Tait DS, Latimer M, Woodson W, Brown VJ (2001) Cholinergic lesions of the thalamic reticular nucleus using 192-IgG-saporin. Neuroscience 2001 Abstracts 313.13. Society for Neuroscience, San Diego, CA.
Summary: The TRN is likely to be involved in attention, based on studies of its anatomy, electrophysiological properties and the effects of lesions (see Guillery et al, 1998, TINS 21:28-32). The cholinergic neurons of the basal forebrain (BF) have also been implicated in attention (Sarter and Bruno, 2000, Neuroscience, 95:933-952). Intriguingly, rostral TRN receives cholinergic innervation from the BF (Hallanger et al, 1987, J Comp Neurol, 262:105-124) and yet the role of acetylcholine in the TRN has not been investigated, in part because of difficulty in selectively manipulating the cholineric input to TRN. 192-IgG-saporin is a conjugation of the ribosome-inactivating protein, saporin, with the monoclonal antibody for the p75 neurotrophin receptor (192-IgG). 192-IgG-saporin, injected into BF or cortical BF-terminal regions, can be used to make selective cholinergic BF lesions. The purpose of the study was to investigate whether it would be possible to lesion the BF cholinergic input to TRN, using the immunotoxin 192-IgG-saporin. Male Lister hooded rats (450-500g) were stereotaxically injected with 192-IgG-saporin into TRN. Doses of 1.4, 1.95 or 2.4μg produced lesions of TRN, with a loss of cholinergic cells observed in the BF at all doses. There was also evidence of depletion of cholinergic input to frontal cortex with all doses. At the highest dose, there was cholinergic depletion in hippocampus. These results suggest that 192-IgG-saporin can be used to lesion the TRN. The behavioural effects of these lesions are under investigation.
Related Products: 192-IgG-SAP (Cat. #IT-01)