Repetitive transcranial magnetic stimulation (rTMS) was shown to
have therapeutic potential for some neurological and psychiatric
disorders. Previous studies reported that low-frequency rTMS
(≤1 Hz) affected synaptic plasticity in rats, however, there were
few investigations to examine the possible effects of rTMS on
structural synaptic plasticity changes in rats, which included the
effects on synaptic morphology in the hippocampus, synaptic
protein markers and Ca2+/calmodulin-dependent protein II
(CaMKII). Sprague-Dawley rats were subject to 500 pulses of
0.5 Hz rTMS for 15 days, or sham stimulation. After last
stimulation, transmission electron microscope (TEM) and
real-time PCR were used to determine the effects of rTMS on
synaptic plasticity. Results showed that rTMS could cause the
change of structural synaptic plasticity, increase the expression of
synaptic protein markers: synaptophysin (SYN) and increase the
expression of CaMKII, relative to normal rats. suggesting
a modulatory effect of chronic rTMS on synaptic plasticity that
may be attributed to the increased expression of CaMKII in rats.
Activation of calmodulin dependent protein kinase (CaMK)II by exercise is beneficial in controlling membrane lipids associated with type 2 diabetes and obesity. Regulation of lipid metabolism is crucial in the improvement of type 2 diabetes and obesity associated symptoms. The role of CaMKII in membrane associated lipid metabolism was the focus of this study. Five to six weeks old male Wistar rats were used in this study. GC×GC-TOFMS technique was used to determine the levels of polyunsaturated fatty acids (linoleic acid, arachidonic acid and 11,14-eicosadienoic acid). Carnitine palmitoyltransferase (Cpt-1) and acetyl-CoA carboxylase (Acc-1) genes expression were assessed using quantitative real time PCR (qPCR). From the results, CaMKII activation by exercise increased the levels of arachidonic acid and 11,14-eicosadienoic acid while a decrease in the level of linolenic acid was observed in the skeletal muscle. The results indicated that exercise-induced CaMKII activation increased CPT-1 expression and decreased ACC-1 expression in rat skeletal muscle. All the observed increases with activation of CaMKII by exercise were aborted when KN93, an inhibitor of CaMKII was injected in exercising rats. This study demonstrated that CaMKII activation by exercise regulated lipid metabolism. This study suggests that CaMKII can be a vital target of
therapeutic approach in the management of diseases such as type 2 diabetes and obesity that have increased to epidemic proportions recently.