Table 1.
- | Depression | Anxiety | PTSD | Schizophrenia |
---|---|---|---|---|
Cannabinoid receptors | The activation of the CB1 cannabinoid receptor induces depression-like behavior The role of the CB2 cannabinoid receptor in depression is unknown |
The absence of the CB1 cannabinoid receptor increases depression-like behavior The role of the CB2 cannabinoid receptor in anxiety is unknown |
Th activation of the CB1 cannabinoid receptor reduces PTSD symptoms The engagement of the CB2 cannabinoid receptor role in PTSD is unknown |
The levels of the CB1 cannabinoid receptor mRNA in schizophrenia is decreased The role of the CB2 cannabinoid receptor role in schizophrenia is unknown |
AEA and 2-AG | The levels of the endocannabinoids in depression are decreased | Stress reduces levels of the endocannabinoids | The contents of the endocannabinoids in PTSD are decreased | The levels of the endocannabinoids in schizophrenia are increased |
NAPE, NAPE-PLD, FAAH, AMT, DAGL, and MAGL | The NAPE-PLD contents are decreased in depression The FAAH gene has been related to depression The FAAH levels are enhanced in depression The DAGL contents are decreased in depression The MAGL levels are increased in depression The AMT activity in depression is unknown |
The blockade of FAAH and MAGL activity decreases anxiety-like behavior The role of NAPE, NAPE-PLD, AMT, DAGL, and MAGL in depression is unknown |
Inconclusive results of role of FAAH in PTSD The role of NAPE, NAPE-PLD, AMT, DAGL, and MAGL in PTSD is unknown |
The FAAH and MAGL levels are enhanced in schizophrenia The NAPE and DAGL contents are decreased in schizophrenia The NAPE-PLD and AMT levels in schizophrenia are unknown |