Tessitore Maria Eduarda, Pereira-Rufino Laís da Silva, Panfilio Carlos Eduardo, de Cassia Sinigaglia Rita, Júnior Odair Aguiar, Maluf Luciana Le-Sueur, Conte Rafael, Ladd Fernando Vagner Lobo, Céspedes Isabel Cristina
Departamento de Biociências, Universidade Federal de São Paulo, campus Baixada Santista-UNIFESP, 11015-020, Brazil.
Departamento de Morfologia e Genética, Escola Paulista de Medicina, Universidade Federal de São Paulo-UNIFESP, 04023-062, Brazil.
IBRO Neurosci Rep. 2022 Aug 17;13:177-186. doi: 10.1016/j.ibneur.2022.08.004. eCollection 2022 Dec.
Alcoholic neuropathy (AN), a debilitating condition that mainly affects chronic alcohol drinkers, is thought to cause lesions in the peripheral nervous system leading to sensory, autonomic, and motor dysfunctions. Despite many studies, the pathogenesis of these lesions is still not completely understood. We investigated few aspects on the development of alcohol-induced peripheral neuropathy, by assessing sensory, motor and autonomic functions, as well as stereological analysis of axonal fibers and myelin sheath of the sciatic nerve. Twelve male Wistar rats were divided into Control group and Alcohol group that was submitted to Two Bottle-Choice Paradigm of intermittent and voluntary alcohol solution intake (20%; v/v) during eight weeks. At the end of treatment, three different sensorium-motor tests were applied - Tactile Sensitivity, Thermal Sensitivity, and Functional Observational Battery (FOB). Quantitative morphometric analysis of sciatic nerve structures was performed by stereological method. Alcohol concentration in the blood was measured to analyze possible correlation between availability of alcohol in the blood and the magnitude of the peripheral nerve lesion. Our data showed a peripheral effect of chronic alcohol intake associated with hyperalgesia and a process of demyelination with a strong correlation with alcohol consumption. This process was associated with increased tactile sensitivity, with behavioral reflexes such as locomotor hyperactivity, changes in gait and balance, and autonomic reflexes such as piloerection.
酒精性神经病变（AN）是一种主要影响慢性饮酒者的使人衰弱的病症，被认为会导致周围神经系统的损伤，进而引发感觉、自主神经和运动功能障碍。尽管进行了许多研究，但这些损伤的发病机制仍未完全明确。我们通过评估感觉、运动和自主神经功能，以及对坐骨神经轴突纤维和髓鞘进行体视学分析，研究了酒精诱导的周围神经病变发展的几个方面。将12只雄性Wistar大鼠分为对照组和酒精组，酒精组在八周内采用两瓶选择范式间歇性自愿摄入酒精溶液（20%；v/v）。治疗结束时，进行了三种不同的感觉运动测试——触觉敏感性、热敏感性和功能观察组合测试（FOB）。通过体视学方法对坐骨神经结构进行定量形态计量分析。测量血液中的酒精浓度，以分析血液中酒精含量与周围神经损伤程度之间可能存在的相关性。我们的数据显示，慢性酒精摄入具有外周效应，伴有痛觉过敏以及脱髓鞘过程，且该过程与酒精消耗量密切相关。这一过程与触觉敏感性增加有关，伴有诸如运动亢进等行为反射、步态和平衡变化，以及诸如竖毛等自主神经反射。
