Leaky Synapses

subsets of neurons, or they may have more of a scaffolding function. A scenario of multiple transsynaptic signaling proteins for different subsets of glutamate synapses is a rather daunting possibility that must now be considered. Such a possibility would allow for the extensive heterogeneity found in molecular composition of individual gluta-matergic postsynaptic specializations, depending on pre-and postsynaptic cell type, stage of development, and activity (Rao et al., 1998). Interestingly, there are two proteins closely related to Narp, neuronal pentraxin 1 and neuronal pentraxin receptor (Dodds et al., 1997). The latter has a putative transmembrane domain, and all three can bind to each other in a calcium-regulated manner. These proteins may function in overlapping sets of neurons to regulate glutamatergic synaptogenesis. Considering the complexity and diversity of central syn-assumed that transmission at these synapses is point Department of Cell and Structural Biology to point. Yet, during the past few years, evidence has University of Illinois accumulated suggesting that for excitatory synapses Urbana, Illinois 61801 glutamate may, under some conditions, be able to spread out of the synapse and activate both pre-and released glutamate can rapidly activate glutamate trans-37–43. 1997), indicating that glutamate is capable of spilling out 407–418. the olfactory bulb that the synaptic release of glutamate can spread from one cell and activate NMDARs on a neighboring cell. Mitral cells, the primary relay neurons of the olfactory bulb, release glutamate from their den-drites onto the processes of inhibitory granule cells, Leaky Synapses which in turn release GABA directly back onto the mitral cell dendrite (see figure) When this inhibitory feedback is removed pharmacologically by a The concept that neurotransmitters can act diffusely and at some distance from their release site has long GABA antagonist, a direct self-excitation of mitral cells by glutamate is revealed (Nicoll and Jahr, 1982). Isacc-been associated with monoamine-and peptide-mediated synaptic transmission, in which communication is son now shows that this action is entirely due to the direct activation of NMDARs. This synaptic response dictated more by the location of the receptors than by the specific site of transmitter release. On the other appears to be very efficient. The release of glutamate