Regulation of kinesin light chain 1 level correlates with the development of morphine reward in the mouse brain.

Persistent changes that take place during the development of opioid addiction are thought to be due to reorganization of synaptic connections in relevant brain circuits. This neuronal plasticity requires trafficking of signaling molecules that are controlled by kinesins. In neurons, kinesin light chain 1 (KLC1) acts as the primary regulator of kinesin action. We observed that KLC1 was enriched in sub-cortical regions of the brain in C57Bl/6J mice. KLC1 expression was especially enriched in the striatum, hippocampus and amygdala, which are known to be involved in opioid addiction. Our study revealed that conditioning of C57Bl/6J mice with morphine elevated KLC1 levels in the amygdala, frontal cortex and hippocampus, but not in the striatum. Further study revealed that alterations in KLC1 protein levels in the studied brain regions correlated with the expression of morphine-induced conditioned place preference. In the cortex, hippocampus and amygdala, KLC1 co-localized with calcium/calmodulin-dependent protein kinase II (CaMKII), suggesting that KLC1 was present in the cell bodies and dendrites of pyramidal neurons. Our findings indicate that KLC1, a molecule involved in dendritic and axonal transport in the brain, is affected during chronic morphine treatment and may be involved in the development of opioid addiction.