Intra-mPFC microinjection of naloxonazine (a mu-opioid receptor antagonist, 1 μg/0.25 μL) and AM251 (a cannabinoid CB1 receptor antagonist, 1 μg/0.25 μL) increased both phases of pain intensity.
The endocannabinoid system involving the central nervous system (CNS), the human cannabinoid receptor 1 (CB1), is an important drug target and its variability has implications for disease susceptibility and altered drug and pain response.
Considering that the endocannabinoid system via CB1 receptors play a crucial role in pain modulation, we also assessed the possible role of the VH cannabinoid CB1 receptors in the functional interaction between minocycline and morphine in acute pain.
Here, the role of vlPAG OX1Rs and their interaction with cannabinoid 1 (CB1) receptor was evaluated in anxiety-like behavior following capsaicin-induced dental pulp pain.
Cannabinoid receptor 1 (CB<sub>1</sub>) is a potential therapeutic target for the treatment of pain, obesity and obesity-related metabolic disorders, and addiction.
Indeed, systemic administration of specific bacteria can reduce abdominal pain through the involvement of cannabinoid receptor 1 in the rat; on the other hand, PEA reduces inflammation markers in a murine model of inflammatory bowel disease (IBD), and butyrate, producted by gut microbiota, is effective in reducing inflammation and pain in irritable bowel syndrome and IBD animal models.
Evaluation of CB1R and MOR spatial expression demonstrated differential modulation of CB1R and MOR in the periaqueductal gray matter (PAG) of ESI-treated rats in sub-areas involved in pain processing/modulation.
Microinjection of the CB1 receptor antagonist AM251 into the ventrolateral periaqueductal gray (vlPAG) can reversed the EA effect on pain hypersensitivity and DNIC function.
Thus, NAPE-PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain.
Intraperitoneal injections of low dose of THC resulted in increased positive and negative BOLD signals compared to vehicle and high dose in areas rich in cannabinoid receptor 1, as well as throughout the pain and hippocampal neural systems.
The inhibitions of CB1R and its downstream ERK and JNK signaling pathways may alleviate the sprouted innervation that has been involved in ENDO-associated pain.
GW405833, widely accepted as a cannabinoid receptor 2 (CB<sub>2</sub>) agonist, suppresses pathologic pain in preclinical models without the unwanted central side effects of cannabinoid receptor 1 (CB<sub>1</sub>) agonists; however, recent in vitro studies have suggested that GW405833 may also behave as a noncompetitive CB<sub>1</sub> antagonist, suggesting that its pharmacology is more complex than initially appreciated.
Heterozygous rare coding variants in CNR1, which encodes the type 1 cannabinoid receptor (CB1), were found to be significantly associated with pain sensitivity (especially migraine), sleep and memory disorders-alone or in combination with anxiety-compared to a set of controls without such CNR1 variants.
The monosodium iodoacetate model was used to evaluate the affective and cognitive manifestations of osteoarthritis pain in type 1 (CB1R) and type 2 (CB2R) cannabinoid receptor knockout and wild-type mice and the ability of CB1R (ACEA) and CB2R (JWH133) selective agonists to improve these manifestations during a 3-week time period.
For CNR1 (AAT)n, gene-by-phenotype interactions were observed for colonic transit at 24 (P = 0.06) and 48 h (P = 0.002) and gas (P = 0.046, highest for IBS-D, P = 0.034), but not pain sensation; the strongest association with transit was in controls, not in IBS.
Symptom scores for abdominal discomfort or pain were higher in patients with the CNR1 >10/>10 genotype than in patients with the other genotypes (P<0.05).
The effects of cannabinoid receptor agonists and antagonists on pain-related responses to CRD were assessed in rats and in wild-type and CB(1) receptor knock-out mice.
Our results suggest that spinal endocannabinoids and CB1 receptors on inhibitory dorsal horn interneurons act as mediators of heterosynaptic pain sensitization and play an unexpected role in dorsal horn pain-controlling circuits.