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Two distinguished neuroscientists distil general principles from more than a century of scientific study, “reverse engineering” the brain to understand its design. Neuroscience research has exploded, with more than fifty thousand neuroscientists applying increasingly advanced methods. A mountain of new facts and mechanisms has emerged. And yet a principled framework to organize this knowledge has been missing. In this book, Peter Sterling and Simon Laughlin, two leading neuroscientists, strive to fill this gap, outlining a set of organizing principles to explain the whys of neural design that allow the brain to compute so efficiently. Setting out to “reverse engineer” the brain—disassembling it to understand it—Sterling and Laughlin first consider why an animal should need a brain, tracing computational abilities from bacterium to protozoan to worm. They examine bigger brains and the advantages of “anticipatory regulation”; identify constraints on neural design and the need to “nanofy”; and demonstrate the routes to efficiency in an integrated molecular system, phototransduction. They show that the principles of neural design at finer scales and lower levels apply at larger scales and higher levels; describe neural wiring efficiency; and discuss learning as a principle of biological design that includes “save only what is needed.” Sterling and Laughlin avoid speculation about how the brain might work and endeavor to make sense of what is already known. Their distinctive contribution is to gather a coherent set of basic rules and exemplify them across spatial and functional scales.

Because the mouse retina has become an important model system, we have begun to identify its specific neuron types and their synaptic connections. Here, based on electron micrographs of serial sections, we report that the wild-type mouse retina expresses the standard rod pathways known in other mammals: (1) rod --> cone (via gap junctions) to inject rod signals into the cone bipolar circuit; and (2) rod --> rod bipolar --> AII amacrine --> cone bipolar --> ganglion cell. The mouse also expresses another rod circuit: a bipolar cell with cone input also receives rod input at symmetrical contacts that express ionotropic glutamate receptors (Hack et al., 1999, 2001). We show that this rod-cone bipolar cell sends an axon to the outer (OFF) strata of the inner plexiform layer to form ribbon synapses with ganglion and amacrine cells. This rod-cone bipolar cell receives direct contacts from only 20% of all rod terminals. However, we also found that rod terminals form gap junctions with each other and thus establish partial syncytia that could pool rod signals for direct chemical transmission to the OFF bipolar cell. This third rod pathway probably explains the rod responses that persist in OFF ganglion cells after the well known rod pathways are blocked (Soucy et al., 1998).

IN: Allostasis, Homeostasis, and the Costs of Adaptation J. Schulkin Cambridge University Press 20041 Principles of allostasis: optimal design, predictive regulation, pathophysiology and rational therapeutics.

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