Vertebrate brain theory

According to the author, the vertebrates developed from the segmented Bilateria. Therefore, the vertebrate brain will also have developed from the brain of the segmented Bilateria. However, only a few lines led to the vertebrates. It will be shown that one of these lines led to the mammals and all their precursors, while another line ended with the reptiles and another with the birds. As a result, the reptilian, avian and mammalian brains differ in certain structures. However, since part of the developmental path was common, they have just as many similarities.

The central nervous system of vertebrates developed gradually over the course of a development process lasting many millions of years. Even in unicellular organisms there was the ability to react to a wide range of stimuli. In multicellular organisms a specialization of cells could take place, different cell classes developed. Simplest nervous systems could develop. Receptors were able to react to stimuli and activate nerve cells. These could in turn activate muscles, which contracted. Movements became possible.

The development of receptors, nerve cells and muscles favoured the manifold reaction possibilities to external and internal stimuli.

A certain spatial concentration of similar cells was observed in contiguous cell formations, which formed organs.

We begin our theory of the origin of the vertebrate brain in the living beings of replication stage 2, which were simple multicellular organisms, formed by the independence of colonies of unicellular organisms.

As the number of cells in such organisms increased, a division of labour and specialisation of the cells began. The number of cells eventually exceeded the number of different tasks. At the same time, there was often a spatial concentration of those cells that performed the same tasks. This is how organs developed.

Spatial concentration was also possible with neurons. Such accumulations of neurons are called neuron nuclei in neurology. We interpret them here as neural organs. However, since nerve cells also had to perform different tasks, a wide variety of neuron nuclei were formed.

We will systematize these neuron nuclei of simple multicellular organisms. For the sake of simplicity, we will assume that the multicellular organisms under consideration were already bilaterally structured, because only such organisms could develop into vertebrates in the course of the long evolution. Initially, these neuron nuclei may have consisted of extremely few neurons. Only later did they become neuronal centres with a larger number of neurons.

3.1  The formation of neuronal centers in simple bilateria

The first neuronal centres emerged when nerve cells joined together to form cell clusters to perform life-supporting tasks.

receptors analysed variables that were important for the control of the various life-support systems. Thus, it was necessary to recognize, find and eat food, digest it and excrete the residual substances. Nutrients had to be taken in from food and provided throughout the body via the bloodstream, while at the same time oxygen had to be distributed and carbon dioxide removed. The heart had to adapt its pumping capacity to the respective situation, the concentration of the various substances in the blood had to be monitored and corresponding reactions had to be triggered. All these complicated regulations and controls required information of all kinds. Therefore, there were many different receptors in the body, which provided this information and passed it on to the corresponding control and regulation centres. Since this information always referred to the whole organism, the responsible receptors were spatially distributed in the body and the result was obtained by combining the signals. Therefore, mainly signal mean values were evaluated. This is why we also refer to these neuronal control centres as mean value centres. Since there were several task complexes of life assurance, several such mean value centres were also created. They differed by the use of different transmitters and are still present in the nervous system of vertebrates. In vertebrates, these mean value systems include the Formatio reticularis, the raphe nuclei, the locus caeruleus, the substantia nigra pars compacta and the area tegmentalis ventralis, but also the central amygdala, or more precisely its magnocellular part.  

Theorem of the mean value centres

In the animals of replication stage 2, neuronal control centres were formed which derived the control signals for life support from mean value signals of different receptors. Different mean value centres used different transmitters, their neurons controlled different target structures. These centres were arranged bilaterally.

By using different transmitters, the different averaging systems could control different target structures, no obstructive signal mixing occurred.

In addition to neuronal centres for the control of life-support systems, neuronal centres were also formed which served to control movement. Compared to plants, animals were able to move actively. The movement could be triggered by stimuli that were perceived via sensory receptors. These receptors excited nerve cells, which in turn activated the motor neurons. The latter led to muscle contractions, which caused motor reactions.

Therefore, the bilateral animals had two centres, one sensory and one motor centre, on each of the two halves of the body.

Theorem of the sensory and motor centre

In the animals of replication stage 2, neuronal centres were formed which served to control movement. On each side of the body there was a sensory centre and a motor centre. The neuronal signals of the receptors arrived at the sensory centre and were transferred to projection neurons of class 3, which in turn controlled the motor neurons in the motor centre. The motor neurons controlled the muscles and thus induced motor responses to stimuli.

We subdivide the neurons in the developing primordial brain into different neuron classes, to each of which we assign a class number in order to be able to distinguish them more easily in later descriptions. It should be noted here that we will find these neuron classes, six in number, in the human brain.

We assign neuron class 3 to the projection neurons in the sensory centers that project to the ipsilateral motor centers.

  Notice:

Class 3 neurons are always located in the sensory center, receive receptor signals from the respective side of the body and project to the motor neurons of the corresponding motor center of the same side of the body.

The motor neurons of the motor centre project to the target muscles on the same side of the body.

The axons of the class 3 neurons of the sensory center ran to the motor center and docked synaptically to the motoneurons, so that sensory stimuli activated the muscles via the sensory center.

In this monograph, we will refer to essential statements as theorems, each of which we will also assign its own designation. In this way, one can clearly refer to the respective statement by the designation. This is easier than specifying the page number or unclear paraphrases.

We assume that the growth direction of axons was controlled by the concentration gradient of markers. In this respect, we can assume the existence of a sensory marker that directed the growth direction of axons of receptors or mediating neurons towards the sensory center. Similarly, there may have been a motor marker that directed the axons of class 3 neurons from the sensory to the motor centre. Further motor markers guided the axons of the motor neurons to the target muscles.

Each (motor receptor) formed the beginning of a signaling pathway that ultimately ended at the muscles. It can be assumed that there were only very few muscles in the initial phase, possibly the first muscle was a ring muscle at the throat.

Since the signal strength of the sensory and motor signals also had to be considered in the life support control systems, these signals were also needed in the mean value centres. The signal transmission was carried out by special projection neurons of class 6, which established a separate class of neurons in these two centers.

Theorem of projections to the centres of mean

In the motor and sensory centers, neurons class 6 were created, whose neurons integrated the excitation and projected to the different mean centers of the system. In this way, they also received information about the mean sensory and motor excitation and were able to take this into account in the control signals for the life-support systems.

The mean value centres not only controlled the life-support systems, but could also have an effect on sensors and motor functions, as well as on other subsystems. For example, it made sense to activate the sensory receptors - in particular the olfactory sensors - in the event of a lack of energy in order to make it easier to find existing prey. The activation raised the sensitivity threshold. The mean value centre responsible for energy evaluation excited the odour sensors, but only subliminally. This pre-excitation made them more sensitive. Analog signal feedback was also provided by the other averaging systems. A special signal feedback in the human brain is caused by the ascending reticular activation system (ARAS), which activates the cortex from the reticular formation and via the thalamus.

Theorem of the feedback of the mean value excitation

In the sensory and motor centre, neuron class 1 developed, which used an excitatory transmitter. The mean value signals of the different mean value centers were transmitted from these centers to class 1 neurons located in the sensory center and in the motor center, respectively. These transmitted this mean value excitation to the class 3 neurons or to the motor neurons, so that these were subject to additional pre-excitation. This was not sufficient to trigger action potentials, but increased the response threshold. Thus, internal conditions in the system could cause neuronal activation, which ultimately also affected the sensors and motor functions.

We assign easily understandable names to such inner states, for example hunger or thirst. Hunger as an inner state could be interpreted as the excitation of receptors that evaluated the energy supply and, when it decreased, produced a neuronal excitation that in turn activated the motor function, sharpened the sense of smell and stimulated a search for food. A feedback effect of inner states on motor function can already be demonstrated in unicellular organisms, even if it is not realized there by neuronal signaling pathways. Since there were different mean value centres specialising in different tasks, there was in principle such an activation of the motor and sensory centre by everyone.

With the formation of inhibitory interneurons, it became possible that mean value centers could not only excite but also inhibit the sensory and motor functions. This should become more important in the development of striatum in the basal ganglia. Here we first consider the excitatory effect of mean-value centers on sensory and motor functions as an example.

A particular advance began with the development of inhibitory interneurons. They formed in all neuronal nuclei and caused stronger signals to inhibit the weaker ones. This led to an increase in contrast in the signals, with the stronger signals dominating the output.

Theorem of lateral inhibition for contrast enhancement

Within all neuronal centers, inhibitory interneurons were formed which caused lateral inhibition. As a result, stronger signals were preferentially passed on, while weaker ones were weakened or even completely suppressed by the stronger ones.

The range of action of these interneurons was generally limited to the respective centre in which they were located. Only projection neurons were capable of transmitting excitations from one neuronal center to another.

Such inhibitory interneurons were formed in both the sensory and motor centre, as well as in all mean value centres.

We therefore assume that, from a certain evolutionary stage of development onwards, there were inhibitory interneurons in the sensory and motor centres, as well as in all mean-value centres.

In the course of evolution, the inhibitory interneurons acquired a new, additional function in bilateria when a signal exchange developed between similar centres on the left and right side of the body. In this case, an exciting projection to the contralateral, similar centre took place. However, this did not end at the mirror image projection neurons, but at an inhibitory interneuron, which in turn inhibited this mirror image projection neuron. This applied firstly to the two motor centers, which now inhibited each other in a 1:1 projection. Secondly, this contralateral inhibition occurred in the two sensory centers. Thirdly, we assume that this contralateral inhibition was also present in the bilaterally present mean value centers. In this case, however, one center does not inhibit all contralateral averaging centers, but only the mirror image center with the identical work task. The projection to the corresponding contralateral neuron center was realized by projection neurons, to which we assign neuron class 2. The inhibition strength was certainly low in the beginning and increased step by step in the course of evolution.

Theorem of contralateral inhibition in unsegmented bilateria

Summary: Nervous system of simple Bilateria

Class 3 neurons were located on both sides of the body in a sensory center and projected into the ipsilateral motor center.

Motor neurons received the excitation of the ipsilateral sensory center and projected to the target muscles.

In the sensory and motor centre, class 6 neurons took over the excitation there and projected into various ipsilateral mean value centres, which evaluated these signals for the life support systems.

In the sensory and motor centre, class 1 neurons received a pre-excitation from the ipsilateral mean value centres, passed it on to the existing projection neurons and thus raised the activation threshold of the projection neurons without generating action potentials.

In the sensory, motor and mean value centers, inhibitory interneurons provided lateral inhibition and caused contrast enhancement of the signals.

Between each neuronal center and its contralateral counterpart there was a contralateral inhibition, which was realized via excitatory projection neurons of class 2 with downstream inhibitory interneurons.

Contralateral inhibition affected both sensory and motor signals as well as the mean value signals.  

This nervous system in the simple Bilateria of replication stage 2 forms the basis for the nervous system of the segmented Bilateria, which have developed via the intermediate stage of budding and colony formation. These segmented bilateria were living beings of replication stage 3, where during embryonic development in the process of budding, the neuronal centres of a segment were neuronally linked to the neuronal centres forming in the new bud. Thus the nervous system of the segmented bilateria was created.