Gill Institute for Neuroscience, Indiana University, 1101 E 10th St, Bloomington, IN, 47401, USA.
Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA.
Sci Rep. 2024 Nov 4;14(1):26720. doi: 10.1038/s41598-024-77761-4.
Salivation is easily taken for granted, but without normal salivation, simple essential tasks such as chewing and swallowing become difficult, with consequences for quality of life, nutrition and oral health. Many important drug classes cause dry mouth as a side effect, contributing substantially to patient non-compliance. Available treatments are mostly palliative. Cannabis user complaints of dry mouth prompted a study that showed that basal salivation is likely regulated by cannabinoid CB1 receptors on neurons that innervate the submandibular gland. But what about stimulated salivation? The adjoining parotid gland releases saliva in response to olfactory or other cues and contributes a large portion of the net salivation in humans. We investigated cannabinoid regulation of stimulated salivation using functional and protein-expression studies in mice. In developing a model of stimulated salivary responses to food-related odorants in mice, we noted sex-dependent responses to food-related cues. Only male mice learned to salivate in response to the odor of peanut butter while only female mice responded to a chocolate hazelnut spread. Both males and females responded to sugar or marmite. Testing peanut butter, we found that the cannabinoid receptor agonist CP55940 (0.5 mg/kg, IP) lowered baseline salivation, as shown previously, but also prevented the odorant-induced increase in salivation. CB1 receptors are expressed in axons innervating the parotid gland, paralleling our findings in the submandibular gland. Notably, we also found that CB1 deletion impaired some responses (those to peanut butter and chocolate hazelnut spread) but not others (sugar or marmite). In mice, the CB1 antagonist SR141716 (4 mg/kg, IP) prevented a previously learned salivary response to peanut butter. We find that CB1 receptors are expressed in a subset of glomeruli in coronal sections of olfactory bulb that may serve as a site of action for scent-specific effects of CB1 receptors. We additionally observe CB1 expression in accessory olfactory bulb. In summary, we find a novel sex-dependence in responses to a subset of food-related odorant cues and that cannabinoid receptors regulate some of these responses. We propose that CB1 receptors act at the parotid gland to inhibit stimulated salivation but also in the olfactory system, where functional CB1 receptors are required for salivary responses to specific appetitive odors.
唾液分泌很容易被认为是理所当然的,但如果没有正常的唾液分泌,像咀嚼和吞咽这样简单的基本任务都会变得困难,从而影响生活质量、营养和口腔健康。许多重要的药物类别都会引起口干作为副作用,这大大增加了患者的不依从性。现有的治疗方法大多是姑息性的。大麻使用者抱怨口干,这促使一项研究表明,支配下颌下腺神经的神经元上的大麻素 CB1 受体可能调节基础唾液分泌。但是,刺激性唾液分泌呢?毗邻的腮腺会响应嗅觉或其他提示释放唾液,并且在人类中贡献了大部分净唾液分泌。我们使用功能性和蛋白表达研究在小鼠中研究了大麻素对刺激性唾液分泌的调节。在开发小鼠对食物相关气味的刺激性唾液反应模型时,我们注意到对食物相关提示存在性别依赖性反应。只有雄性小鼠学会了对花生酱的气味产生唾液反应,而只有雌性小鼠对巧克力榛子酱有反应。雄性和雌性小鼠都对糖或马麦酱有反应。在测试花生酱时,我们发现大麻素受体激动剂 CP55940(0.5mg/kg,IP)降低了基础唾液分泌,如前所述,但也阻止了气味引起的唾液分泌增加。CB1 受体表达在支配腮腺的轴突中,与我们在下颌下腺中的发现平行。值得注意的是,我们还发现 CB1 缺失会损害一些反应(对花生酱和巧克力榛子酱的反应),但不会损害其他反应(对糖或马麦酱的反应)。在小鼠中,CB1 拮抗剂 SR141716(4mg/kg,IP)阻止了先前对花生酱的唾液反应。我们发现,CB1 受体在嗅球冠状切片中的一小部分肾小球中表达,这可能是 CB1 受体对气味特异性作用的作用部位。我们还观察到 CB1 在副嗅球中的表达。总之,我们发现对一组食物相关气味提示存在新的性别依赖性,大麻素受体调节其中一些反应。我们提出,CB1 受体在腮腺中起作用以抑制刺激性唾液分泌,但也在嗅觉系统中起作用,在该系统中,功能性 CB1 受体是对特定食欲气味产生唾液反应所必需的。