Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: brain ; Germany ; LONG-TERM ; GENE ; PROTEIN ; transcription ; TRANSCRIPTION FACTOR ; REDUCTION ; WATER ; MEMORY ; FORM ; CAMP ; CELL-SURVIVAL ; conditioned taste aversion ; CONDITIONED TASTE-AVERSION ; CREB ; DEFICITS ; DELETION ; ELEMENT ; ELEMENT-BINDING PROTEIN ; ELEMENT-BINDING-PROTEIN ; fear conditioning ; hippocampus ; ISOFORM ; ISOFORMS ; knockout ; LATE-PHASE ; learning ; LONG-TERM POTENTIATION ; LTD ; LTP ; MAP KINASE ; MOUSE ; MOUSE-BRAIN ; MUTANT ; NERVOUS-SYSTEM ; NO ; PERFORMANCE ; PROBE ; RESPONSE ELEMENT ; score ; STAGE ; synaptic plasticity ; TARGETED MUTATION ; TRANSCRIPTION FACTORS ; TRANSGENIC MICE ; TRIAL ; TRIALS ; WATER MAZE
    Abstract: Previous studies addressing the role of the transcription factor cAMP response element-binding protein (CREB) in mammalian long-term synaptic plasticity and memory by gene targeting were compromised by incomplete deletion of the CREB isoforms. Therefore, we generated conditional knock-out strains with a marked reduction or complete deletion of all CREB isoforms in the hippocampus. In these strains, no deficits could be detected in lasting forms of hippocampal long-term potentiation (LTP) and long-term depression (LTD). When tested for hippocampus-dependent learning, mutants showed normal context-dependent fear conditioning. Water maze learning was impaired during the early stages, but many mutants showed satisfactory scores in probe trials thought to measure hippocampus-dependent spatial memory. However, conditioned taste aversion learning, a putatively hippocampus-independent memory test, was markedly impaired. Our data indicate that in the adult mouse brain, loss of CREB neither prevents learning nor substantially affects performance in some hippocampus-dependent tasks. Furthermore, it spares LTP and LTD in paradigms that are sensitive enough to detect deficits in other mutants. This implies either a species-specific or regionally restricted role of CREB in the brain and/or a compensatory upregulation of the cAMP response element modulator (CREM) and other as yet unidentified transcription factors
    Type of Publication: Journal article published
    PubMed ID: 12867515
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: brain ; RECEPTOR ; EXPRESSION ; Germany ; DISEASE ; GENE ; MICE ; RATS ; MEMORY ; hippocampus ; MOUSE ; synaptic plasticity ; UP-REGULATION ; STRESS ; BEHAVIOR ; RE ; NEUROENDOCRINE ; LEVEL ; LOSSES ; BLOCKADE ; ANTAGONISTS ; ADULT MICE ; GLUCOCORTICOID-RECEPTORS ; PITUITARY-ADRENOCORTICAL AXIS
    Abstract: Corticosteroid action in the brain is mediated by the mineralocorticoid (MR) and the glucocorticoid (GR) receptor. Disturbances in MR- and GR-mediated effects are thought to impair cognition, behavior, and endocrine control. To assess the function of the limbic MR in these processes, we inactivated the MR gene in the forebrain of the mouse using the Cre/loxP-recombination system. We screened the mice with a limbic MR deficiency in various learning and exploration tests. The mutant mice show impaired learning of the water-maze task and deficits in measures of working memory on the radial maze due to behavioral perseverance and stereotypy. They exhibit a hyperreactivity toward a novel object but normal anxiety-like behavior. The behavioral changes are associated with abnormalities of the mossy fiber projection and an up-regulation of GR expression in the hippocampus. Adult mutant mice show normal corticosterone levels at circadian trough and peak. This genetic model provides important information about the consequences of a permanently altered balance between limbic MR and GR, with implications for stress-related neuroendocrine and neuropsychiatric diseases
    Type of Publication: Journal article published
    PubMed ID: 16368758
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    ISSN: 0300-9629
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...