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Vol. 55, Issue 3, 557-563, March 1999
and 
Isoforms
Shanghai Institute of Cell Biology, Chinese Academy of Sciences,
Shanghai, People's Republic of China
Calcium/calmodulin-dependent protein kinase II (CaMK II) has been shown
to be involved in the regulation of opioid receptor signaling. The
present study showed that acute morphine treatment significantly
increased both Ca2+/calmodulin-independent and
Ca2+/calmodulin-dependent activities of CaMK II in the rat
hippocampus, with little alteration in the protein level of either 
or 
isoform of CaMK II. However, chronic morphine treatment, by
which rats were observed to develop apparent tolerance to morphine,
significantly down-regulated both
Ca2+/calmodulin-independent and
Ca2+/calmodulin-dependent activities of CaMK II and
differentially regulated the expression of and isoforms of CaMK
II at protein and mRNA levels. Application of naloxone or
discontinuation of morphine treatment after chronic morphine
administration, which induced the withdrawal syndrome of morphine,
resulted in the overshoot of CaMK II (at both protein and mRNA levels)
and its kinase activity. The phenomena of overshoot were mainly
observed in the isoform of CaMK II but not in the isoform. The
effects of both acute and chronic morphine treatments on CaMK II could
be completely abolished by the concomitant application of naloxone,
indicating that the effects of morphine were achieved through
activation of opioid receptors. Our data demonstrated that both acute
and chronic morphine treatments could effectively modulate the activity and the expression of CaMK II in the hippocampus.
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