1. Counting GABA Release Sites and Active Zones
gota A. Bir, Nomi B. Holderith, and Zoltan Nusser

The tradition of quantal analysis of synaptic transmission, which began at the neuromuscular junction, is extended this week to the inhibitory synapse between cholecystokinin- expressing interneurons and hippocampal CA3 pyramidal cells. Bir et al. first determined the quantal amplitude and the number of functional release sites from measurements of unitary IPSCs. Next, they counted the number of boutons and active zones on nerve terminals by light and electron microscopy (EM). The authors report that things dont add up: they found many more functionally determined release sites than anatomically defined active zones as defined by three- dimensional EM reconstructions. Using kinetic modeling, the authors estimated that an approximately fivefold increase in the peak GABA concentration was required for the fivefold enhancement of the postsynaptic response at a single synapse, consistent with multivesicular release at each active zone when release probability is high.

2. -Catenin Signaling in Cortical Precursors
Gregory J. Woodhead, Christopher A. Mutch, Eric C. Olson, and Anjen Chenn

They say that with evolution, us mammals got smarter, thanks to an increase in our cerebral cortex. A clue to the molecules involved in cortical expansion comes from transgenic mice overexpressing -catenin, a component of the Wnt signaling pathway. These mice have enlarged brains with an increased cortical surface area, presumably because a greater proportion of transgenic cortical precursors reenter the cell cycle after mitosis, thereby enlarging the pool of precursor cells. This week, Woodhead et al. used cre-mediated gene excision in utero to knock out -catenin in the ventricular zone of developing mouse embryos. The loss of -catenin increased the number of precursors that exited the cell cycle early, differentiated into n
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Contact: Sara Harris
sharris@sfn.org
202-962-4000
Society for Neuroscience
28-Nov-2006