Question: 

During the pathogenesis of Alzheimer's Disease (AD), the amyloid precursor protein (APP) plays a central role as it leads to the production of Ab, which is involved in the formation of amyloid plaques. As the Ca_v2.3 calcium channel was found to interact with the structurally related protein amyloid precursor like protein 1 (APLP1) (Radhakrishnan et al., 2012), we sought to investigate changes in APP and questioned whether APP's expression level may be modified during experimentally induced epilepsy, in an epilepsy model, in which Ca_v2.3 is known to be involved in signalling of neurodegeneration (Weiergräber et al., 2007).

Methods: 

In our in vivo experiments with Ca_v2.3-deficient mice and their counterparts we focused on the protein expression of APP in the neocortex after kainate-induced epilepsy after a 24-hour period. The injection of kainic acid (20 mg / kg. i.p.) as a chemical medium to induce neurotoxic effects such as epilepsy showed that Ca_v2.3-deficient mice displayed a reduced response compared to Ca_v2.3(+|+) mice during progressing epileptogenesis.

Results & Conclusion: 

We examined the quantity of APP in neocortical tissue of both genotypes and identified significant differences between the APP expression after kainic acid injection in the neocortex of Ca_v2.3 (+|+) and Ca_v2.3 (-|-) mice after 24 hours. Expression of APP was significantly lower in Ca_v2.3 (-|-) mice compared to controls, leading to the assumption that signalling in neurodegeneration in epilepsy and M. Alzheimer may include common pathways (Noebels, 2011) involving pharmacoresistant voltage-gated Ca²⁺-channels.