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From a molecular point of view, the necroptosis pathway is initiated by auto- and trans-phosphorylation of RIPK1 and RIPK3 at Ser-227, resulting in stimulation of their kinase activity and assembly of a heterodimer protein complex termed necrosome via their RIPK homotypic interaction motif domains (Fulda, 2013

The RRP consists of a small fraction of total vesicles that are physically docked at the active zone, molecularly primed by active zone proteins (such as RIM and Munc13) into a SNARE-assembled, fusion-competent state (Kaeser and Regehr, 2017)

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These effects can further reduce neuron damage and apoptosis