The olfactory bulb’s external plexiform layer is dominated by lateral interactions between mitral and tufted cells, which extend long lateral dendrites across the layer, and inhibitory granule cell interneurons, the dendrites of which are perpendicular to the M/T cell lateral dendrites.  Their matrix of interconnections governs the transformations of afferent olfactory input performed in this layer.  In this set of biophysical simulations, based on the olfactory bulb model of Li and Cleland (2013), McIntyre and Cleland demonstrate that the basic architecture of these interactions is based on long-range excitation and local inhibition, based simply on established biophysical principles.  Based on this essential framework, future work can better ask how the weights in this network are determined and regulated.

McIntyre AB, Cleland TA (2016)  Biophysical constraints on lateral inhibition in the olfactory bulb.  Journal of Neurophysiology 115(6):2937-2949.
Abstract:  The mitral cells (MCs) of the mammalian olfactory bulb (OB) constitute one of two populations of principal neurons (along with middle/deep tufted cells) that integrate afferent olfactory information with top-down inputs and intrinsic learning and deliver output to downstream olfactory areas. MC activity is regulated in part by inhibition from granule cells, which form reciprocal synapses with MCs along the extents of their lateral dendrites. However, with MC lateral dendrites reaching over 1.5 mm in length in rats, the roles of distal inhibitory synapses pose a quandary. Here, we systematically vary the properties of a MC model to assess the capacity of inhibitory synaptic inputs on lateral dendrites to influence afferent information flow through MCs. Simulations using passivized models with varying dendritic morphologies and synaptic properties demonstrated that, even with unrealistically favorable parameters, passive propagation fails to convey effective inhibitory signals to the soma from distal sources. Additional simulations using an active model exhibiting action potentials, subthreshold oscillations, and a dendritic morphology closely matched to experimental values further confirmed that distal synaptic inputs along the lateral dendrite could not exert physiologically relevant effects on MC spike timing at the soma. Larger synaptic conductances representative of multiple simultaneous inputs were not sufficient to compensate for the decline in signal with distance. Reciprocal synapses on distal MC lateral dendrites may instead serve to maintain a common fast oscillatory clock across the OB by delaying spike propagation within the lateral dendrites themselves.