Trends in Neurosciences
ReviewWhere is the trace in trace conditioning?
Section snippets
Delay and trace conditioning paradigms
Neural substrates of Pavlovian eyeblink and fear conditioning are among the most elaborated and best understood of all learning and memory circuits. Continued exploration of these seemingly simple behaviors and their underlying circuitry reveals the exquisite complexity of brain processing even for the most fundamental forms of learning. Tones, lights or somatosensory stimuli usually serve as the conditioned stimulus (CS) that is paired with an unconditioned stimulus (US) such as an air puff to
Traditional perspective of cerebellar cortex in eyeblink classical conditioning
The cerebellar cortex and hippocampus are normally activated in delay eyeblink conditioning [22], but for decades it has been known that hippocampal lesions do not prevent acquisition or retention in the delay paradigm 23, 24, 25. Hippocampal lesions block acquisition and retention of recently acquired learning in trace eyeblink conditioning 26, 27, 28. For some years, the only study examining the effect of cerebellar cortical lesions upon the retention of previously learned trace CRs reported
Trace eyeblink classical conditioning: independent of cerebellar cortex?
The cerebellar interpositus nucleus is essential in trace eyeblink classical conditioning as demonstrated in rabbits with electrolytic lesions [10] and reversible chemical lesions [48]. In rats tested in trace eyeblink conditioning, there was activation in the posterior interpositus nucleus as assessed by a marker of metabolic activity, [14C]2-deoxyglucose [19]. In addition to the interpositus nucleus in trace eyeblink classical conditioning, an intact hippocampus 26, 27, 28, medial prefrontal
Summary and new research directions
The role of the cerebellum in trace eyeblink conditioning has received far less research attention than it has in delay eyeblink conditioning. It appears that forebrain regions are able to bridge the temporal gap in trace conditioning through pontine–cerebellar nuclear connections, but that a cerebellar cortical LTD-like process is required to support normal delay conditioning. Additional studies of cerebellar cortical and nuclear involvement in forebrain-dependent trace eyeblink classical
Acknowledgements
We would like to thank Steven Purcell and Roberto Galvez for their contributions to Figure 1, and Craig Weiss for his contribution to Figure 3. Comments on and suggestions for the manuscript by Indira Raman and Craig Weiss are very much appreciated. This research was supported by grants from the National Institute on Aging, 1 R01 AG021925 and 1 R01 AG023742, to D.S.W-P. and from the National Institute of Mental Health, 1 R01 MH47340, and the National Institute on Aging, 2 R37 AG08796, to J.F.D.
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