These results provide a new strategy for angina treatment and show that the pre and postsynaptic influx of Ca2+ is important for CMI-induced synaptic potentiation. One interesting finding was that the Ca2+ permeable AMPAR receptor subunits replaced the GluR2 in the synaptic region after coronary artery ligation. It is already well documented that the NMDA receptor is important for CT99021 GSK-3 inhibitor triggering synaptic plasticity induced by various stimuli, such as learning, fear and pain induction and for triggering the postsynaptic accumulation of GluR1 and the replacement of GluR2 with GluR1/3. Thus, it is likely that the potentiated postsynaptic response is initiated by overexcited NMDAR and the mediated by subsequent trafficking of GluR1/3 in the PSD. Actually, in our pilot work, we have found that NMDAR subunit NR2A and NR2B were overexpressed in the NTS with CMI. Tang et al. also report that tetanic stimulation of the aortic depressor nerve potentiated the A-fiber evoked responses in the NTS, which can be blocked by NMDA receptor antagonists, indicating the role of NMDAR in the potentiation of synaptic transmission. However, more works should be carried out in the future to clarify the role of NMDAR for the synaptic plasticity in the NTS. Another interesting finding is that the increased expression of synaptophysin-ir puncta and Fos-ir neurons mainly occurred in the SolM and SolC. Because the SolM and SolC but not SolL are the main targets for afferent vagal fibers, it is likely that nociceptive information from the heart will increase the amount of afferent vagal terminals and then activate the neurons within the SolMand SolC. Actually, our previous work showed that microinjection of the NMDA receptor antagonist MK801 into the SolC but not the SolL inhibits the acute cardiacsomatic reflex. However, we cannot rule out that the increased afferent terminals may also come from the ascending fibers of the spinal cord. To address this question, selective vagotomy or sympathectomy should be explored in the future. This represents a huge social and economic burden worldwide. Individuals that are continuously exposed to malaria infection in endemic regions eventually develop clinical immunity that protects them from severe disease, complications, and death; however, sterile immunity is never achieved under natural conditions. These individuals also develop immune responses that reduce or completely block parasite transmission from humans to the mosquito vector in what has been called transmission blocking immunity. It has been experimentally demonstrated that specific antibodies targeting Plasmodium antigens which are expressed on gametocytes, zygote, gametes and ookinete stages can block parasite transmission from a variety of malaria animal hosts, including humans and non-human primates, to mosquitoes. Therefore TB immune mechanism may represent an important method to prevent human malaria transmission and may eventually contribute to malaria elimination. However, the malaria TB process appears to be complex and depends on multiple factors such as target antigens, time of antigen expression, antibody concentration, and in some cases, on complement activation. In P. falciparum, as in other species, several gametocyte antigens, i.e., Pfs230 and Pfs48/45, as well as oocyst/ookinete antigens, i.e., Pfs25 and Pfs28, which have been identified as potential TB vaccine candidates, have been expressed as recombinant proteins. However, efforts to express some of these BEZ235 proteins with their proper conformation to induce antibodies with TB capacity have been hampered by the presence of the high number of cysteine residues that usually lead to complex protein structures.