Abstract
In neurons of the central nervous system, the integrative function depends on the somato-dendritic distribution and properties of voltage-gated ion channels, pumps and transporters. These membrane-associated proteins are highly regulated by an intracellular second-messenger system consisted of a variety of functional molecules and divalent cations including Ca2+. In this talk, particular emphasis is placed on results concerning Ca2+ dependent modulation of excitability in CNS dendrites. We examined how Ca2+ signals play pivotal roles in 1) the hippocampal neuronal death after transient forebrain ischemia, and in 2) protein kinase C (PKC) signaling in cerebellar Purkinje cells. A combination of intracellular recording and fluorescence Ca2+ imaging was applied to each neuron in the brain slice obtained from rodents. In the former study, we found that excitatory synaptic inputs induced relatively larger calcium transients in the apical dendrites of post-ischemic CA1 neurons than in those of normal neurons, although somatic depolarization induced smaller increases in dendritic signals than those of the control. These results suggest that the Ca2+ homeostasis at the apical dendrite is impaired in CA1 pyramidal neurons following transient ischemia. In the later study, we found propagation of Ca2+ dependent γPKC translocation along Purkinje cell dendrites. The present results suggest that local intracellular signals activated by parallel fiber input could transmit to the other parts of cell through dendritic arbor. Our findings obtained from those studies may provide us a new insight for understanding molecular mechanisms of the integrative function in CNS dendrites. [Jpn J Physiol 55 Suppl:S18 (2005)]
