c-kit Receptor and Ligand Expression in Developing Nervous System Blocked c-kit Function by ACK2.
- Author:
Heanam HONG
;
Jonghwan LEE
;
Donghou KIM
- Publication Type:Original Article
- MeSH:
Animals;
Cerebellum;
In Situ Hybridization;
Injections, Intraperitoneal;
Mice;
Nervous System*;
Neurons;
Proto-Oncogene Proteins c-kit*;
Purkinje Cells;
RNA, Messenger;
Stem Cells;
Synapses;
Synaptophysin
- From:Korean Journal of Anatomy
1998;31(4):619-628
- CountryRepublic of Korea
- Language:English
-
Abstract:
The objective of the present study was to investigate the expression of KL ligand and synaptophysin during postnatal development of the cerebellum blocked c-kit function by ACK2 to determine whether the c-kit receptor and KL ligand interacting system could play a role during the migration of cerebellar neuronal cells and during establishment of functional synapses of all cerebellar neurons. In this study, we used in situ hybridization technique in order to examine the expression of KL mRNA in the cerebellar tissue following intraperitoneal injections of ACK2 and to study the localization of synaptophysin and protein products of KL ligand (SCF: Stem Cell Factor) during postnatal development we used immunohistochemical methods. Our findings are that the intensity of immunoreaction to SCF (protein product of KL ligand) antibody is increased while an immunoreactivity to anti-synaptophysin is decreased in the Purkinje cell bodies in the cerebellum of the mouse given ACK2 from the postnatal day 3 (P3) to Pl4. The overexpression of KL mRNA is detected in the Purkinje cell bodies at Pl4 in the cerebellum blocked c-kit function. At postnatal day 21, the period of which establishment of functional connections of all cerebellar neurons is complete, immunoreactivities of SCF and synaptophysin in the ACK2 treated cerebellum is recovered to the same level being observed in the control. With above results, we suggest a role for the c-kit receptor in the synaptogenesis and migration of developing cerebellar neurons with interaction of ckit receptor/KL ligand system. And the overexpression of KL ligand mRNA and protein product in the Purkinje cells is supposed to be one of mechanisms compensate for the lack of c-kit function in the cerebellum induced by ACK2 during postnatal development.
