Human brain theory

14.4 Movement generation at the simple joint

In the previous chapter, it was explained how a start signal from the mean value system for life support - triggered, for example, by a lack of energy - produced two mutually phase-shifted and periodic continuous oscillations that appeared suitable for motor control of the body.

Now the reader may expect some new, hitherto unknown neuronal circuit that could generate movements from these two motor clock signals. Some will expect a complicated, possibly quite opaque circuit in the brain. But this is not the case!

The circuits that generate movements from two motor clock signals have been present in the vertebrate brain for ages and are quite simple. One way to generate movements from clock signals is to use ordinary divergence modules (also called divergence grids in my earlier monographs).

Divergent modules and convergent modules differ in terms of input and output. Divergent modules are located in the ascending sensory branch of the cord ladder system or on the sensory half of the neural tube.

Convergence modules, on the other hand, are found on the motor side.

Both types of modules arose from the need to protect neuronal circuits against the failure of individual neurons. For this purpose, neuronal signals were distributed among several neurons. This happens in divergence modules. In convergence modules, the signal divergence was reversed. In both cases, there was the option of initially arranging these reserve neurons as vertical neuron columns. This had the advantage that the topological arrangement was preserved in the area. Thus, the neurons in the visual cortex, but also in the corpus geniculatum laterale, are well-ordered in such neuron columns, which are called ocular dominance columns.

These simplest divergence modules are also the ones that first emerged in the course of evolution and are still found today in reptiles and birds. They are divergence modules with vertical signal propagation.

It should be noted that the input for such divergence modules with vertical signal propagation basically consists of a pair of mutually inverse signals that are fed into the neuron column at the top and bottom, respectively. If an original quantity, for example brightness, produces a firing rate in a receptor that increases with the strength of the original quantity, this signal is referred to as the on signal. The signal inverse to this decreases in strength with the firing rate when the strength of the primal quantity increases. Both signals are inverse to each other.

In the divergence module with vertical signal propagation, the neurons of the on-signal form a thin neuron layer. The neurons of the off-signal form a second thin neuron layer. Between the two input layers there is a relatively thick output layer, which could also be understood as a stack of thin output layers. With increasing evolution, the number of stacks becomes larger; initially, there was only one thin outpup layer.

Whether the on-layer is located at the top and the off-layer at the bottom depends on which type of receptor was present earlier in evolution.

This is where the cerebellum comes into play. After the development of the cerebellum, it was no longer necessary for each type of signal to form an inverse type of signal. In the visual area - which developed very early - such a splitting of signals into on-types and off-types could develop. This did not happen with many types of receptors that concerned motor functions. There are no "inverse" muscle spindles whose signal strength decreases with increasing muscle tension. There are no "inverse" tendon organs whose firing rate increases with decreasing muscle tension. The task of forming an inverse signal to a motor-effective signal was taken over by the cerebellum. In both the vestibulocerebellum and the spinicerebellum, signal inversion was originally the main task.

The cerebellum output found its way - in the course of evolution and certainly quite early - to the cortex, i.e. to the top floor of the early cord ladder system or to the cortical floor of the neuroanatomical system. Since it also changed sides, it arrived in the cortex together with the original signals. The original signals already existed before the development of the cerebellum, so they were the evolutionarily older signals. They therefore formed the lower input layer in the frontal lobe. The cerebellum signals, which arose through signal inversion, formed the upper input layer in the frontal cortex. They were arranged in a topologically well-ordered way so that the corresponding input neuron with the off-signal from the cerebellum was located exactly above each input neuron that received a certain on-signal. Between them were the output neurons, which received the input of the output neurons above or below them via a myriad of interneurons. They formed the output column, so to speak. The signal propagation was basically vertical, hence the name divergence modules with vertical signal propagation.

So while the on-signal from the lower input layer propagated vertically upwards, the off-signal from the upper input layer fought its way downwards. All output neurons of the vertical neuron column between the two input neurons with the signals inverted to each other received both signal components because they propagated vertically via interneurons. We can combine these neurons into an output column. This is the typical organisation in the vertebrate cortex. There were no contacts with the neighbouring output neurons of the neighbouring columns, the distance was too great and the neurons were not signal-compatible - they belonged to other muscle groups.

Now, if the joint in question did not produce any signals because both muscles were slack, then there was no output at all in the output column in question.

Now, signal propagation in the divergence lattice is not lossless. On its way from the two input neurons to the output neurons of the cell column, a non-linear signal attenuation occurred. The neuronal excitation of a nerve cell ultimately resulted from the difference in concentration of the differently charged ions. Since there was a drop in concentration in the cell membrane due to constantly open ion channels and the movement of the ions was hindered by the electrical resistance of the cell plasma, the signal attenuation increased with increasing distance from the input source. We establish here a quadratic dependence on the distance.

But how could such a divergence grid move a joint?

 

Here we make a recourse to the mean value system. As described in the previous section, this generates two mutually phase-shifted clock signals, one of the on-type and one of the off-type. We now recall the back-projection of all mean value systems into activation neurons of neuron class 1.

We also find these activation neurons in the cortex. We assume that the motor clock signals - formed from motorically effective mean value signals - end in the cortical target area where the motor control signals of the muscles are also located. Therefore, these clock signals - among others - also end up near the neuronal column that is assigned to our joint.

The signals from the tendon organs of this muscle travel to the sensory centre and contact a class 4 neuron via the axons of the receptors. This neuron transports the signal to the sensory part of the frontal lobe with the interposition of further class 4 neurons. A class 3 neuron takes over the excitation and projects into a class 5 motor projection neuron, which again projects via further interconnected class 5 neurons to a motor neuron of the floor in which the siglal-producing muscle is located.

If the muscle is flaccid, the signalling pathway via the described neuron chain exists, but it is signal-free. This changes when the neuronal clock signal, the origin of which we have described, excites a cortical activation neuron of class 1 from the associated mean centre. Then this excitation is transmitted by interneurons to the neuron of class 4 or class 5, which lies in the signalling pathway of the muscle concerned. Via the descending projection from the cortex to the motor neuron, the muscle is excited and therefore contracts.

 

We assume that the on-tact signal is located below the on-inpuch layer. The associated activation neuron has a larger axon radius and distributes its excitation into the surrounding area.

The associated off-beat signal lands above the on-input layer, where there was the original layer of class 1 activation neurons.

Thus, the on signal of the motor clock signal is fed to the neuron column of the joint from below, while the motor off signal is fed from above. The on signal excites one of the joint's contraction muscles, the off signal excites the opposite. And since the firing rate of the motor on-stroke signal resembles a sinusoid, as being periodic, the one muscle of the joint is contracted periodically, while the motor off-stroke is contracted out of phase each time, since it is excited inversely by the cerebellum. This triggers a periodic movement in the joint.

A periodic movement of a joint (with one degree of freedom) is thus generated by the motor clock signal formed from average values.

In the case described, we had located the motor output neurons in the frontal cortex. However, this is not absolutely necessary.

Likewise, we could have located these neuron columns in the torus semicircularis. This system is connected to the basal ganglia system on the one hand and to the spinocerebellum on the other, and both were involved in the mean system. The formation of the neuronal columns in the torus semicircularis could therefore have taken place in an earlier evolutionary period, and later the frontal contex took over more specific tasks. The reason for this was the splitting of the modalities and segments above the torus semicircularis, so that certain joints received their own spatial representations in the frontal cortex and could thus be controlled separately. This expanded the possible range of movement of the vertebrate.

In any case, it could be explained why an animal whose cortex has been removed is still capable of higher movements, such as walking, if it is supported by suitable measures so that the legs can still swing freely. Here, motor control takes place in the deeper brain nuclei.