Present address: Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria, 3010, Australia
Anterior thalamic lesions stop immediate early gene activation in selective laminae of the retrosplenial cortex: evidence of covert pathology in rats?
Version of Record online: 24 JUN 2004
European Journal of Neuroscience
Volume 19, Issue 12, pages 3291–3304, June 2004
How to Cite
Jenkins, T. A., Vann, S. D., Amin, E. and Aggleton, J. P. (2004), Anterior thalamic lesions stop immediate early gene activation in selective laminae of the retrosplenial cortex: evidence of covert pathology in rats?. European Journal of Neuroscience, 19: 3291–3304. doi: 10.1111/j.0953-816X.2004.03421.x
- Issue online: 24 JUN 2004
- Version of Record online: 24 JUN 2004
- Received 3 February 2004, revised 4 April 2004, accepted 6 April 2004
- Alzheimer's disease;
- anterior thalamus;
- immediate early genes;
- retrosplenial cortex;
Lesions involving the anterior thalamic nuclei stopped immediate early gene (IEG) activity in specific regions of the rat retrosplenial cortex, even though there were no apparent cytoarchitectonic changes. Discrete anterior thalamic lesions were made either by excitotoxin (Experiment 1) or radiofrequency (Experiment 2) and, following recovery, the rats foraged in a radial-arm maze in a novel room. Measurements made 6–12 weeks postsurgery showed that, in comparison with surgical controls, the thalamic lesions produced the same, selective patterns of Fos changes irrespective of method. Granular (caudal granular cortex and rostral granular cortex), but not dysgranular (dysgranular cortex), retrosplenial cortex showed a striking loss of Fos-positive cells. While a loss of between 79 and 89% of Fos-positive cells was found in the superficial laminae, the deeper layers appeared normal. In Experiments 3 and 4, rats 9–10 months postsurgery were placed in an activity box for 30 min. Anterior thalamic lesions (Experiment 3) led to a pronounced IEG decrease of both Fos and zif268 throughout the retrosplenial cortex that now included the dysgranular area. These IEG losses were found even though the same regions appeared normal using standard histological techniques. Lesions of the postrhinal cortex (Experiment 4) did not bring about a loss of retrosplenial IEG activity even though this region is also reciprocally connected with the retrosplenial cortex. This selective effect of anterior thalamic damage upon retrosplenial activity may both amplify the disruptive effects of anterior thalamic lesions and help to explain the posterior cingulate hypoactivity found in Alzheimer's disease.