Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive thalamus

John C. Dalrymple-Alford, Bruce Harland, Elena A. Loukavenko, Brook Perry, Stephanie Mercer, David A. Collings, Katharina Ulrich, Wickliffe C. Abraham, Neil McNaughton, Mathieu Wolff
Neuroscience & Biobehavioral Reviews. 2015-07-01; 54: 145-160
DOI: 10.1016/j.neubiorev.2014.12.007

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1. Neurosci Biobehav Rev. 2015 Jul;54:145-60. doi: 10.1016/j.neubiorev.2014.12.007.
Epub 2015 Jan 29.

Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive
thalamus.

Dalrymple-Alford JC(1), Harland B(2), Loukavenko EA(2), Perry B(2), Mercer S(2),
Collings DA(3), Ulrich K(4), Abraham WC(4), McNaughton N(4), Wolff M(5).

Author information:
(1)New Zealand Brain Research Institute, and Department of Psychology, University
of Canterbury, Christchurch 8140, New Zealand; Department of Medicine, University
of Otago, Christchurch, New Zealand. Electronic address:
.
(2)New Zealand Brain Research Institute, and Department of Psychology, University
of Canterbury, Christchurch 8140, New Zealand.
(3)School of Biological Sciences, University of Canterbury, Christchurch, New
Zealand.
(4)Department of Psychology and Brain Health Research Centre, University of
Otago, Dunedin, New Zealand.
(5)University of Bordeaux, INCIA, UMR 5287, F-33400 Talence, France; CNRS, INCIA,
UMR 5287, F-33400 Talence, France.

Injury to the anterior thalamic nuclei (ATN) and their neural connections is the
most consistent neuropathology associated with diencephalic amnesia. ATN lesions
in rats produce memory impairments that support a key role for this region within
an extended hippocampal system of complex overlapping neural connections.
Environmental enrichment is a therapeutic tool that produces substantial,
although incomplete, recovery of memory function after ATN lesions, even after
the lesion-induced deficit has become established. Similarly, the neurotrophic
agent cerebrolysin, also counters the negative effects of ATN lesions. ATN
lesions substantially reduce c-Fos expression and spine density in the
retrosplenial cortex, and reduce spine density on CA1 neurons; only the latter is
reversed by enrichment. We discuss the implications of this evidence for the
cognitive thalamus, with a proposal that there are genuine interactions among
different but allied thalamo-cortical systems that go beyond a simple summation
of their separate effects.

Copyright © 2015. Published by Elsevier Ltd.

DOI: 10.1016/j.neubiorev.2014.12.007
PMID: 25637779 [Indexed for MEDLINE]

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