Table 4 Autophagy in acute neuronal injury.

Hypoxia/Ischemia

Mixed results after hypoxic treatments: Knockout of Atg genes in C. elegans decreases survival after hypoxia and autophagy activation by rapamycin treatment leads to injury reduction in rat and rat tissue. On the contrary, Atg7^-/- mice lacking functional autophagy in the CNS are largely protected from neurodegeneration.

[247, 80, 104, 94, 244, 246, 245]

Trauma

Macroautophagy appears to be beneficial: Autophagy can be activated for more than a month following brain trauma (elevated BECN1, MAP1LC3-II, ATG5-12 levels, increased AV numbers) in rodents, autophagy appears activated in human tissue samples. Rapamycin treatment is neuroprotective in mice.

[106, 87, 249, 248, 65, 95, 84, 81, 250]

Pharmacological injury

Autophagy appears to be deleterious: Transient activation of autophagy after injury (elevated MAP1LC3-II, p-mTOR, LAMP2, increased AV numbers) and activation of apoptosis in rodents and primary neuronal culture. 3-MA treatment or RNAi against ATG5 or BECN1 blocks cell death.

[96, 252, 166, 103, 253, 251, 254]

Trophic deprivation

Autophagy appears to be deleterious: Growth factor withdrawal leads to autophagic cell death in rodents or chicken, 3-MA blocks cytochrome C release and delays apoptosis.

[257, 255, 256, 259, 258]