Why do lesions in the rodent anterior thalamic nuclei cause such severe spatial deficits?

Highlights

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  A dual hypothesis is introduced to explain the importance of these thalamic nuclei.

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  ATN are vital for multiple spatial functions.

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  ATN damage disrupts processing across distal limbic sites.

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  Distal pathology caused by ATN damage disrupts plasticity and metabolic activity.

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  ATN lesion effects reflect both their intrinsic importance and distal dysfunctions.

Abstract

Lesions of the rodent anterior thalamic nuclei cause severe deficits to multiple spatial learning tasks. Possible explanations for these effects are examined, with particular reference to T-maze alternation. Anterior thalamic lesions not only impair allocentric place learning but also disrupt other spatial processes, including direction learning, path integration, and relative length discriminations, as well as aspects of nonspatial learning, e.g., temporal discriminations. Working memory tasks, such as T-maze alternation, appear particularly sensitive as they combine an array of these spatial and nonspatial demands. This sensitivity partly reflects the different functions supported by individual anterior thalamic nuclei, though it is argued that anterior thalamic lesion effects also arise from covert pathology in sites distal to the thalamus, most critically in the retrosplenial cortex and hippocampus. This two-level account, involving both local and distal lesion effects, explains the range and severity of the spatial deficits following anterior thalamic lesions. These findings highlight how the anterior thalamic nuclei form a key component in a series of interdependent systems that support multiple spatial functions.