Creb and Memory

Silva, Alcino J.; Kogan, Jeffrey H.; Frankland, Paul W.; Kida, Satoshi

doi:10.1146/annurev.neuro.21.1.127

Cited by 1,349 publications

(1,014 citation statements)

References 100 publications

(162 reference statements)

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“…They concluded that new neurons must be at a specific stage of maturation to be capable of supporting hippocampal-dependent learning. Previous studies have demonstrated a role for CREB in other forms of cellular and behavioral learning and memory (see Silva et al 1998). Localization of phospho-CREB during the critical period of granule cell maturation suggests that this transcription factor may play a role in deciding the functional fate of these new neurons (Figure 6).…”

Section: Colocalization Of Phospho-creb With Markers Of Maturing Neuronsmentioning

confidence: 99%

Regulation of Adult Neurogenesis by Antidepressant Treatment

Duman

Nakagawa

Malberg

2001

Neuropsychopharmacology

428

249

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Demonstration of neurogenesis in adult brainOur understanding of how the brain functions and undergoes adaptation and plasticity has changed dramatically over the past several years. A great deal of work has demonstrated that altered levels of neurotransmitters, second messenger pathways, and gene expression profiles underlie cellular and behavioral plasticity. This includes models of learning and memory as well as models of depression, anxiety, and psychosis, and the long-term actions of psychotropic drugs. However, it is now becoming increasing evident that changes in cellular morphology and even more pronounced alterations in brain structure also contribute to neural plasticity or remodeling. At the cellular level these changes can occur in the form of up or down-regulation of synapse formation and spine density or extension and retraction of dendrites. Another very dramatic example is up or down-regulation of neurogenesis in adult brain. Studies in recent years demonstrate that new cell birth occurs in adult brain and that the rate of neurogenesis and the survival of new neurons is regulated by a number of environmental, endocrine, and pharmacological treatments.In this paper we discuss the evidence that structural remodeling may be involved in the pathophysiology and treatment of mood disorders. The potential role of neurogenesis is also discussed as well as the molecular mechanisms which underlie antidepressant regulation of new cell birth and survival. The studies to date suggest an exciting possibility for the role of neurogenesis

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Section: Colocalization Of Phospho-creb With Markers Of Maturing Neuronsmentioning

confidence: 99%

Regulation of Adult Neurogenesis by Antidepressant Treatment

Duman

Nakagawa

Malberg

2001

Neuropsychopharmacology

428

249

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“…Among the CREB-regulated genes are several genes important for neurotransmission and signalling (Impey et al, 2004). Moreover, CREB is involved in adaptative processes such as learning, memory (Silva et al, 1998), and opiodinduced addiction (Nestler, 2001). As the signalling pathways affected by lithium can also influence CREB, CREB-directed transcription could be a downstream mediator of lithium action.…”

Section: Introductionmentioning

confidence: 99%

Chronic Lithium Salt Treatment Reduces CRE/CREB-Directed Gene Transcription and Reverses Its Upregulation by Chronic Psychosocial Stress in Transgenic Reporter Gene Mice

Böer

Cierny

Krause

et al. 2007

Neuropsychopharmacol

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The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMPresponsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) significantly decreased CRE/CREB-directed gene expression in hippocampus, cortex, hypothalamus, and striatum to 60-70%, and likewise reduced CREB phosphorylation. As bipolar disorder is also considered as a stress-related disorder, the effect of lithium was determined in mice submitted to a paradigm for chronic psychosocial stress. As shown before, stress for 25 days significantly increased CRE/CREB-directed gene expression in several brain regions by 100-150%. Treatment of stressed mice with lithium decreased stress-induced CRE/CREB-directed gene expression to control levels in nearly all brain regions and likewise reduced CREB phosphorylation. Chronic lithium treatment induced b-catenin accumulation and decreased cAMP levels, indicating an inhibitory effect of lithium on glycogen synthase kinase 3 and the adenylate cyclase/protein kinase A signalling cascade, which are known to modulate CREB activity. We here for the first time show that lithium regulates CRE/CREB-directed gene transcription in vivo and suggest CREB as a putative mediator of the neuronal adaptation after chronic lithium treatment.

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“…The role of the cyclic AMP cascade in memory processes has been recently evidenced. Genetic and pharmacological studies in mice and rats demonstrated that the cyclic AMP responsive element binding protein (CREB) is required for a variety of complex forms of memory, including spatial and social learning (Silva et al, 1998). The activation of the cyclic AMP-dependent protein kinase (PKA) induces long-term memory (Muller, 2000) and the inhibition of cyclic AMP phosphodiesterase reverses memory de®cits in the radial arm maze task (Zhang et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Differential prevention of morphine amnesia by antisense oligodeoxynucleotides directed against various Gi‐protein α subunits

Galeotti¹,

Ghelardini²,

Bartolini³

2001

British J Pharmacology

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1 The e ect of the i.c.v. administration of pertussis toxin (PTX) and antisense oligodeoxynucleotide directed against the a subunit of di erent Gi-proteins (anti-Gia 1 , anti-Gia 2 , anti-Gia 3 ) on amnesia induced by morphine was evaluated in the mouse passive avoidance test. 2 The administration of morphine (6 ± 10 mg kg 71 i.p.) immediately after the training session produced amnesia that was prevented by PTX (0.25 mg per mouse i.c.v.) administered 7 days before the passive avoidance test. 3 Anti-Gia 1 (6.25 mg per mouse i.c.v.) and anti-Gia 3 (12.5 mg per mouse i.c.v.), administered 18 and 24 h before the training session, prevented the morphine amnesia. By contrast, pretreatment with anti-Gia 2 (3.12 ± 25 mg per mouse i.c.v.) never modi®ed the impairment of memory processes induced by morphine. 4 At the highest e ective doses, none of the compounds used impaired motor coordination, as revealed by the rota rod test, nor modi®ed spontaneous motility and inspection activity, as revealed by the hole board test. 5 These results suggest the important role played by Gi 1 and Gi 3 protein subtypes in the transduction mechanism involved in the impairment of memory processes produced by morphine.

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Creb and Memory

Cited by 1,349 publications

References 100 publications

Regulation of Adult Neurogenesis by Antidepressant Treatment

Regulation of Adult Neurogenesis by Antidepressant Treatment

Chronic Lithium Salt Treatment Reduces CRE/CREB-Directed Gene Transcription and Reverses Its Upregulation by Chronic Psychosocial Stress in Transgenic Reporter Gene Mice

Differential prevention of morphine amnesia by antisense oligodeoxynucleotides directed against various Gi‐protein α subunits

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