Abstract
Until recently, neural-glial communication has been assumed to be mediated by low concentration transients of transmitter that result from spillover from the synaptic cleft. Therefore such communication has been thought to be a secondary effect of synaptic transmission between neurons. In the cerebellum, Bergmann glia cell (BG) processes encase synapses between presynaptic climbing fiber and parallel fiber elements and postsynaptic Purkinje cell (PC) spines and glutamate released from these fibers can activate Ca2+-permeable AMPA receptors on BGs. We have found evidences that support the idea that this rapid neural signaling to BGs is mediated not by spillover but by ectopic vesicular release of glutamate from presynaptic elements directly facing the BG membrane. It has been suggested that such neural-glial communication is responsible for the encasement and isolation of excitatory synapses on PCs by BGs. Therefore we have started to employ two-photon microscopy to study the impact of neural-glial communication on BG morphology. Rapid remodeling of the extracellular space caused by spontaneous motility of BG protrusions was observed and synaptic activation lead to enhanced motility of these protrusions. Synaptic activation also lead to Ca2+ influx at the tip of the protrusions via Ca2+-permeable AMPA receptors followed by a broader propagation of Ca2+ increase throughout the entire process possibly via activation of ATP receptors. We are currently trying to understand the mechanism of BG motility and how neural-glial communication leads to the refinement of synaptic and glial complex environment. [J Physiol Sci. 2007;57 Suppl:S26]
