Excitotoxic lesions of the parafascicular nucleus produce deficits in a socially transmitted food preference

The parafascicular (PF) nucleus, a posterior component of the intralaminar nuclei of the thalamus, is considered to be an essential structure in the feedback circuits of basal ganglia-thalamo-cortical systems that critically participate in cognitive processes. To study the PF contribution to process...

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Veröffentlicht in:Neurobiology of learning and memory 2006-11, Vol.86 (3), p.256-263
Hauptverfasser: QUIROZPADILLA, M, GUILLAZOBLANCH, G, VALEMARTINEZ, A, MARTINICOLOVIUS, M
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Sprache:eng
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Zusammenfassung:The parafascicular (PF) nucleus, a posterior component of the intralaminar nuclei of the thalamus, is considered to be an essential structure in the feedback circuits of basal ganglia-thalamo-cortical systems that critically participate in cognitive processes. To study the PF contribution to processing of behaviorally significant information during specific episodes of learning, we investigated the effects of damaging the PF nucleus in the acquisition of a natural form of social olfactory learning, the socially transmitted food preference (STFP) task. This task is a non-spatial paradigm that exhibits some of the characteristics of relational memory because it requires that animals use information obtained in one episode to guide later behavior in different circumstances. Adult male Wistar rats were submitted to pretraining bilateral N-methyl- d-aspartate (0.15 M, pH 7.4) lesions of the PF (0.4 μl/side, 0.2 μl/min). The behavioral effects of PF lesions were compared to vehicle- and sham-operated control groups and two retention delays were considered in separate groups: immediately (Lesion-I, Vehicle-I, and Sham-I groups) and 24 h after training (Lesion-24, Vehicle-24, and Sham-24 groups). PF lesions produced delay-independent impairments in the STFP suggesting that this nucleus might modulate the acquisition of this odor–odor association task. Results are discussed in the context of medial prefrontal cortex deafferentation induced by PF damage.
ISSN:1074-7427
1095-9564
DOI:10.1016/j.nlm.2006.03.007