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Attentional Functions of the Thalamic Reticular Nucleus in the Rat: The Role of Acetylcholine

Verity Brown and David S. Tait
School of Psychology, University of St. Andrews, Scotland, UK

There is widespread behavioural evidence for the involvement of the basal forebrain cholinergic system in attentional function and, with projections to prefrontal cortex, hippocampus and thalamic reticular nucleus (TRN), it is likely that a variety of attentional processes are influenced by the basal forebrain.

Previous work from this laboratory has shown that the TRN is involved in selective attention to visual and auditory stimuli. We have also shown that shifting of visuospatial attention is speeded by systemic nicotine and the same task is impaired by lesions of the TRN, but not by lesions of frontal cortex. From these data, it would be parsimonious to suggest that it is the basal forebrain cholinergic input to the TRN – rather than the projection to cortex – that is particularly significant in this aspect of attention. Our recent research has addressed the issue of whether this is true of all aspects of attention. Data will be presented from a test of acquisition and shifting of ‘attentional set’ in the rat. Performance by monkeys in an attentional set-shifting task is impaired by excitotoxic lesions of the basal forebrain, resulting in a behavioural rigidity suggestive of perseveration (Roberts et al., 1992; Neuroscience 47: 251-264). The development of the selective immunotoxin, 192-IgG-saporin, which targets neurons bearing the p75 rat nerve growth factor receptor that is found almost exclusively on basal forebrain cholinergic projection neurons, has allowed dissociation between processes mediated by the basal forebrain cholinergic system, and those mediated by non-cholinergic basal forebrain neurons. In rats, excitotoxic lesions of the basal forebrain induce a similar behavioural rigidity. However, these effects are not seen after cholinergic lesions of the basal forebrain, using 192-IgG-saporin. This would suggest that certain basal forebrain-mediated attentional processes arise from non-cholinergic projections.

When attentional deficits have been reported following basal forebrain cholinergic depletion, these deficits have generally been assumed to be due to loss of cortical cholinergic input. Data will also be presented from studies into the effect of administration of 192-IgG-saporin into rostral TRN. Cholinergic depletion was found throughout the rostro-caudal extent of the TRN and also in cortex, suggesting that the cholinergic neurons that project to TRN from basal forebrain may have multiple collaterals to cortex and other areas of the TRN. From these data, we conclude that selective lesioning of basal forebrain cholinergic innervation of TRN versus cortex may not, therefore, be possible and conclusions about the functions of the basal forebrain cholinergic projections must include consideration of the projection to TRN