Balance: Bipeds Need It; Where Did It Come From?
As upright walkers, human beings are subject to damage from falls. Our center of gravity, near the navel, is much higher than that of a dog or rat that is balanced on four feet. Howard Glicksman and Steve Laufmann note in Your Designed Body that you have only a half second from losing your balance to hitting the ground.
Many of us know loved ones who have fallen and incurred major injuries to the head, hips, spine, or other body parts. The commercial line “Help! I’ve fallen and I can’t get up!” reminds us of the danger of falls for the elderly who have lost their youthful balance and reaction time. The young would be at the same risk were it not for intricately designed mechanisms for rapid correction from loss of balance. Before there were ambulances and emergency rooms, this would have likely ended the human race, because in Darwinian thinking, individuals must reach reproductive age to achieve the mystical property called “fitness.” How many falls would it take for the young to each earn a “Darwin Award” for eliminating themselves from the gene pool?
“We All Fall Down”
Without a suite of protective systems for preventing serious injuries from falls, would any human ancestors survive to puberty? Babies fall, as parents know, but they live closer to the ground and retain a good deal of cushioning body fat till they master the art of walking on two legs. Pre-pubertal adolescents are already at risk of falling; plus, they tend to be foolhardier and more energetic. The simplistic just-so story of apes descending from the trees and learning to walk upright on the ground (the Savannah hypothesis) should end with the nursery rhyme, “We all fall down.”
Fortunately, we have such a suite of protective equipment. Glicksman discusses one fine-tuning specialization, the myelin sheath encasing many neurons in the central nervous system. Myelin speeds up neural transmission by a factor of a hundred, giving us time to respond to a loss of balance. Another remarkable specialization is found in the middle ear: the vestibular apparatus, consisting of the utricle, saccule, and semicircular canals. These balance organs inform the brain rapidly, giving us precious fractions of a second to try to catch ourselves. With that extra time, we can move our feet, knees, arms, and hands to avoid hitting the ground, grab onto something with our hands, or if we cannot stop, we can roll onto our side to absorb the shock. The success of these protections can be seen in gymnasts, teens on skateboards, specialists in parkour, or experts in any high-velocity sport who make rapid adjustments in moves that would otherwise be debilitating or fatal.
Fastest Signals in the Body
Physiologists have marveled at the rapidity of the neurons in the vestibular organs — the fastest in the body — but did not understand how they work. A new paper in Current Biology notes that these neurons are arranged by “birthdate” in an orderly manner, giving them a “previously hidden functional topography.” This means that “directional selectivity to body tilts followed soma position and birthdate.”
Taken together, we find that development reveals organization within the vestibular brainstem, its peripheral inputs, and its motor outputs (Figure 7). We propose that time plays a causal role in fate determination, topographic organization, and, by extension, vestibular circuit formation. Our data suggest mechanisms for projection neuron fate specification. More broadly, our findings offer insights into how time shapes vertebrate sensorimotor circuits. [Emphasis added.]
A team of researchers from Rice, Yale, and the University of Chicago, publishing in PNAS, looked further at the synapses in vestibular neurons and found them to be uniquely designed for rapid response. Most neurons transfer electrical signals across synapses with neurotransmitters in what’s called “quantal transmission” (QT). QT has an inherent delay as the information crosses a synaptic gap. Vestibular neurons, by contrast, operate with “a mysterious form of electrical transmission that does not involve gap junctions, termed nonquantal transmission (NQT).”
The ability of the vestibular system to drive the fastest reflexes in the nervous system depends on rapid transmission of mechanosensory signals at vestibular hair cell synapses. In mammals and other amniotes, afferent neurons form unusually large calyx terminals on certain hair cells, and communication at these synapses includes nonquantal transmission (NQT), which avoids the synaptic delay of quantal transmission. We present a quantitative model that shows how NQT depends on the extent of the calyx covering the hair cell and attributes the short latency of NQT to changes in synaptic cleft electrical potential caused by current flowing through open potassium channels in the hair cell. This mechanism of electrical transmission between cells may act at other synapses.
Hair cells perform mechanotransduction — the transfer of mechanical energy to electrical energy. When the tiny hairs are deflected, they trigger the flow of ions from the surrounding fluid, called endolymph, into the adjacent cell, triggering an ionic train that travels down the neurons. The hair cells in the cochlea perform mechanotransduction for hearing. The hair cells in the utricle “drive neural circuits controlling gaze, balance, and orientation.”
What’s unique about a vestibular hair cell is the large goblet-shaped calyx surrounding its base. This is where the rapid “nonquantal” mechanotransduction was understood to occur, but the mechanism was unknown.
How it Works
Unlike normal synapses between neurons, vestibular hair cells do not need to traverse a gap junction, where the electrical energy must be converted to chemical energy and back again. In a synapse, signal “quanta” are packetized by exocytosis of vesicles containing neurotransmitters. Each packet must cross the synapse and be re-absorbed by endocytosis into the neuron. In vestibular hair cells, by contrast, the calyx structure has a very narrow “synaptic cleft” between the hair cell body and the neuron that “involves neither exocytosis of packets (vesicles or quanta) of neurotransmitter nor gap junctions.” This reduces the latency of gap junctions and speeds the electrical impulse on its way to the brain.
A deflection of only 1 micrometer (one millionth of a meter) in the hair cell is sufficient to trigger a response. Because the synaptic cleft is lined with potassium and sodium channels, multiple channels in the cup-shaped calyx can respond simultaneously to the change in electrical potential.
The synaptic cleft is a dynamic system where electric potentials, ion concentrations, and ionic currents interact. The changes in cleft electrical potential and ion concentrations shown in Fig. 2 are driven by currents through voltage-sensitive ion channels … on the hair cell basolateral membrane and on the calyx inner face, and in turn modulate these currents (Fig. 3). NQT is bidirectional: we first describe the roles of key channels during anterograde (hair cell to calyx) NQT and later discuss retrograde (calyx to hair cell) NQT.
The description gets correspondingly “hairy” at this part of the paper. The authors discuss signal gain, frequency response, electrical potentials, voltage, resistance, capacitance, and other terms that make the paper seem like it belongs under electrical engineering instead of biology. Suffice it to say that a great deal happens quickly, with forward and backward feedback.
These results indicate that fast retrograde events seen in electrophysiological recordings of the hair cell and calyx are caused by changes in electrical potential in the synaptic cleft. It has been suggested that the bidirectional nature of NQT, which our VHCC model captures, could be used to modulate the sensitivity of both the calyx and the hair cell.
A key point is that NQT depends on the morphology of the calyx. One other thing to keep in mind is that the “large number” of ion channels that line the synaptic cleft in the calyx are wonderfully complex in themselves: K+ channels, Na+channels, and Ca2+ channels. Each type includes a selectivity filter that can discriminate the nanoscopic ions allowed through. Their placement in both number and orientation along the synaptic cleft, furthermore, are additional functional requirements to achieve the rapid response, so that the organism doesn’t break its skull when suddenly shifted off balance. The rapidity of the system can be appreciated by watching an ice skater breaking a dizzying spin or sticking the landing of a triple lutz.
A Question of Origins
It is true that all amniotes, including fish, amphibians, and mammals, contain the calyx structure in their vestibular organs. It is not unique to bipeds like humans. An evolutionist would have to consider this a “pre-design” for the bipeds and figure skaters to come hundreds of millions of years later. Rob Raphael, the lead author at Rice for the paper, speculated that the calyx
is an example of how evolution drives morphological specialization. A compelling argument can be made that once animals emerged from the sea and began to move on land, swing in trees and fly, there were increased demands on the vestibular system to rapidly inform the brain about the position of the head in space. And at this point the calyx appeared.
“The calyx appeared”! A more magical explanation could hardly be fabricated. The argument may be compelling to Dr. Raphael, but can it be believed that needs create solutions on their own? Fish are not at risk of falling, so where was the selective pressure to evolve NQT? Did an amphibian summon cosmic rays to hit its germ cells just right to start the evolution of nonquantal transmission in its offspring? Human engineers can observe needs and build solutions, but to expect a multi-part, irreducibly complex piece of supremely efficient electrical engineering to “evolve” by sheer dumb luck simply because an animal might benefit from it stretches credulity. If anything, what the authors describe represents over-design — a concept foreign to Darwinism, which lacks foresight.
The common implementation of calyx NQT among different animals is not evidence of common ancestry. Each animal could, instead, enjoy the shared design tailored to its particular lifestyle. The authors note that larger calyces reduce delay and observe that “calyces vary in their shape in different regions of amniote vestibular epithelia.” Not every animal needs the human specification. ID advocates might want to investigate the tailoring of calyces to lifestyle.
For those of us not beholden to evolutionary explanations, NQT is another lifesaving wonder that most of us probably never heard of before. Glicksman says that neural reflexes travel at 200 miles per hour in the spine, allowing us to react in 0.01 seconds — 50 times faster than a fall. Awareness of a loss of balance begins with nonquantal transmission in the utricle.
Our vestibular organs are tiny marvels inside our heads that keep us on balance and oriented in 3-D space and time. They work flawlessly most of the time for up to a century or more. How many times have you put your vestibular organs to the test: swimming, riding roller coasters, leaping, rock-hopping across a stream, doing handstands, or engaging in sports? One episode of vertigo accompanied by a painful fall is enough to shudder at what would be the norm without these tiny organs working properly. The astonishing thing is not that these systems begin to slow down in old age, but that they ever worked in the first place.