21:I[432972,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/1270dead247da766.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/2d7aa753e81324a8.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/263f2cdcb9aa2341.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 22:T520,Cannabinoid CB₂ receptor (CB₂) agonists are potential analgesics void of psychotropic effects. Peripheral immune cells, neurons and glia express CB₂; however, the involvement of CB₂ from these cells in neuropathic pain remains unresolved. We explored spontaneous neuropathic pain through on-demand self-administration of the selective CB₂ agonist JWH133 in wild-type and knockout mice lacking CB₂ in neurons, monocytes or constitutively. Operant self-administration reflected drug-taking to alleviate spontaneous pain, nociceptive and affective manifestations. While constitutive deletion of CB₂ disrupted JWH133-taking behavior, this behavior was not modified in monocyte-specific CB₂ knockouts and was increased in mice defective in neuronal CB₂ knockouts suggestive of increased spontaneous pain. Interestingly, CB₂-positive lymphocytes infiltrated the injured nerve and possible CB₂transfer from immune cells to neurons was found. Lymphocyte CB₂depletion also exacerbated JWH133 self-administration and inhibited antinociception. This work identifies a simultaneous activity of neuronal and lymphoid CB₂that protects against spontaneous and evoked neuropathic pain.

#	Concept	H-Index	Publications	Citations
1	Medicine	1	1	39
2	Cell Biology	1	1	39
3	Pharmacology	1	1	39
4	Inflammation	1	1	39
5	Physiology	1	1	39

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