Linked Life Data

14988037

Source:http://linkedlifedata.com/resource/pubmed/id/14988037

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-2-27
pubmed:abstractText
The present work focuses on characterization of glutamate receptor subtypes mediating cone signal transmission to ON bipolar cells (BCs) in the carp retina, using intracellular recording techniques. Glutamate (5 mM) hyperpolarized cone-dominant ON BCs, which was associated with a suppression of light responses, whereas Co(2+) (1 mM) depolarized these cells and suppressed their light responses. On the other hand, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) of 20 microM caused a membrane depolarization and blocked depolarizing light responses, L-2-amino-4-phosphonobutryic acid (l-AP4) was without effect. The effects of AMPA were reversed by coapplication of GYKI 52466, an AMPA receptor selective non-competitive antagonist, but persisted in the presence of picrotoxin and strychnine. For rod-dominant ON BCs, both l-AP4 and AMPA reversibly blocked depolarizing light responses, but with membrane potential changes of opposite polarities (hyperpolarization for l-AP4 and depolarization for AMPA). In the inner retina, AMPA depolarized transient ON-OFF amacrine cells and blocked both ON and OFF cone-driven depolarizing responses, but l-AP4 did not. These results suggest that AMPA receptors, but not l-AP4 receptors, are involved in synaptic transmission of cone signal to ON bipolar cells in carp retina.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
1002
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
86-93
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
AMPA receptor is involved in transmission of cone signal to ON bipolar cells in carp retina.
pubmed:affiliation
Institute of Neurobiology, Institutes of Brain Science, Fudan University, 220 Handan Road, Shanghai 200433, China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't