Diencephalic amnesia is thought to be the result of damage to a single thalamic structure that is responsible for the memory impairment. However, an alternative view is that different thalamic structures contribute to the memory impairment in subtly different ways. Paired-associate learning is one important measure of learning and memory that is highly sensitive to disruption in people with amnesia or dementia. The current study will investigate the influence of lesions to two thalamic subregions, the anterior thalamic nuclei (AT) and the lateral thalamic nuclei (LT) in an object-odour paired associate learning task. Each of these subregions has been suggested by the literature as critical for amnesia after thalamus injury. The current study does not involve a place/ space component. Both AT and LT lesions caused impairments in the object-odour paired associate task, but not in the simple discrimination tasks. The results of this study provide new evidence to suggest that the anterior thalamic region may be responsible for more than spatial memory processing. This result is inconsistent with those of Aggleton & Brown (1999) that consider the AT to be part of an 'extended hippocampal system'. The deficits observed from LT lesions in this study provide new insight into the lateral thalamic region's role in pattern processing.

Diencephalic amnesia is thought to be the result of damage to a single thalamic structure that is responsible for the memory impairment. However, an alternative view is that different thalamic structures contribute to the memory impairment in subtly different ways. Paired-associate learning is one important measure of learning and memory that is highly sensitive to disruption in people with amnesia or dementia. The current study will investigate the influence of lesions to two thalamic subregions, the anterior thalamic nuclei (AT) and the lateral thalamic nuclei (LT) in an object-odour paired associate learning task. Each of these subregions has been suggested by the literature as critical for amnesia after thalamus injury. The current study does not involve a place/ space component. Both AT and LT lesions caused impairments in the object-odour paired associate task, but not in the simple discrimination tasks. The results of this study provide new evidence to suggest that the anterior thalamic region may be responsible for more than spatial memory processing. This result is inconsistent with those of Aggleton & Brown (1999) that consider the AT to be part of an 'extended hippocampal system'. The deficits observed from LT lesions in this study provide new insight into the lateral thalamic region's role in pattern processing.

Episodic memory is processed by the extended hippocampal system, and pathology or injury to individual components of this system can result in deficits in spatial learning and memory (Aggleton & Brown, 1999). Extensive research regarding spatial memory has been carried out on the anterior thalamic nuclei, a component of the extended hippocampal system, but the contribution of the laterodorsal thalamic nuclei, an adjacent structure with similar neural connections, is less clear. The purpose of the present study was to compare the effects of selective anterior thalamic nuclei lesions (AT) with selective laterodorsal thalamic nuclei lesions (LD) in a novel land-based spatial reference memory task. This assessed the use of proximal and distal visual cues on the propensity to use allocentric or egocentric navigation strategies to locate a specific place in space, as well as the temporal evolution of these navigation strategies. AT lesion impairments were observed in the acquisition trials in both proximal and distal cue conditions. LD lesion rats were unimpaired in the acquisition trials in both visual cue conditions. Across the probe trials, lesion effects were not observed when tested for general navigation, egocentric or allocentric strategies, and there was no clear improvement in performance over the four weeks of probe trials. However, performance was consistently poorer for all groups when proximal cues facilitated navigation compared to distal cues. Performance differences related to cue proximity may reflect the influence of motion parallax, the perceived displacement rate of visual cues. The absence of lesion effects across probes were thought to be due to the preferential use of cued navigation, which was reliant on a single salient beacon, and the lack of integration between cued and place navigation, which was reliant on the formation of a spatial representation.

The anterior thalamic nuclei (ATN) are a critical part of an extended hippocampal system that supports key elements of episodic memory. Damage or disconnection of the ATN is a component of clinical conditions associated with severe anterograde amnesisa such as the Korsakoff’s syndrome, thalamic stroke, and neurodegenerative disorders. Previous studies have demonstrated that the ATN and hippocampus are often interdependent, and that ATN damage can result in ‘covert pathology’ in ostensibly healthy distal regions of the extended hippocampal system. Adult male rats with neurotoxic bilateral ATN lesions or sham surgery were post-operatively housed in an enriched environment or standard housing after a lesion-induced spatial working memory deficit had been established. These rats were retested on cross-maze and then trained in radial-arm maze spatial memory tasks. Other enriched rats received pseudo-training only after the enrichment period. The detailed neuromorphology of neurons was subsequently examined in the hippocampal CA1. Soma characteristics were also examined in the retrosplenial granular b cortex and the prelimbic cortex. In Experiment 1, ATN lesions produced clear deficits in both the cross-maze and radial-arm maze tasks and reduced hippocampal CA1 dendritic complexity, length, and spine density, while increasing the average diameter of the dendrites. Post-operative enrichment reversed the ATN lesion-induced deficits in the cross-maze and radial-arm maze, and returned CA1 basal and apical spine density to a level comparable to that of sham standard housed trained rats. The sham enriched rats exhibited improved radial-arm maze performance and increased CA1 branching complexity and spine density in both basal and apical arbors compared to sham standard housed rats. The neuromorphological changes observed in the enriched ATN and sham rats may be in part responsible for the spatial working memory improvements observed. Experiment 2 provided support for this contention by demonstrating that the CA1 spine changes were explicitly relevant to spatial learning and memory, because trained enriched sham and ATN rats had increased spines, particularly in the basal tree when compared to closely comparable pseudo-trained enriched rats. Interestingly, spatial memory training increased the numbers of both thin and mushroom spines, whereas enrichment was only associated with an increase in thin spines. In Experiment 3, ATN lesions increased cell body size in layer II of the retrosplenial granular b cortex, whereas enrichment decreased cell body size in layer V of this region. Neither ATN lesions nor enrichment had any effect on cell body morphology in the prelimbic cortex. The current research provides some of the strongest evidence to date of ATN and hippocampal interdependence within the extended hippocampal system, and provides the first evidence of neuromorphological correlates of recovery after ATN lesions.