Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-3-3
pubmed:abstractText
To address the role of D1 receptors in the medial prefrontal cortex, we combined pharmacological and genetic manipulations to examine long-term synaptic potentiation (LTP)/long-term synaptic depression (LTD) in brain slices of rats and mice. We found that the D1 antagonist SCH23390 selectively blocked the maintenance but not the induction of LTP in the prefrontal cortex. Conversely, activation of D1 receptors facilitated the maintenance of LTP, and this effect is impaired in heterozygous D1 receptor knockout mice. Low-frequency stimulation induced a transient depression in the medial prefrontal cortex. This depression could be transformed into LTD by coapplication of dopamine. Coapplication of dopamine, however, shows no facilitating effect on LTD in heterozygous D1 receptor knockout mice. These results provide pharmacological and genetic evidence for a role of D1 receptors in the bidirectional modulation of synaptic plasticity in the medial prefrontal cortex. The absence of this modulation in heterozygous knockout mice shows that a dysregulation of dopamine receptor expression levels can have dramatic effects on synaptic plasticity in the prefrontal cortex.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-10515982, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-10648725, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-10818167, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-11069975, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-112679, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-11784805, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-11906719, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-11978847, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-1825731, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-2213602, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-4744179, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-4856104, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7326577, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7708662, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7722001, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7757261, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7792056, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7809078, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-7862943, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9024661, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9334425, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9405523, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9427321, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9454866, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9639264, http://linkedlifedata.com/resource/pubmed/commentcorrection/14981263-9786225
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3236-41
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors.
pubmed:affiliation
Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't