Table 1 Endocannabinoids and endocannabinoid modulation in TBI models

Synthetic 2-AG administration

0.1, 5, 10 mg/kg

i.v.

15 min post-injury

Weight-drop TBI (closed-head)

Sabra mice, males

Treatment educed edema; reduced infarct volume; reduced cell death (hippocampus); and improved functional recovery

[39]

2-AG augmentation (via MAGL inhibitor MJN110)

0.5, 1, 2.5 mg/kg

i.p.

30 min after each injury, then daily for 5 days (8 × total)

Repetitive closed-head injury (CCI device); three impacts delivered 24 h apart

C57BL/6 mice, males

Treatment reduced inflammatory markers; attenuated cell death; restored glutamate and GABA receptors changes; improved cognition; and improved locomotor function

[59]

2-AG augmentation (via astrocyte-specific MAGL knockout)

n/a

n/a

n/a

Repetitive closed-head injury (CCI device); three impacts delivered 24 h apart

Mgll^flox/flox mice (astrocyte-specific MAGL knockout), males and females

Knockout reduced neuroinflammation; reduced TBI-induced gene expression changes; and prevented neurodegenerative pathology and cognitive impairment, among other injury-induced effects

[60]