Does cAMP Response Element-Binding Protein Have a Pivotal Role in Hippocampal Synaptic Plasticity and Hippocampus-Dependent Memory?

Balschun, Detlef; Wolfer, David P; Gass, Peter; Mantamadiotis, Theo; Welzl, Hans; Schütz, Günther; Frey, Julietta U.; Lipp, Hans Peter

doi:10.1523/jneurosci.23-15-06304.2003

Cited by 229 publications

(183 citation statements)

References 49 publications

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“…The memory phenotype in mice with various CREB mutations is sensitive to training parameters (Bourtchuladze et al 1994;Kogan et al 1997;Gass et al 1998;Balschun et al 2003); however, this is the first study to show that different sequences of Morris water-maze training parameters also play a role in this memory phenotype. In the current study, CREB ‫מ␦␣‬ -deficient mice first exposed to a successful learning experience, (i.e., MWM4/ MWM4R) continued to learn well under more demanding test conditions in which they are known to be impaired.…”

Section: Discussionmentioning

confidence: 85%

“…Spatial learning and memory performance of CREB ‫מ␦␣‬ -deficient mice in different genetic backgrounds have been reported to show either a genetically dose-dependent effect (Gass et al 1998) or no impairment at all (Graves et al 2002). Further, various CREB mutants (in the 129SvEv ‫ן‬ C57BL/6 background) with either a marked reduction or complete loss of hippocampal CREB exhibit only modestly impaired water maze learning (Balschun et al 2003).…”

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confidence: 99%

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Cognitive performance is highly sensitive to prior experience in mice with a learning and memory deficit: Failure leads to more failure

Hebda-Bauer¹,

Watson²,

Akil³

2005

Learn. Mem.

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The impact of a previously successful or unsuccessful experience on the subsequent acquisition of a related task is not well understood. The nature of past experience may have even greater impact in individuals with learning deficits, as their cognitive processes can be easily disrupted. Mice with a targeted disruption of the ␣ and ␦ isoforms of the cAMP-response element-binding protein (CREB) gene (CREB ␣␦− -deficient mice) have a genetic vulnerability to impaired learning and memory that is highly influenced by experimental conditions. Thus, we studied the impact of prior successful and unsuccessful experiences on the degree to which CREB ␣␦− -deficient mice exhibit impaired spatial learning and memory in the Morris water maze (MWM). In Experiment 1, we replicated the cognitive deficit of CREB ␣␦− -deficient mice when given two trials per day with a 1-min intertrial interval (MWM2), and labeled this experience as a "failure." We rescued the deficit using four trials per day with a 3-to 5-min intertrial interval (MWM4) and labeled this experience a "success." In Experiment 2, a new, naive set of wild-type (WT) and CREB ␣␦− -deficient mice were randomly assigned to one of two sequence protocols to assess the influence of a success or a failure on subsequent performance. In Group 1, mice were first exposed to the MWM4 condition, followed by the more difficult MWM2 task. As expected, CREB ␣␦− -deficient mice performed well in the MWM4; they also performed well during reversal testing (MWM4R) where the goal location is changed. With this initial successful learning experience, the CREB ␣␦− -deficient mice then performed as well as WT mice in the MWM2, the condition in which they are known to be impaired. In contrast, CREB ␣␦− -deficient mice in Group 2 had an unsuccessful experience when first exposed to the MWM2 condition, and then also showed impairment in the MWM4, the condition in which they would normally perform well. This deficit was amplified when CREB ␣␦− -deficient mice were then tested in the reversal test. Sex differences in learning among CREB ␣␦− -deficient mice were amplified upon exposure to an unsuccessful learning experience. These data indicate that, under conditions of cognitive impairment, past experience can-depending on its nature-significantly facilitate or hinder future performance.

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Section: Discussionmentioning

confidence: 85%

mentioning

confidence: 99%

Cognitive performance is highly sensitive to prior experience in mice with a learning and memory deficit: Failure leads to more failure

Hebda-Bauer¹,

Watson²,

Akil³

2005

Learn. Mem.

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“…Importantly, histone acetylation is increased by the same amount in CREB␣⌬ mutant mice and wild-type littermates after TSA treatment (data not shown), demonstrating that TSA has similar overall effects on histone acetylation even in the presence of the CREB␣⌬ mutation. Much research suggests that CREB and CREB-mediated transcription (Bourtchuladze et al, 1994;Kogan et al, 1997;Gass et al, 1998;Josselyn et al, 2001Josselyn et al, , 2004Barco et al, 2002;Graves et al, 2002;Kida et al, 2002;Pittenger et al, 2002;Balschun et al, 2003) is involved in both hippocampus and amygdala function during memory formation, although the studies are at times contradictory. For example, confounding effects of genetic background and gene dosage on behavioral phenotypes of CREB mutant mice exist and partly explain the disparity in fear conditioning results observed by different laboratories (for review, see Bucan and Abel, 2002;Lonze and Ginty, 2002;Kaplan and Abel, 2003).…”

Section: Discussionmentioning

confidence: 99%

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Vecsey¹,

Hawk²,

Lattal³

et al. 2007

Journal of Neuroscience

759

761

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Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance both memory and synaptic plasticity. The current model for the action of HDAC inhibitors assumes that they alter gene expression globally and thus affect memory processes in a nonspecific manner. Here, we show that the enhancement of hippocampus-dependent memory and hippocampal synaptic plasticity by HDAC inhibitors is mediated by the transcription factor cAMP response element-binding protein (CREB) and the recruitment of the transcriptional coactivator and histone acetyltransferase CREB-binding protein (CBP) via the CREB-binding domain of CBP. Furthermore, we show that the HDAC inhibitor trichostatin A does not globally alter gene expression but instead increases the expression of specific genes during memory consolidation. Our results suggest that HDAC inhibitors enhance memory processes by the activation of key genes regulated by the CREB:CBP transcriptional complex.

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“…Conditioned taste aversion (CTA) is a form of classical conditioning, in which mice associate drinking saccharin (conditioned stimulus-CS) with a subsequent unpleasant sensation, that is, nausea (unconditioned stimulus-US) induced by lithium chloride (LiCl) (Balschun et al, 2003; see Supplementary Methods for details).…”

Section: Conditioned Taste Aversionmentioning

confidence: 99%

Adult AMPA GLUA1 Receptor Subunit Loss in 5-HT Neurons Results in a Specific Anxiety-Phenotype with Evidence for Dysregulation of 5-HT Neuronal Activity

Weber

Vogt

Gartside

et al. 2014

Neuropsychopharmacol

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Both the glutamatergic and serotonergic (5-HT) systems are implicated in the modulation of mood and anxiety. Descending cortical glutamatergic neurons regulate 5-HT neuronal activity in the midbrain raphe nuclei through a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors. To analyze the functional role of GLUA1-containing AMPA receptors in serotonergic neurons, we used the Cre-ERT2/loxP-system for the conditional inactivation of the GLUA1-encoding Gria1 gene selectively in 5-HT neurons of adult mice. These Gria1 5-HT À / À mice exhibited a distinct anxiety phenotype but showed no alterations in locomotion, depression-like behavior, or learning and memory. Increased anxiety-related behavior was associated with significant decreases in tryptophan hydroxylase 2 (TPH2) expression and activity, and subsequent reductions in tissue levels of 5-HT, its metabolite 5-hydroxyindoleacetic acid (5-HIAA), and norepinephrine in the raphe nuclei. However, TPH2 expression and activity as well as monoamine levels were unchanged in the projection areas of 5-HT neurons. Extracellular electrophysiological recordings of 5-HT neurons revealed that, while a1-adrenoceptor-mediated excitation was unchanged, excitatory responses to AMPA were enhanced and the 5-HT 1A autoreceptor-mediated inhibitory response to 5-HT was attenuated in Gria1 5-HT À / À mice. Our data show that a loss of GLUA1 protein in 5-HT neurons enhances AMPA receptor function and leads to multiple local molecular and neurochemical changes in the raphe nuclei that dysregulate 5-HT neuronal activity and induce anxiety-like behavior.

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Does cAMP Response Element-Binding Protein Have a Pivotal Role in Hippocampal Synaptic Plasticity and Hippocampus-Dependent Memory?

Cited by 229 publications

References 49 publications

Cognitive performance is highly sensitive to prior experience in mice with a learning and memory deficit: Failure leads to more failure

Cognitive performance is highly sensitive to prior experience in mice with a learning and memory deficit: Failure leads to more failure

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Adult AMPA GLUA1 Receptor Subunit Loss in 5-HT Neurons Results in a Specific Anxiety-Phenotype with Evidence for Dysregulation of 5-HT Neuronal Activity

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