Expression and Kinetics of Endogenous Cannabinoids in the Brain and Spinal Cord of a Spare Nerve Injury (SNI) Model of Neuropathic Pain

This study explores the role of 2-arachidonoyl glycerol (2-AG), an endogenous cannabinoid, in neuropathic pain using a spare nerve injury (SNI) mouse model. The researchers used desorption electrospray ionization mass spectrometry imaging (DESI-MSI) to examine the expression and distribution of 2-AG in the brain and spinal cord. The study found that 2-AG expression decreased in certain brain regions (hypothalamus, midbrain, and periaqueductal gray) but increased in the lumbar spinal cord in the SNI model during the early stages (days 3 and 7) after the injury. These findings suggest that 2-AG might play a role in pain control, with decreased levels in the brain potentially contributing to a lower pain threshold and increased levels in the spinal cord potentially serving to prevent the sending of more signals than necessary from the local area.

• 1
  On days 3 and 7 after SNI treatment, 2-AG expression decreased in the hypothalamus, midbrain, and especially in the periaqueductal gray (PAG) region.
• 2
  On days 3 and 7 after SNI treatment, 2-AG expression increased in the lumbar spinal cord.
• 3
  On day 21, the SNI model showed decreased 2-AG expression in the hypothalamus, but the difference from the control was not significant, and there were no differences in 2-AG expression between the lumbar spinal cord, midbrain, or PAG.