Medical Hypotheses, Journal Year: 2009, Volume and Issue: 73(6), P. 892 - 899
Published: July 30, 2009
Language: Английский
Medical Hypotheses, Journal Year: 2009, Volume and Issue: 73(6), P. 892 - 899
Published: July 30, 2009
Language: Английский
Neuroscience & Biobehavioral Reviews, Journal Year: 2007, Volume and Issue: 32(3), P. 581 - 597
Published: Dec. 5, 2007
Language: Английский
Citations
330Pharmacology & Therapeutics, Journal Year: 2008, Volume and Issue: 120(2), P. 102 - 128
Published: Aug. 16, 2008
Language: Английский
Citations
320Neuropharmacology, Journal Year: 2011, Volume and Issue: 61(7), P. 1109 - 1122
Published: April 9, 2011
Language: Английский
Citations
320The Lancet Neurology, Journal Year: 2009, Volume and Issue: 8(12), P. 1140 - 1149
Published: Nov. 12, 2009
Language: Английский
Citations
288Experimental Neurology, Journal Year: 2014, Volume and Issue: 259, P. 64 - 74
Published: Feb. 6, 2014
Language: Английский
Citations
241International 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
193Journal 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
278Annals 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
242Neuropharmacology, Journal Year: 2008, Volume and Issue: 56, P. 177 - 185
Published: May 9, 2008
Language: Английский
Citations
225Annals 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