Mouse cerebellar Purkinje cell damage induced by diphenylhydantoin acute intoxication

作     者：Orlando J.CASTEJÓN 

作者机构：Biological Research Institute and Faculty of MedicineZulia UniversityMaracaiboVenezuela 

出 版 物：《BIOCELL》 (生物细胞（英文）)

年 卷 期：2015年第39卷第2期

页      面：33-39页

核心收录：

学科分类：08[工学] 080502[工学-材料学] 0805[工学-材料科学与工程（可授工学、理学学位）] 

基　　金：a subvention obtained from Biological Research Institute.Faculty of Medicine.Zulia University the Council for Humanistic and Scientific Devel-opment of Zulia University(CONDES LUZ) and Castejón Foundation.The technical digital help of Lic.Orlando Caste-jón Depablos is deeply appreciated.The author declares no conflicts of interests 

主　　题：Purkinje cell cytotoxic edema diphenylhydantoin toxicity electron microscopy 

摘      要：Twenty one days old Swiss albino mice that received diphenylhydantoin(25 mg/kg,i.p.,daily for 15 days)progressively developed gait alterations,changes of behavior and cerebellar *** slices were processed by conventional transmission electron *** body of Purkinje cells exhibited fragmented limiting plasma membranes,dilated nuclear envelopes,swelling and disassembly of nuclear pores,enlargement of rough and smooth endoplasmic reticulum and a notable detachment of membrane associated ribosomes,to-gether with distorted vacuoles of smooth endoplasmic reticulum,bizarre shaped and swollen mitochondria with dilated cristae,as well as disrupted limiting lysosomal *** axosomatic synapses apparently corresponding to basket cell axonal endings were *** Purkinje cell axon initial segments exhibited vacuolar degeneration of myelin sheath,dilated axoplasmic tubular bundles,fragmented axonal mem-branes,swollen mitochondria,and disassembly of cytoskeletal *** edematous and clear secondary and tertiary dendrites exhibited areas of dilated cisterns of smooth endoplasmic reticulum,clear and dark mul-tivesicular bodies,and coated *** dendritic ramifications exhibited an electron dense *** and large climbing fiber endings were observed making axodendritic synapses with edematous Purkinje *** presynaptic endings appeared depleted or containing few synaptic *** syn-apses did not exhibit pre-and postsynaptic *** the molecular layer,the edematous synaptic varicosities of parallel fibers containing pleomorphic synaptic vesicles and dense extravesicular substance were observed making asymmetric synaptic contacts with swollen Purkinje dendritic *** findings are postulated as pathogenic mechanisms of mouse cerebellar ataxia.