Department of Psychological and Brain Sciences, Gill Center for Biomolecular Science, Program in Neuroscience, Indiana University, Bloomington, IN, 47405, USA.
Indiana University, 1101 E 10th St, Bloomington, IN, 47401, USA.
Sci Rep. 2022 Aug 19;12(1):14182. doi: 10.1038/s41598-022-17987-2.
Saliva serves multiple important functions within the body that we typically take for granted, such as helping prepare food for swallowing and defense against oral pathogens. Dry mouth is a primary symptom of Sjӧgren's syndrome and is a side effect of many drug treatments. Cannabis users frequently report dry mouth, but the basis for this is still unknown. If the effects occur via the endogenous cannabinoid signaling system, then this may represent a novel mechanism for the regulation of salivation. We examined expression of cannabinoid CB1 receptors in submandibular salivary gland using immunohistochemistry and tested regulation of salivation by THC and cannabinoid-related ligands. We now report that CB1 receptors are expressed in the axons of cholinergic neurons innervating the submandibular gland. No staining is seen in submandibular gland epithelial cells (acinar and ductal), or myoepithelial cells (MECs). Treatment with THC (4 mg/kg, IP) or the cannabinoid receptor agonist CP55940 (0.5 mg/kg) reduced salivation in both male and female mice 1 h after treatment. CBD had no effect on its own but reversed the effect of THC in a concentration-dependent manner. Neither the CB1 receptor antagonist SR141716 (4 mg/kg) nor the CB2-selective agonist JWH133 (4 mg/kg) had an effect on salivation. We also found that fatty acid amide hydrolase (FAAH), the enzyme that metabolizes the endocannabinoid anandamide and related lipids, regulates salivation. Salivation was reduced in FAAH knockout mice as well as mice treated with the FAAH blocker URB597 (4 mg/kg). URB597 had no effect in CB1 knockout mice. FAAH protein is detected intracellularly in acinar but not ductal epithelial cells. In lipidomics experiments, we found that FAAH knockout mice chiefly had elevated levels of acylethanolamines, including anandamide, and reduced levels of acyglycines. Our results are consistent with a model wherein endocannabinoids activate CB1 receptors on cholinergic axons innervating the submandibular gland. THC likely acts by plugging into this system, activating CB1 receptors to reduce salivation, thus offering a mechanism underlying the dry mouth reported by cannabis users.
唾液在体内发挥着多种重要功能,我们通常认为这是理所当然的,例如帮助吞咽食物和抵御口腔病原体。口干是干燥综合征的主要症状,也是许多药物治疗的副作用。大麻使用者经常报告口干,但这一现象的基础尚不清楚。如果这种作用是通过内源性大麻素信号系统发生的,那么这可能代表了一种调节唾液分泌的新机制。我们使用免疫组织化学方法研究了下颌下腺中大麻素 CB1 受体的表达,并测试了 THC 和大麻素相关配体对唾液分泌的调节作用。我们现在报告,CB1 受体表达在下颌下腺胆碱能神经元的轴突中。在下颌下腺上皮细胞(腺泡和导管)或肌上皮细胞(MEC)中未见染色。腹腔注射 THC(4mg/kg)或大麻素受体激动剂 CP55940(0.5mg/kg)后 1 小时,均可减少雄性和雌性小鼠的唾液分泌。CBD 本身没有作用,但以浓度依赖的方式逆转了 THC 的作用。CB1 受体拮抗剂 SR141716(4mg/kg)和 CB2 选择性激动剂 JWH133(4mg/kg)均对唾液分泌没有影响。我们还发现,脂肪酸酰胺水解酶(FAAH),即代谢内源性大麻素大麻二酚和相关脂质的酶,调节唾液分泌。FAAH 基因敲除小鼠以及用 FAAH 阻断剂 URB597(4mg/kg)处理的小鼠的唾液分泌减少。URB597 在 CB1 基因敲除小鼠中没有作用。FAAH 蛋白在腺泡上皮细胞中检测到,但在导管上皮细胞中未检测到。在脂质组学实验中,我们发现 FAAH 基因敲除小鼠主要表现为酰基乙醇胺水平升高,包括大麻二酚,而酰基甘油水平降低。我们的结果与内源性大麻素激活支配下颌下腺的胆碱能轴突上的 CB1 受体的模型一致。THC 可能通过插入该系统发挥作用,激活 CB1 受体以减少唾液分泌,从而为大麻使用者报告的口干提供了一种机制。