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. Author manuscript; available in PMC: 2016 Feb 5.
Published in final edited form as: Epilepsy Behav. 2014 Jan 13;38:117–124. doi: 10.1016/j.yebeh.2013.12.001

Table 1.

Outcome of NSC Grafting in Hippocampal Injury/Neurodegeneration Prototypes on Memory and Mood Function

Type of Injury Type of NSCs and Species Region and Timing of grafting Effect on Memory Function Effect on Mood Function
KA-induced unilateral hippocampal injury in rat [39] NSCs from the postnatal SVZ Injured CA3 Region at 5 days after injury Prevented spatial and recognition memory deficits Prevented depressive-like behavior
KA-induced bilateral hippocampal injury in mouse [60] NSCs from the postnatal SVZ transduced with IGF-1 Injured hippocampus at 4 days after injury Reduced Memory Deficits Not Examined
KA-induced unilateral hippocampal injury in rat [64] Human NSCs transduced with ChAT Injured hippocampus at 4 weeks after injury Improved memory function Not examined
Fluid Percussion prototype of TBI in rat [61] Human fetal NSCs Injured hippocampus one-day after TBI Improved Memory Function Not examined
Triple transgenic AD mouse (3xTg-AD) [38] NSCs from the entire postnatal day 1 brain hippocampus of 18-month old mice exhibiting Aβ plaques and NFTs Improved Memory Function Not examined
Status epilepticus (SE) induced hippocampal injury in rat [40] NSCs from the postnatal SVZ Injured hippocampi (bilateral) 7-days after SE Prevented recognition memory dysfunction Prevented depressive-like behavior

Aβ, amyloid beta; AD, Alzheimer’s disease; BDNF, brain derived neurotrophic factor; ChAT, choline acetyltransferase; GD, gestation day; IGF-1, insulin-like growth factor-1; KA, kainic acid; NFTs, neurofibrillary tangles; NSCs, neural stem cells; SE, status epilepticus; SVZ, subventricular zone; TBI, traumatic brain injury.