The absence of a major Ca2+ signaling pathway in GABAergic neurons of the hippocampus
AUTOR(ES)
Sík, Attila
FONTE
The National Academy of Sciences
RESUMO
The Ca2+/calmodulin-dependent protein phosphatase 2B or calcineurin (CN) participates in several Ca2+-dependent signal transduction cascades and, thus, contributes to the short and long term regulation of neuronal excitability. By using a specific antibody to CN, we demonstrate its absence from hippocampal interneurons and illustrate a physiological consequence of such CN deficiency. Consistent with the lack of CN in interneurons as detected by immunocytochemistry, the CN inhibitors FK-506 or okadaic acid significantly prolonged N-methyl-d-aspartate channel openings recorded in the cell-attached mode in hippocampal principal cells but not those recorded in interneurons. Interneurons were also devoid of Ca2+/calmodulin-dependent protein kinase IIα, yet many of their nuclei contained the cyclic AMP-responsive element binding protein. On the basis of the CN and Ca2+/calmodulin-dependent protein kinase IIα deficiency of interneurons, entirely different biochemical mechanisms are expected to govern Ca2+-dependent neuronal plasticity in interneurons versus principal cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=19727Documentos Relacionados
- Ca2+ buffering and action potential-evoked Ca2+ signaling in dendrites of pyramidal neurons.
- Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease
- Structural role of countertransport revealed in Ca2+ pump crystal structure in the absence of Ca2+
- Ca2+ dynamics in the lumen of the endoplasmic reticulum in sensory neurons: direct visualization of Ca2+-induced Ca2+ release triggered by physiological Ca2+ entry
- Ca2+ activity at GABAB receptors constitutively promotes metabotropic glutamate signaling in the absence of GABA