Linked Life Data

19619137

Source:http://linkedlifedata.com/resource/pubmed/id/19619137

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-9-23
pubmed:abstractText
The neurotransmitter serotonin is synthesized in the retina by one type of amacrine neuron but accumulates in bipolar neurons in many vertebrates. The mechanisms, functions and purpose underlying serotonin accumulation in bipolar cells remain unknown. Here, we demonstrate that exogenous serotonin transiently accumulates in a distinct type of bipolar neuron. KCl-mediated depolarization causes the depletion of serotonin from amacrine neurons and, subsequently, serotonin is taken-up by bipolar neurons. The accumulation of endogenous and exogenous serotonin by bipolar neurons is blocked by selective reuptake inhibitors. Exogenous serotonin is specifically taken-up by bipolar neurons even when serotonin-synthesizing amacrine neurons are destroyed; excluding the possibility that serotonin diffuses through gap junctions from amacrine into bipolar neurons. Further, inhibition of monoamine oxidase A prevents the degradation of serotonin in bipolar neurons, suggesting that monoamine oxidase A is present in these neurons. However, the vesicular monoamine transporter 2 is present only in amacrine cells suggesting that serotonin is not transported into synaptic vesicles and reused as a transmitter in the bipolar neurons. We conclude that the serotonin-accumulating bipolar neurons perform glial functions in the retina by actively transporting and degrading serotonin that is synthesized in neighboring amacrine cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-14
pubmed:dateRevised
2010-12-3
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Serotonin released from amacrine neurons is scavenged and degraded in bipolar neurons in the retina.
pubmed:affiliation
Department of Neuroscience, The Ohio State University, Columbus, Ohio, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural