In the vast and diverse world of the mammalian brain, some species get no more attention than the kind of cranial borings described here.
In particular, the brain of the baboon—a single-celled organism that, in a small population at most, can be considered the world’s oldest living group of primates—was largely ignored in the entire history of neuroscience. But now, at last, scientists have compiled long-awaited data on the “alphabet soup” of baboon brain structures.
All the “receiver centers” in a baboon brain.
That library now includes more than 1,100 distinct structures and over 400,000 individual genes. The research was published this week in the prestigious Proceedings of the National Academy of Sciences.
The largest structure is a “central central nucleus” (CDN) made of approximately 3,000 receptors and wireless units—a very large complex by other terms that humanity has often used to describe, say, a freeway or a credit card.
Called the CDN, the receptor cell complexes are organized like cheese and cream containers. Each has its own “data base” (or memory), although the data is not stored or recorded in the CSF, but rather from a nearby hippocampus-like region.
Photos of baboons at the Center for Comparative Medicine at King’s College London with the latest maps of the “alphabet soup” of baboon brain structures, the largest yet compiled.
At the CDN is a library of thousands of complex protein complexes. These binding points, known as “master receptors,” are located in a central region called a “range center” (R1) and the neck region at R2. These master receptors transmit chemical messages in response to stimuli such as light and sound. In the baboon, the R1 and R2 are more like switches than receptors. They turn on the master receptors and put them into low-power dormitory mode when they sense the neurotransmitter GABA. This dormitory activity (called gamma-aminobutyric acid or GABA-D) is a prerequisite for social behavior (like stand-up comedy). When baboons switch from dormancy to action, they knock out the dormitory neurons.
In “home” territory, these response mechanisms are relatively simple and just “switch on” at the start of interaction between an individual and other baboons, causing mild harassment and forcing the primate to use fewer brain cells (which rely on feedback from R1 and R2 to operate).
In contact, however, the exchange is not a pleasant one. When a BDNF molecule in the BDNF-protein complex binds an GABA molecule in the well-known theta pathway, an alpha-like “biological punch” to the temporal and occipital lobes changes the amygdala (the almond-shaped brain structure known as the reward center) and releases a neurotransmitter called norepinephrine. This combined neural action increases vigilance. Conversely, when BDNF is blocked by BDNF inhibitors (which has happened with Parkinson’s Disease), the chain reaction doesn’t happen. BDNF relies on BDNF-like proteins in BDNF-protein complexes (In the baboon’s case, BDNF-αα complexes). These complexes are more complex than the master receptors and more complex than the wireless receptors. They do not rely on the hippocampus-like brain region.
Receptor cells (receiver) in the CDN of a baboon brain.
Collaborators in this project included neurobiologists Christine Schenk and Roger Shumway, at the Center for Comparative Medicine at King’s College London, and researchers from Portugal’s Center for Neuropharmacology in Carvalho da Alabardiera.