LAUSR

ABSTRACT Previously we reported that prenatal morphine exposure during embryonic days 5–8 can cause cognitive deficits of one‐trial passive avoidance learning (PAL) in one‐day old chicks. Because protein kinase C (PKC) has been associated with memory capacity, we investigated the effects of prenatal morphine exposure on PKC isoforms expression in the left intermediate medial mesopallium (IMM) of chick brain at a time when memory tests were performed at 30, 120 and 360 min respectively following training in PAL paradigm. We found that the level of PKC&agr; in the membrane fractions in left IMM was decreased but that in the cytosol fractions showed a increased trend in prenatally morphine‐exposed chicks with impaired long‐term memory (120 and 360 min). Moreover, the translocation of PKC &dgr; from cytosol to membrane in left IMM was shown in prenatal morphine group which had significantly impaired long‐term memory at 360 min after training. Furthermore, there were no statistical differences between the two groups regarding the expressions of PKC&agr; and PKC &dgr; in the membrane fraction, although their levels in the cytosol fraction of prenatal morphine group which showed impaired intermediate‐term memory at 30 min after training, were quite different from that of prenatal saline group. Taken together, these results indicate that PKC&agr; and PKC &dgr; in the left IMM are differentially involved in the impairments of long‐term memory induced by prenatal morphine exposure. Neither PKC&agr; nor PKC &dgr; in left IMM may be associated with the disruption of intermediate‐term memory of chicks prenatally exposed to morphine.