signal-regulated kinase 1/2 (ERK1/2) embryonic central nervous system (CNS) regulation adult brain function. ERK1/2, one most well characterized members mitogen-activated protein family, regulates range from metabolism, motility inflammation, cell death survival. In system, ERK1/2 synaptic plasticity, repair memory formation. is also potent effector neuronal neuroinflammation many CNS diseases. This review summarizes recent findings neurobiological research, with special emphasis on that clarify our understanding processes regulate plethora isoform-specific ERK functions under Finally, we suggest potential therapeutic strategies associated agents acting prevent or treat neurological

Language: Английский

Citations

193

Cell Surface AMPA Receptors in the Rat Nucleus Accumbens Increase during Cocaine Withdrawal But Internalize after Cocaine Challenge in Association with Altered Activation of Mitogen-Activated Protein Kinases DOI Creative Commons

Amy C. Boudreau,

Jeremy M. Reimers,

Michael Milovanovic

et al.

Journal of Neuroscience, Journal Year: 2007, Volume and Issue: 27(39), P. 10621 - 10635

Published: Sept. 26, 2007

Although some studies report increased responsiveness of nucleus accumbens (NAc) AMPA receptors (AMPARs) after withdrawal from repeated cocaine treatment, others decreased plus challenge. Here we examine this apparent contradiction by quantifying cell surface and intracellular AMPAR subunits in the NAc before a challenge injection behaviorally sensitized rats. Because MAPKs (mitogen-activated protein kinases) regulate trafficking are implicated addiction, also evaluated phosphorylation extracellular signal-regulated kinase (ERK), c-Jun N-terminal (JNK), p38. Glutamate receptor 1 (GluR1) GluR2 surface/intracellular (S/I) ratios were 14 d rats but 24 h with (which elicited locomotor response) or saline conditioned locomotion). These findings suggested redistribution GluR1/2-containing receptors, possibility supported immunoprecipitation experiments indicating that most AMPARs GluR1/2 GluR2/3, few homomeric GluR1 GluR1/3 receptors. In rats, ERK during normalized JNK withdrawal, challenge, it was inversely related to S/I ratios. After p38 increased. summary, expression internalized single reexposure cocaine-related cues. paralleled expression. results complex, may be involved internalization respectively.

Language: Английский

Citations

278

Cocaine‐induced neuroadaptations in glutamate transmission DOI
Heath D. Schmidt, R. Christopher Pierce

Annals of the New York Academy of Sciences, Journal Year: 2010, Volume and Issue: 1187(1), P. 35 - 75

Published: Jan. 8, 2010

A growing body of evidence indicates that repeated exposure to cocaine leads profound changes in glutamate transmission limbic nuclei, particularly the nucleus accumbens. This review focuses on preclinical studies cocaine-induced behavioral plasticity, including sensitization, self-administration, and reinstatement seeking. Behavioral, pharmacological, neurochemical, electrophysiological, biochemical, molecular biological associated with plasticity systems are reviewed. The ultimate goal these lines research is identify novel targets for development therapies craving addiction. Therefore, we also outline progress prospects modulators treatment

Language: Английский

Citations

242

Role of ventral medial prefrontal cortex in incubation of cocaine craving DOI
Eisuke Koya,

Jamie L. Uejima,

Kristina A. Wihbey

et al.

Neuropharmacology, Journal Year: 2008, Volume and Issue: 56, P. 177 - 185

Published: May 9, 2008

Language: Английский

Citations

225

The epigenetic landscape of addiction DOI
Ian Maze, Eric J. Nestler

Annals of the New York Academy of Sciences, Journal Year: 2011, Volume and Issue: 1216(1), P. 99 - 113

Published: Jan. 1, 2011

Drug‐induced alterations in gene expression throughout the reward circuitry of brain are likely components persistence drug‐addicted state. Recent studies examining molecular mechanisms controlling drug‐induced transcriptional, behavioral, and synaptic plasticity have indicated a direct role for chromatin remodeling regulation stability drug‐mediated neuronal programs, subsequent promulgation addictive behaviors. In this review, we discuss recent advances our understanding phenomena—or epigenetics, by one definition—that contribute to drug addiction, with hope that such mechanistic insights may aid development novel therapeutics future treatments addiction.

Language: Английский

Citations

214