Multiple studies have found the MPT to be a key factor in the damage to neurons caused by excitotoxicity.
The induction of MPT, which increases mitochondrial membrane permeability, causes mitochondria to become further depolarized, meaning that Δψ is abolished. When Δψ is lost, protons and some molecules are able to flow across the outer mitochondrial membrane uninhibited.
Loss of Δψ interferes with the production of adenosine triphosphate (ATP), the cell's main source of energy, because mitochondria must have an electrochemical gradient to provide the driving force for ATP production.
In cell damage resulting from conditions such as neurodegenerative diseases and head injury, opening of the mitochondrial permeability transition pore can greatly reduce ATP production, and can cause ATP synthase to begin hydrolysing, rather than producing, ATP. This produces an energy deficit in the cell, just when it most needs ATP to fuel activity of ion pumps. 
MPT also allows Ca to leave the mitochondrion, which can place further stress on nearby mitochondria, and which can activate harmful calcium-dependent proteases such as calpain.
Reactive oxygen species (ROS) are also produced as a result of opening the MPT pore.  MPT can allow antioxidant molecules such as glutathione to exit mitochondria, reducing the organelles ability to neutralize ROS.  In addition, the electron transport chain (ETC) may produce more free radicals due to loss of components of the ETC, such as cytochrome c', through the MPTP. Loss of ETC components can lead to escape of electrons from the chain, which can then reduce molecules and form free radicals.
MPT causes mitochondria to become permeable to molecules smaller than 1.5 kDa, which, once inside, draw water in by increasing the organelles osmolar load.  This event may lead mitochondria to swell and may cause the outer membrane to rupture, releasing cytochrome c.  Cytochrome c can in turn cause the cell to go through apoptosis ("commit suicide") by activating pro-apoptotic factors.  Other researchers contend that it is not mitochondrial membrane rupture that leads to cytochrome c' release, but rather another mechanism, such as translocation of the molecule through channels in the outer membrane, which does not involve the MPTP.
Much research has found that the fate of the cell after an insult depends on the extent of MPT.  If MPT occurs to only a slight extent, the cell may recover, whereas if it occurs more it may undergo apoptosis. If it occurs to an even larger degree the cell is likely to undergo necrotic cell death.