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Developmental localization of potassium chloride co-transporter 2 in granule cells of the early postnatal mouse cerebellum with special reference to the synapse formation.
Neuroscience 2006; 143(3):757-67N

Abstract

In the adult CNS, GABA is the predominant inhibitory neurotransmitter, mediating the hyperpolarization of membrane potential and regulating the glutamatergic activity. In the immature CNS, on the other hand, GABA mediates depolarization and is involved in controlling morphogenesis. This developmental shift in GABA actions from depolarization to hyperpolarization occurs as a result of decreasing the intracellular chloride ion (Cl(-)) concentration ([Cl(-)](i)) which is regulated by the potassium (K(+))-Cl(-) co-transporter 2 (KCC2). To clarify the time-course of changes in the GABA actions during development, we examined the developmental localization of the KCC2 in the granule cells of the postnatal mouse cerebellum using specific antibodies against KCC2. The granule cell precursors and migrating granule cells were devoid of immunoreactivity against KCC2 antibodies. At postnatal day 3 (P3), the KCC2-immunolabeling was negative in the internal granular layer, although synaptophysin-positive mossy fiber terminals were detected. At P5, we first detected the KCC2-immunolabeling at the somata of granule cells and their dendrites before granule cells received inhibitory input from Golgi cells. Almost all KCC2-positive dendrites (more than 98%) attached to and formed synapses with mossy fiber terminals. As development proceeded, the number of KCC2-positive granule cells increased, and all granule cells became positive by P21. These results suggested that GABAergic transmission on granule cells might shift from excitation to inhibition after the synapse formation, and the excitatory synapse-formation and related factors might be the triggers for the expression and localization of the KCC2 in the granule cells. Furthermore, it was also suggested that formation of the GABAergic synapses and GABAergic transmission were not necessary for the KCC2-expression in the mouse cerebellar granule cells in vivo.

Authors+Show Affiliations

Department of Molecular Neuroanatomy, Hokkaido University School of Medicine, Kita-15 Nishi-7, Kita-Ku, Sapporo 060-8638, Japan. takachan@med.hokudai.ac.jpNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17008020

Citation

Takayama, C, and Y Inoue. "Developmental Localization of Potassium Chloride Co-transporter 2 in Granule Cells of the Early Postnatal Mouse Cerebellum With Special Reference to the Synapse Formation." Neuroscience, vol. 143, no. 3, 2006, pp. 757-67.
Takayama C, Inoue Y. Developmental localization of potassium chloride co-transporter 2 in granule cells of the early postnatal mouse cerebellum with special reference to the synapse formation. Neuroscience. 2006;143(3):757-67.
Takayama, C., & Inoue, Y. (2006). Developmental localization of potassium chloride co-transporter 2 in granule cells of the early postnatal mouse cerebellum with special reference to the synapse formation. Neuroscience, 143(3), pp. 757-67.
Takayama C, Inoue Y. Developmental Localization of Potassium Chloride Co-transporter 2 in Granule Cells of the Early Postnatal Mouse Cerebellum With Special Reference to the Synapse Formation. Neuroscience. 2006;143(3):757-67. PubMed PMID: 17008020.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Developmental localization of potassium chloride co-transporter 2 in granule cells of the early postnatal mouse cerebellum with special reference to the synapse formation. AU - Takayama,C, AU - Inoue,Y, Y1 - 2006/09/27/ PY - 2006/05/16/received PY - 2006/07/26/revised PY - 2006/08/17/accepted PY - 2006/9/30/pubmed PY - 2007/3/7/medline PY - 2006/9/30/entrez SP - 757 EP - 67 JF - Neuroscience JO - Neuroscience VL - 143 IS - 3 N2 - In the adult CNS, GABA is the predominant inhibitory neurotransmitter, mediating the hyperpolarization of membrane potential and regulating the glutamatergic activity. In the immature CNS, on the other hand, GABA mediates depolarization and is involved in controlling morphogenesis. This developmental shift in GABA actions from depolarization to hyperpolarization occurs as a result of decreasing the intracellular chloride ion (Cl(-)) concentration ([Cl(-)](i)) which is regulated by the potassium (K(+))-Cl(-) co-transporter 2 (KCC2). To clarify the time-course of changes in the GABA actions during development, we examined the developmental localization of the KCC2 in the granule cells of the postnatal mouse cerebellum using specific antibodies against KCC2. The granule cell precursors and migrating granule cells were devoid of immunoreactivity against KCC2 antibodies. At postnatal day 3 (P3), the KCC2-immunolabeling was negative in the internal granular layer, although synaptophysin-positive mossy fiber terminals were detected. At P5, we first detected the KCC2-immunolabeling at the somata of granule cells and their dendrites before granule cells received inhibitory input from Golgi cells. Almost all KCC2-positive dendrites (more than 98%) attached to and formed synapses with mossy fiber terminals. As development proceeded, the number of KCC2-positive granule cells increased, and all granule cells became positive by P21. These results suggested that GABAergic transmission on granule cells might shift from excitation to inhibition after the synapse formation, and the excitatory synapse-formation and related factors might be the triggers for the expression and localization of the KCC2 in the granule cells. Furthermore, it was also suggested that formation of the GABAergic synapses and GABAergic transmission were not necessary for the KCC2-expression in the mouse cerebellar granule cells in vivo. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/17008020/Developmental_localization_of_potassium_chloride_co_transporter_2_in_granule_cells_of_the_early_postnatal_mouse_cerebellum_with_special_reference_to_the_synapse_formation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(06)01110-9 DB - PRIME DP - Unbound Medicine ER -