1 To assess the alteration in cell viability, calcium-dependent death signaling cascades, cytosolic Ca2+ levels and mitochondrial dynamics (in term of mitochondrial structures, mitochondrial fission and fusion proteins levels and oligomerization) of neuron cells in response to METH-induced neurotoxicity.
2. To determine the role of Drp1 (fission protein) inhibitor against METH-induced toxicity, cytosolic calcium overload and mitochondrial fission in neuron cells (in term of cell viability, calcium-dependent death signaling cascades, mitochondrial structure and mitochondrial function).
3. To determine the neuroprotection providing by calpastatin (calpain inhibitor protein) and melatonin against METH-induced calcium overload leading to alteration in cell viability, calcium-dependent death signaling cascades, and mitochondrial dynamics (in term of mitochondrial structures, mitochondrial fission and fusion proteins levels and oligomerization) in neuron cells.
