title: Immunohistochemical localization of calbindin D28-k, parvalbumin, and calretinin in the cerebellar cortex of the circling mouse.
abstract: The spontaneous mutant circling mouse has an autosomal recessive pattern of inheritance and is an animal model for deafness, which is characterized by circling, head tossing, and hyperactivity. Since the main pathology in circling mice lies in the organ of Corti, most studies on deaf mice have focused on auditory brain stem nuclei. No studies regarding behavior-related CNS changes in circling mice have been reported. The major center of sensory input for modulation of motor activity is best-studied in the cerebellum. Considering the importance of calcium homeostasis in numerous processes, calcium-binding proteins (CaBPs), such as calbindin D-28k (CB), parvalbumin (PV), and calretinin (CR), may play crucial roles in preserving cerebellar coordinated motor function. Thus, the distribution of CB, PV, and CR was determined in the cerebellum using immunohistochemical methods to compare immunoreactivity (IR) of CaBPs between wild-type (+/+), heterozygous (+/cir), and homozygous (cir/cir) mice. The IR of CB and PV was predominantly observed in the Purkinje cell layer of all three genotypes. Compared with the +/+ genotype, the relative mean density of CB and PV IR in the Purkinje cell layer and CR IR in the granular layer was significantly decreased in the cir/cir genotype. Changes in calcium homeostasis in parallel fiber/Purkinje cell synapses could diminish cerebellar control of motor coordination. A number of deficiencies among the CaBPs lead to distinct alterations in brain physiology, which may affect normal behavior.
authors.affiliation: Department of Anatomy, Dankook University, Cheonan-si, Chungnam, South Korea.
authors.forename: Dhiraj
authors.initials: D
authors.lastname: Maskey
authors.forename: Jonu
authors.initials: J
authors.lastname: Pradhan
authors.forename: Hye-Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Ki Sup
authors.initials: KS
authors.lastname: Park
authors.forename: Seung Cheol
authors.initials: SC
authors.lastname: Ahn
authors.forename: Myeung Ju
authors.initials: MJ
authors.lastname: Kim
mesh_terms: D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D020013:Calcium Signaling / Q000235:genetics; D002525:Cerebellar Cortex / Q000378:metabolism* / Q000473:pathology; D002526:Cerebellar Diseases / Q000235:genetics* / Q000378:metabolism*; D015536:Down-Regulation / Q000235:genetics; D005838:Genotype; D051379:Mice; D008810:Mice, Inbred C57BL; D008818:Mice, Neurologic Mutants; D010320:Parvalbumins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D011689:Purkinje Cells / Q000378:metabolism / Q000473:pathology; D064030:S100 Calcium Binding Protein G / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D022142:Secretory Vesicles / Q000235:genetics / Q000378:metabolism
chemical_list: C576511:Calb2 protein, mouse; D064032:Calbindin 2; D064026:Calbindins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G