Amlashi Fazel Isapanah, Besharat Sima, Jahanshahi Mehrdad, Shirzad-Aski Hesamaddin, Torshizi Fatemeh Nassaj
Golestan Research Center of Gastroenterology and Hepatology, GolestanUniversity of Medical Sciences, Gorgan, Iran.
Neuroscience Research Center, Golestan University of Medical Sciences, Gorgan, Iran.
BMC Gastroenterol. 2025 Mar 13;25(1):171. doi: 10.1186/s12876-025-03745-x.
Hyperalgesia and hypersensitivity in patients with Inflammatory Bowel Disease (IBD) can be related to central nervous system (CNS) changes, particularly in the pain pathways. The objective of this study was to examine the neuronal density of the cingulate cortex area (CC) and amygdala in an animal model of colitis.
In this experiment, 13 male Wistar rats were subjected to study. Colitis was induced in the rats by transrectally administering 1 cc of acetic acid 3% under sedation with xylazine 10% (5 mg/kg). After 14 days of colitis, the rats were euthanized under high doses of anesthesia with ketamine (50 mg/kg), xylazine (10 mg/kg), and diazepam (2.5 mg/kg). Their brains were then removed surgically. Six-micrometer-thick brain slices were stained with cresyl violet, and the neuronal density of the amygdala, area 1 of the cingulate cortex area (CC1), and area 2 of the cingulate cortex area (CC2) was assessed via microscopic imaging.
The mean ± standard deviation (SD) of the neuronal density in CC1 was significantly decreased in rats with colitis compared to the control group in both the right CC1 (43.53 ± 9.63 vs. 62.7 ± 11.89; p-value ˂ 0.001), and left CC1 (41.19 ± 9.05 and 63.1 ± 7.44; p-value ˂ 0.001). Additionally, the neuronal density of CC2 in the colitis group was found to be significantly lower than that of the controls in both the right CC2 (57.8 ± 13.23 vs. 87.95 ± 8.76; p-value ˂ 0.001), and left CC2 (55.42 ± 11.3 vs. 98 ± 8.99; p-value ˂ 0.001). Furthermore, the amygdala had a lower neuronal density in both hemispheres in rats with colitis in comparison to the controls bilaterally: right hemisphere (24.51 ± 5.49 and 36.3 ± 7.44; p-value = 0.360), and left hemisphere (24.52 ± 5.53 VS. 35.25 ± 5.6; P-value = 0.869).
This study showed that colitis can reduce the neuronal density within cortical areas and amygdala of both hemispheres. Considering the cingulate cortex's role in suppressing pain perception, any harm inflicted upon this region of the brain can has the ability to impact the cognitive and sensory aspects of pain.
炎症性肠病(IBD)患者的痛觉过敏和超敏反应可能与中枢神经系统(CNS)变化有关,尤其是在疼痛传导通路中。本研究的目的是在结肠炎动物模型中检测扣带回皮质区域(CC)和杏仁核的神经元密度。
在本实验中,对13只雄性Wistar大鼠进行研究。在10%甲苯噻嗪(5mg/kg)镇静下,经直肠向大鼠注射1cc 3%的醋酸诱导结肠炎。结肠炎14天后,用高剂量的氯胺酮(50mg/kg)、甲苯噻嗪(10mg/kg)和地西泮(2.5mg/kg)麻醉大鼠后实施安乐死。然后通过手术取出它们的大脑。将6微米厚的脑片用甲酚紫染色,并通过显微镜成像评估杏仁核、扣带回皮质区域1(CC1)和扣带回皮质区域2(CC2)的神经元密度。
与对照组相比,结肠炎大鼠CC1的神经元密度平均值±标准差(SD)在右侧CC1(43.53±9.63对62.7±11.89;p值<0.001)和左侧CC1(41.19±9.05和63.1±7.44;p值<0.001)均显著降低。此外,发现结肠炎组右侧CC2(57.8±13.23对87.95±8.76;p值<0.001)和左侧CC2(55.42±11.3对98±8.99;p值<0.001)的CC2神经元密度均显著低于对照组。此外,与双侧对照组相比,结肠炎大鼠双侧杏仁核的神经元密度均较低:右侧半球(24.51±5.49和36.3±7.44;p值=0.360),左侧半球(24.52±5.53对35.25±5.6;p值=0.869)。
本研究表明,结肠炎可降低双侧皮质区域和杏仁核内的神经元密度。考虑到扣带回皮质在抑制痛觉感知中的作用,对该脑区造成的任何损害都有可能影响疼痛的认知和感觉方面。