rdf:type |
|
lifeskim:mentions |
umls-concept:C0001675,
umls-concept:C0015127,
umls-concept:C0021469,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0027882,
umls-concept:C0042817,
umls-concept:C0392747,
umls-concept:C0439831,
umls-concept:C0445254,
umls-concept:C0678594,
umls-concept:C1314792,
umls-concept:C1517945,
umls-concept:C1708517
|
pubmed:issue |
5
|
pubmed:dateCreated |
2011-9-9
|
pubmed:abstractText |
A fundamental property of neuronal circuits is the ability to adapt to altered sensory inputs. It is well established that the functional synaptic changes underlying this adaptation are reflected by structural modifications in excitatory neurons. In contrast, the degree to which structural plasticity in inhibitory neurons accompanies functional changes is less clear. Here, we use two-photon imaging to monitor the fine structure of inhibitory neurons in mouse visual cortex after deprivation induced by retinal lesions. We find that a subset of inhibitory neurons carry dendritic spines, which form glutamatergic synapses. Removal of visual input correlates with a rapid and lasting reduction in the number of inhibitory cell spines. Similar to the effects seen for dendritic spines, the number of inhibitory neuron boutons dropped sharply after retinal lesions. Together, these data suggest that structural changes in inhibitory neurons may precede structural changes in excitatory circuitry, which ultimately result in functional adaptation following sensory deprivation.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
1097-4199
|
pubmed:author |
|
pubmed:copyrightInfo |
Copyright © 2011 Elsevier Inc. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:day |
8
|
pubmed:volume |
71
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
869-82
|
pubmed:meshHeading |
pubmed-meshheading:21903080-Animals,
pubmed-meshheading:21903080-Brain Mapping,
pubmed-meshheading:21903080-Dendritic Spines,
pubmed-meshheading:21903080-Diagnostic Imaging,
pubmed-meshheading:21903080-Glutamate Decarboxylase,
pubmed-meshheading:21903080-Glutamic Acid,
pubmed-meshheading:21903080-Green Fluorescent Proteins,
pubmed-meshheading:21903080-Inhibitory Postsynaptic Potentials,
pubmed-meshheading:21903080-Mice,
pubmed-meshheading:21903080-Mice, Transgenic,
pubmed-meshheading:21903080-Neural Inhibition,
pubmed-meshheading:21903080-Neuropeptide Y,
pubmed-meshheading:21903080-Presynaptic Terminals,
pubmed-meshheading:21903080-Retina,
pubmed-meshheading:21903080-Sensory Deprivation,
pubmed-meshheading:21903080-Sensory Receptor Cells,
pubmed-meshheading:21903080-Time Factors,
pubmed-meshheading:21903080-Vesicular Glutamate Transport Protein 1,
pubmed-meshheading:21903080-Visual Cortex,
pubmed-meshheading:21903080-Visual Pathways,
pubmed-meshheading:21903080-gamma-Aminobutyric Acid
|
pubmed:year |
2011
|
pubmed:articleTitle |
Loss of sensory input causes rapid structural changes of inhibitory neurons in adult mouse visual cortex.
|
pubmed:affiliation |
Max Planck Institute of Neurobiology, Am Klopferspitz 18, D-82152 Martinsried, Germany.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|