Linked Life Data

17767503

Source:http://linkedlifedata.com/resource/pubmed/id/17767503

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-9-4
pubmed:abstractText
The present study examined whether hippocampal lesions disrupt retrosplenial cortex function. The immediate-early genesc-fos and zif268 provided markers of cellular activity, and their levels were compared in different cytoarchitectonic subregions (dysgranular, granular a and granular b) and different layers (superficial or deep) within retrosplenial cortex. Experiments 1-3 examined the impact of hippocampal lesions on retrosplenial cortex function, with the variations in protocol (e.g. lesion method, rat strain, behaviour prior to gene activity measurement) testing the generality of the findings. Experiment 1 showed that radio-frequency hippocampus lesions result in very striking losses of Fos and Zif268 activity in both superficial and deep laminae of all retrosplenial subregions. This pattern of results was repeated for Fos in experiments 2 and 3. Despite the loss of Fos and Zif268, there was no evidence of retrosplenial cortex atrophy as measured by Nissl counts (experiments 1-3) or NeuN-positive cell counts (experiment 3). Likewise, there was little evidence of any overt changes in cellular size, shape or appearance. The specificity of these hippocampal lesion effects was confirmed in experiment 4 as entorhinal cortex lesions did not change retrosplenial Fos levels. These results provide strong support for the notion that the retrosplenial cortex is unusually sensitive to deafferentation from some of its inputs, so that hippocampal damage might produce permanent 'covert pathology' in the retrosplenial cortex. Such dysfunctions could contribute to the pattern of cognitive changes associated with hippocampal lesions and also help to explain the functional interdependency of these two structures.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1254-66
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Hippocampal lesions halve immediate-early gene protein counts in retrosplenial cortex: distal dysfunctions in a spatial memory system.
pubmed:affiliation
School of Psychology, Cardiff University, Tower Building, Park Place, Cardiff, CF10 3AT, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't