Table 4.

Autophagy in acute neuronal injury.

Injury	Autophagy related changes	Ref.
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.	[96,252,166,103,251,254]
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]