title: Lateral and anterior thalamic lesions impair independent memory systems.
abstract: Damage to the medial region of the thalamus, both in clinical cases (e.g., patients with infarcts or the Korsakoff's syndrome) and animal lesion models, is associated with variable amnesic deficits. Some studies suggest that many of these memory deficits rely on the presence of lateral thalamic lesions (LT) that include the intralaminar nuclei, presumably by altering normal function between the striatum and frontal cortex. Other studies suggest that the anterior thalamic nuclei (AT) may be more critical, as a result of disruption to an extended hippocampal system. Here, highly selective LT and AT lesions were made to test the prediction that these two regions contribute to two different memory systems. Only LT lesions produced deficits on a preoperatively acquired response-related (egocentric) working memory task, tested in a cross-maze. Conversely, only AT lesions impaired postoperative acquisition of spatial working memory, tested in a radial maze. These findings provide the first direct evidence of a double dissociation between the LT and AT neural aggregates. As the lateral and the anterior medial thalamus influence parallel independent memory processing systems, they may each contribute to memory deficits, depending on lesion extent in clinical and experimental cases of thalamic amnesia.
authors.affiliation: Van der Veer Institute for Parkinson's and Brain Research, and Department of Psychology, University of Canterbury, Christchurch 8020, New Zealand. anna.mitchell@psy.ox.ac.uk
authors.forename: Anna S
authors.initials: AS
authors.lastname: Mitchell
authors.forename: John C
authors.initials: JC
authors.lastname: Dalrymple-Alford
mesh_terms: D000647:Amnesia / Q000503:physiopathology*; D000818:Animals; D020643:Anterior Thalamic Nuclei / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D020646:Intralaminar Thalamic Nuclei / Q000502:physiology*; D018782:Maze Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D051381:Rats