Molecular basis of long-term plasticity underlying addiction (Q29620539)

Europe PubMed Central

title

Molecular basis of long-term plasticity underlying addiction (English)

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30 April 2017

author name string

Nestler EJ

series ordinal

1

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30 April 2017

language of work or name

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30 April 2017

publication date

February 2001

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Nature Reviews Neuroscience

30 April 2017

published in

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30 April 2017

volume

2

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page(s)

119-28

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issue

2

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The neurobiology of drug addiction

30 April 2017

cites work

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Molecular and cellular basis of addiction

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CREB: a stimulus-induced transcription factor activated by a diverse array of extracellular signals

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Transcriptional regulation by cyclic AMP-responsive factors

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Regulation of cyclic AMP response element-binding protein (CREB) phosphorylation by acute and chronic morphine in the rat locus coeruleus

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Dual regulation of adenylate cyclase accounts for narcotic dependence and tolerance

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A general role for adaptations in G-proteins and the cyclic AMP system in mediating the chronic actions of morphine and cocaine on neuronal function

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Chronic repeated cocaine administration alters basal and opioid-regulated adenylyl cyclase activity

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Increased probability of GABA release during withdrawal from morphine

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Chronic morphine increases GABA tone on serotonergic neurons of the dorsal raphe nucleus: association with an up-regulation of the cyclic AMP pathway.

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Chronic morphine augments adenylyl cyclase phosphorylation: relevance to altered signaling during tolerance/dependence.

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Regulation of expression of cAMP response element-binding protein in the locus coeruleus in vivo and in a locus coeruleus-like cell line in vitro

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Regulation of cocaine reward by CREB.

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Involvement of cAMP-dependent protein kinase in the nucleus accumbens in cocaine self-administration and relapse of cocaine-seeking behavior.

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Cocaine binges differentially alter striatal preprodynorphin and zif/268 mRNAs.

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Induction of a long-lasting AP-1 complex composed of altered Fos-like proteins in brain by chronic cocaine and other chronic treatments.

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Network-level changes in expression of inducible Fos-Jun proteins in the striatum during chronic cocaine treatment and withdrawal

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deltaFosB: a molecular switch underlying long-term neural plasticity.

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Atypical and typical neuroleptic treatments induce distinct programs of transcription factor expression in the striatum.

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Expression of the transcription factor deltaFosB in the brain controls sensitivity to cocaine

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FosB mutant mice: loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine's psychomotor and rewarding effects

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NAC-1 is a brain POZ/BTB protein that can prevent cocaine-induced sensitization in the rat.

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16 Structure, function, and regulation of human cAMP-dependent protein kinases

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Enhanced morphine analgesia in mice lacking beta-arrestin 2

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Mu-opioid receptor desensitization by beta-arrestin-2 determines morphine tolerance but not dependence

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Chronic morphine administration increases beta-adrenergic receptor kinase (beta ARK) levels in the rat locus coeruleus

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Chronic morphine induces visible changes in the morphology of mesolimbic dopamine neurons

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Persistent structural modifications in nucleus accumbens and prefrontal cortex neurons produced by previous experience with amphetamine.

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Alterations in the morphology of dendrites and dendritic spines in the nucleus accumbens and prefrontal cortex following repeated treatment with amphetamine or cocaine.

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Opiates inhibit neurogenesis in the adult rat hippocampus

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Mammalian neural stem cells

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Mini-review: in vivo neurogenesis in the adult brain: regulation and functional implications

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Enhancement of locomotor activity and conditioned reward to cocaine by brain-derived neurotrophic factor.

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Role for GDNF in biochemical and behavioral adaptations to drugs of abuse.

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Regulation of phospholipase Cgamma in the mesolimbic dopamine system by chronic morphine administration

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Regulation of ERK (extracellular signal regulated kinase), part of the neurotrophin signal transduction cascade, in the rat mesolimbic dopamine system by chronic exposure to morphine or cocaine.

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Long-lasting induction of astrocytic basic fibroblast growth factor by repeated injections of amphetamine: blockade by concurrent treatment with a glutamate antagonist.

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Cell adhesion molecules, CREB, and the formation of new synaptic connections

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Synaptic plasticity: A molecular mechanism for metaplasticity

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CREB and the formation of long-term memory

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Neurotrophin regulation of synaptic transmission

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The involvement of brain-derived neurotrophic factor in hippocampal long-term potentiation revealed by gene targeting experiments

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Synaptic plasticity and dynamic modulation of the postsynaptic membrane

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Dopaminergic modulation of neuronal excitability in the striatum and nucleus accumbens

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Amphetamine blocks long-term synaptic depression in the ventral tegmental area.

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Modulation of long-term depression by dopamine in the mesolimbic system.

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LTP mechanisms: from silence to four-lane traffic

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Postsynaptic organization and regulation of excitatory synapses

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Sensitization to morphine induced by viral-mediated gene transfer

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The role of excitatory amino acids in behavioral sensitization to psychomotor stimulants

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Context-specific enhancement of glutamate transmission by cocaine

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https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=11252991

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30 April 2017

Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

1223602

1028328477

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1223602

1 reference

Consolidated OpenCitations Corpus – April 2017

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=11252991

2 references

30 April 2017

Consolidated OpenCitations Corpus – April 2017