Impaired spatial working memory after anterior thalamic lesions: recovery with cerebrolysin and enrichment.
Brain Struct Funct. 2015-03-01; 221(4): 1955-1970
DOI: 10.1007/s00429-015-1015-x
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1. Brain Struct Funct. 2016 May;221(4):1955-70. doi: 10.1007/s00429-015-1015-x. Epub
2015 Mar 1.
Impaired spatial working memory after anterior thalamic lesions: recovery with
cerebrolysin and enrichment.
Loukavenko EA(1), Wolff M(2)(3), Poirier GL(4), Dalrymple-Alford JC(5)(6).
Author information:
(1)Department of Psychology, New Zealand Brain Research Institute, University of
Canterbury, Private Bag 4800, Christchurch, 8140, New Zealand.
.
(2)Univ.Bordeaux,INCIA, UMR 5287, 33400, Talence, France.
.
(3)CNRS, INCIA, UMR 5287, 33400, Talence, France. .
(4)Brain Mind Institute, École Polytechnique Fédérale de Lausanne, AAB201,
Station 19, 1015, Lausanne, Switzerland.
(5)Department of Psychology, New Zealand Brain Research Institute, University of
Canterbury, Private Bag 4800, Christchurch, 8140, New Zealand.
.
(6)Department of Medicine, University of Otago, Christchurch, New Zealand.
.
Lesions to the anterior thalamic nuclei (ATN) in rats produce robust spatial
memory deficits that reflect their influence as part of an extended hippocampal
system. Recovery of spatial working memory after ATN lesions was examined using a
30-day administration of the neurotrophin cerebrolysin and/or an enriched housing
environment. As expected, ATN lesions in standard-housed rats given saline
produced severely impaired reinforced spatial alternation when compared to
standard-housed rats with sham lesions. Both cerebrolysin and enrichment
substantially improved this working memory deficit, including accuracy on trials
that required attention to distal cues for successful performance. The
combination of cerebrolysin and enrichment was more effective than either
treatment alone when the delay between successive runs in a trial was increased
to 40 s. Compared to the intact rats, ATN lesions in standard-housed groups
produced substantial reduction in c-Fos expression in the retrosplenial cortex,
which remained low after cerebrolysin and enrichment treatments. Evidence that
multiple treatment strategies restore some memory functions in the current lesion
model reinforces the prospect for treatments in human diencephalic amnesia.
DOI: 10.1007/s00429-015-1015-x
PMID: 25725627 [Indexed for MEDLINE]