Figure 6.

A schematic diagram illustrating the proposed mechanism by which osmotin protects against glutamate-induced synaptic plasticity and neurodegeneration in the brain of postnatal rats. Glutamate-induced neurodegeneration is caused by the overactivation of glutamate receptors, followed by the increased release of intracellular Ca²⁺ that stimulates the JNK/PI3K/Akt pathway, resulting in widespread neurodegeneration via p53 activation. This activated p53 causes an increase in the Bax/Bcl-2 ratio, leading to the translocation of cytochrome c that then activates caspase-3 and PARP-1 expression, inducing DNA fragmentation and cell apoptosis. However, successively treating with osmotin after glutamate successfully enhances synaptic plasticity and inhibits glutamate receptor activation and neurodegeneration through the JNK/PI3K/Akt pathway