Harding J W, Getchell T V, Margolis F L
Brain Res. 1978 Jan 27;140(2):271-85. doi: 10.1016/0006-8993(78)90460-2.
Intranasal irrigation of mice with 0.17 M ZnSO4 solution results in the immediate and total loss of the ability to find a buried food pellet. This anosmia persists for 6 weeks in at least 80% of the treated mice and for 4 months in half of the animals. This marked behavioral effect is matched by a long-term reduction of the levels of carnosine synthesis and transport in the primary olfactory pathway. These biochemical parameters are virtually undetectable at two weeks after treatment and even at one year after treatment do not exceed 5-10% of average control values. Light microscopic observations of tissues of the primary olfactory pathway at various times after treatment are consistent with these observations and indicate a substantial destruction of the olfactory epithelium with subsequent atrophy of the olfactory bulb. At very long intervals after treatment, some receptor regeneration is apparent with accompanying reinnervation of the olfactory bulb. Estimates from microscopy and biochemistry suggest that much less than 10% of the normal complement of functioning receptor cells is adequate to give apparently normal food-finding behavior.
用0.17M硫酸锌溶液对小鼠进行鼻腔灌洗，会导致其立即完全丧失找到埋藏食物颗粒的能力。这种嗅觉丧失在至少80%的受试小鼠中持续6周，在一半的动物中持续4个月。这种显著的行为效应与初级嗅觉通路中肌肽合成和转运水平的长期降低相匹配。这些生化参数在治疗后两周几乎检测不到，甚至在治疗后一年也不超过平均对照值的5-10%。对治疗后不同时间的初级嗅觉通路组织进行光学显微镜观察，与这些观察结果一致，表明嗅觉上皮有大量破坏，随后嗅球萎缩。在治疗后很长一段时间间隔，一些受体再生明显，伴有嗅球的重新神经支配。显微镜和生化分析估计，功能正常的受体细胞数量少于正常数量的10%，就足以产生明显正常的寻找食物行为。
