Stress Modulation of Opposing Circuits in the Bed Nucleus of the Stria Terminalis

Neuropsychopharmacology, Год журнала: 2015, Номер 41(1), С. 103 - 125

Опубликована: Июнь 22, 2015

Язык: Английский

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The extracellular signal-regulated kinase 1/2 pathway in neurological diseases: A potential therapeutic target (Review)

International Journal of Molecular Medicine, Год журнала: 2017, Номер 39(6), С. 1338 - 1346

Опубликована: Апрель 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

Язык: Английский

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Under the curve: Critical issues for elucidating D1 receptor function in working memory

Neuroscience, Год журнала: 2005, Номер 139(1), С. 263 - 276

Опубликована: Ноя. 29, 2005

Язык: Английский

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Inhibition of ERK pathway or protein synthesis during reexposure to drugs of abuse erases previously learned place preference

Proceedings of the National Academy of Sciences, Год журнала: 2006, Номер 103(8), С. 2932 - 2937

Опубликована: Фев. 10, 2006

Repeated association of drugs abuse with context leads to long-lasting behavioral responses that reflect reward-controlled learning and participate in the establishment addiction. Reactivation consolidated memories is known produce a reconsolidation process during which undergo labile state. We investigated whether reexposure had similar effects. Cocaine administration activates extracellular signal-regulated kinase (ERK) striatum, ERK activation required for acquisition cocaine-induced conditioned place preference (CPP). When mice previously cocaine-place were reexposed cocaine drug-paired compartment after systemic SL327, an inhibitor activation, CPP response was abolished 24 h later. This procedure also phosphorylation glutamate receptor-1 observed ventral dorsal later, test. Erasure by SL327 combination did not result from enhanced extinction. Similarly, morphine presence long-lastingly learned morphine-CPP. The effects on cocaine- or morphine-CPP reproduced protein synthesis inhibition. In contrast, inhibition alter acquired locomotor sensitization cocaine. Our findings show established can be disrupted when reactivation associates both drug administration. involves ERK, treatment preventing erases response. These results suggest potential therapeutic strategies explore

Язык: Английский

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Parsing Molecular and Behavioral Effects of Cocaine in Mitogen- and Stress-Activated Protein Kinase-1-Deficient Mice

Journal of Neuroscience, Год журнала: 2005, Номер 25(49), С. 11444 - 11454

Опубликована: Дек. 7, 2005

Although the induction of persistent behavioral alterations by drugs abuse requires regulation gene transcription, precise intracellular signaling pathways that are involved remain mainly unknown. Extracellular signal-regulated kinase (ERK) is critical for expression immediate-early genes in striatum response to cocaine and Δ9-tetrahydrocannabinol rewarding properties these drugs. Here we show mice a single injection (10 mg/kg) activates mitogen- stress-activated protein 1 (MSK1) dorsal nucleus accumbens. Cocaine-induced phosphorylation MSK1 threonine 581 cAMP element-binding (CREB) serine 133 (Ser ) were blocked SL327, drug prevents ERK activation. Cocaine increased acetylation histone H4 lysine 5 H3 Ser 10 , demonstrating existence drug-induced chromatin remodeling vivo . In knock-out (KO) CREB blocked, c-Fos dynorphin was prevented, whereas Egr-1 (early growth response-1)/zif268/Krox24 unaltered. MSK1-KO had no obvious neurological defect but displayed contrasted phenotype cocaine. Acute effects dopamine D or 2 agonists Sensitivity low doses, not high conditioned place preference paradigm, locomotor sensitization repeated injections decreased markedly. Our results major striatal kinase, downstream from ERK, responsible required specifically as well sensitization.

Язык: Английский

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