Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-8-19
pubmed:abstractText
Encoding of novel information has been proposed to rely on the time-locked release of dopamine in the hippocampal formation during novelty detection. However, the site of novelty detection in the hippocampus remains a matter of debate. According to current models, the CA1 and the subiculum act as detectors and distributors of novel sensory information. Although most CA1 pyramidal neurons exhibit regular-spiking behavior, the majority of subicular pyramidal neurons fire high-frequency bursts of action potentials. The present study investigates the efficacy of dopamine D1/D5 receptor activation to facilitate the induction of activity-dependent long-term potentiation (LTP) in rat CA1 regular-spiking and subicular burst-spiking pyramidal cells. Using a weak stimulation protocol, set at a level subthreshold for the induction of LTP, we show that activation of D1/D5 receptors for 5-10 min facilitates LTP in subicular burst-spiking neurons but not in CA1 neurons. The results demonstrate that D1/D5 receptor-facilitated LTP is NMDA receptor-dependent, and requires the activation of protein kinase A. In addition, the D1/D5 receptor-facilitated LTP is shown to be presynaptically expressed and relies on presynaptic Ca(2+) signaling. The phenomenon of dopamine-induced facilitation of presynaptic NMDA receptor-dependent LTP in subicular burst-spiking pyramidal cells is in accordance with observations of the time-locked release of dopamine during novelty detection in this brain region, and reveals an intriguing mechanism for the encoding of hippocampal output information.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1460-9568
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
598-605
pubmed:meshHeading
pubmed-meshheading:20646048-2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, pubmed-meshheading:20646048-Action Potentials, pubmed-meshheading:20646048-Animals, pubmed-meshheading:20646048-Calcium, pubmed-meshheading:20646048-Cell Membrane, pubmed-meshheading:20646048-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:20646048-Dopamine Agonists, pubmed-meshheading:20646048-Enzyme Activation, pubmed-meshheading:20646048-Female, pubmed-meshheading:20646048-Hippocampus, pubmed-meshheading:20646048-Humans, pubmed-meshheading:20646048-Long-Term Potentiation, pubmed-meshheading:20646048-Male, pubmed-meshheading:20646048-Patch-Clamp Techniques, pubmed-meshheading:20646048-Presynaptic Terminals, pubmed-meshheading:20646048-Rats, pubmed-meshheading:20646048-Rats, Wistar, pubmed-meshheading:20646048-Receptors, Dopamine D1, pubmed-meshheading:20646048-Receptors, Dopamine D5, pubmed-meshheading:20646048-Synapses
pubmed:year
2010
pubmed:articleTitle
Activation of dopamine D1/D5 receptors facilitates the induction of presynaptic long-term potentiation at hippocampal output synapses.
pubmed:affiliation
Department of Psychiatry and Psychotherapy, Charité- Universitätsmedizin Berlin, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't