Having recently shown that extinction of conditioned fear depends on L-type voltage-gated calcium channels (LVGCCs), we have been seeking other protocols that require this unusual induction mechanism. We tested latent inhibition (LI) of fear, because LI resembles extinction except that cue exposures precede, rather than follow, cue-shock pairing. Systemic injections of two LVGCC inhibitors, nifedipine and diltiazem, before pre-exposure blocked LI completely with no evidence of state-dependent learning.
View Article and Find Full Text PDFMany articles have reported that adrenal chromaffin cell transplants produce analgesic effects. Surprisingly, studies conducted in our laboratory failed to detect analgesic effects of adrenal chromaffin cell transplants. Although we have attempted to replicate the procedures reported to produce analgesic effects with adrenal chromaffin transplants, many of the different cell preparation procedures we have examined are fairly complex, and it is possible that our transplants were not sufficiently viable because of some subtle difference in our cell preparation procedures.
View Article and Find Full Text PDFIt has been shown recently that extinction of conditional fear does not depend acutely on NMDA-type glutamate receptors, although other evidence has led to the hypothesis that L-type voltage-gated calcium channels (LVGCCs) play a role in conditional fear. We therefore tested the role of LVGCCs in the acquisition, expression, and extinction of conditional fear of cue and context in mice. Using systemic injections of two LVGCC inhibitors, nifedipine and nimodipine, which both effectively cross the blood-brain barrier, we show that LVGCCs are essential for the extinction, but not for the acquisition or expression, of conditional fear in mice.
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