Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Simulations suggest pharmacological methods for rescuing long-term potentiation.

Journal of theoretical biology - 7 Nov 2014

Smolen Paul, Baxter Douglas A, Byrne John H

Abstract excerpt

Congenital cognitive dysfunctions are frequently due to deficits in molecular pathways that underlie the induction or maintenance of synaptic plasticity. For example, Rubinstein-Taybi syndrome (RTS) is due to a mutation in cbp, encoding the histone acetyltransferase CREB-binding protein (CBP). CBP is a transcriptional co-activator for CREB, and induction of CREB-dependent transcription plays a key role in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Drug Synergism
Share to Histone Deacetylase Inhibitors
Share to Long-Term Potentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Metabolic Networks and Pathways

Share to Neuronal Plasticity

Share to Phosphodiesterase Inhibitors

Share to Rubinstein-Taybi Syndrome

Share to Sialoglycoproteins

Source

Open in PubMed Open full text

Identifiers

PMID: 25034337
DOI: 10.1016/j.jtbi.2014.07.006
PMCID: PMC4162763

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 9 closest

Simulations suggest pharmacological methods for rescuing long-term potentiation.PMID 25034337Read ↗

Rubinstein-Taybi syndrome: molecular findings and therapeutic approaches to improve cognitive dysfunction.Semantic proximity Read ↗

Deficiency of the RIβ subunit of protein kinase A causes body tremor and impaired fear conditioning memory in rats.Semantic proximity Read ↗

Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism.Semantic proximity Read ↗

Amphetamine modulation of long-term potentiation in the prefrontal cortex: dose dependency, monoaminergic contributions, and paradoxical rescue in hyperdopaminergic mutant.Semantic proximity Read ↗

Effects of repeated treatment with phosphodiesterase-4 inhibitors on cAMP signaling, hippocampal cell proliferation, and behavior in the forced-swim test.Semantic proximity Read ↗

Bidirectional regulation of hippocampal long-term synaptic plasticity and its influence on opposing forms of memory.Semantic proximity Read ↗

Understanding intellectual disability through RASopathies.Semantic proximity Read ↗

Synaptic plasticity is altered by treatment with pharmacological levels of retinoic acid acting nongenomically however endogenous retinoic acid has not been shown to control synaptic plasticitySemantic proximity Read ↗

Inducible, pharmacogenetic approaches to the study of learning and memory.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.