Theory of the neuronal circuity of the brain and analytical thinking

ISBN 978-3-00-037458-6
ISBN 978-3-00-042153-2

Monograph of Dr. rer. nat. Andreas Heinrich Malczan

Part 2.4 Compartmentalization of the neural system of the brain

A closer examination of the striatum revealed the parallel existence of two systems. On the one hand the striatum consists of the matrix. Its main neurons are excited by the cortex output and have huge dendritic fields that tap the cortex output. From the substantia nigra pars compacta, dopaminergic axons move to these main neurons and inhibit them, since these matrix main neurons possess the D2 receptors.

On the other hand, so-called striosomes are embedded in this matrix, similar to raisins in a cake. They form a coherent skeleton that seems to run through the matrix. The axons, which grow from the substantia nigra pars compacta, have a stimulating effect on these main neurons, as the D1 receptors are now active.

Such a dichotomy of the spatial system has system-theoretical causes, as this monograph has shown. The striosomes represent the magnocellular mean system of the brain. Within this system, a climbing fibre signal is generated - depending on the excitation situation in the associated cortex cluster. It leads to the automatic storage of new signal combinations of the cortex cluster in the associated cerebellum cluster. If the current signal combination is already known to the cerebellum, the Purkinje cell whose own signal best matches the input will inhibit the transmission of the active climbing fibre signal from the olive to the cerebellum cluster. This prevents multiple storage of this signal combination.

The signal neurons of the cortex clusters belong to the parvocellular system of the brain. These-these are represented in the striatum by the matrix. Significantly, there is a previously unexplained projection of the matrix into the striosomes. It is realized by the transmitter acetylcholine. This transmitter also enables the visualization of the two subsystems. The matrix is rich in acetylcholine, while this transmitter hardly exists in the striosomes. Therefore, the division of the striatum into matrix and striosomes could be made visible by suitable methods.

Both areas - matrix and striosomes - receive input from the substantia nigra pars compacta. Therefore, for a long time it was assumed that the compartmentalization of the striatum could be found in the substantia nigra pars compacta.

This assumption was supported by the finding that the substantia nigra pars com-pacta contains two subtypes of neurons. One population - the subtype D1 - has an excitatory effect on the main neurons of the striosomes. The other population of nigra pars com-pacta belongs to subtype D2 and has an inhibitory effect on the matrix neurons.

The recent dissertation by Marlene Kanter, submitted to the Medical Faculty of the University of Leipzig in 2010 and supervised by Professor Thomas Arendt, is well worth reading. It examines the question of which organisational principles are present in the substantia nigra of the human being and what relationship there is to Parkinson's disease. Chapter 5.2 "Nigrostriatal projections" explains that the substantia nigra is compartmentalised into nigrosomes and matrix. On the one hand, there are contiguous areas, which are called nigrosomes. In the rat, five such nigrosomes are called nigrosomes. The already analogous compartmentalization of the striatum into strio-somes and matrix is pointed out.

Compartmentalization of the substantia nigra in the rat brain was achieved by the calbidine method described by Damier et al (1999). (Quote from the paper - page 61:) "The calbidine-positive neuropil of the SN (substantia nigra) also appears to be formed by the afferent fibres of the gabaergic striatal neurons (Kiyama et al, 1990). Since the distribution of substance P is very similar to that of calbidine in SN, it appears to be almost the same polarity of projection neurons. The notch in the substance P-positive neuropil corresponds in part to the nigrosomes in the calbidine-positive neuropil" (end of quote)

Although this compartmentalisation in the rat brain is not directly transferable to humans because there are no calbidin-positive neurons in the substantia nigra of the human brain, the division into nigrosomes and matrix is nevertheless safe. Here, the striosomes of the striatum seem to correspond to the nigrosomes of the substantia nigra, while the striatal matrix corresponds to the nigral matrix.

This is particularly interesting with regard to the degenerative processes in basal ganglia diseases. In theory, the magnocellular system is the evolutionarily older one. This is at least the view of the author of this monograph. Only much later the parvocel-lular layers of the cerebral cortex seem to have developed.

The cited dissertation by Marlene Kanter describes how the nigrosomal neurons of the substantia nigra suffer a greater loss of neurons in Parkinson's disease than the matrix of the substantia nigra. This is what we read on page 63 of this dissertation (beginning of quotation):

"There was found to be more neuronal loss in the nigrosomes than in the matrix...

 (end of quote) 

It seems, therefore, that in Parkinson's disease the degeneration of the nigral neurons begins in the evolutionarily older subsystem - the nigrosomes.

Since the nigrosomes have been assigned to the magnocellular system and the magnocellular system of the brain generates the climbing fibre signals for learning the future own signals of the associative matrix in the cerebellum, this sub-system collapses completely in case of neurodegeneration. This is associated with a loss of learning ability. However, not only the intellectual ability to learn is lost. The formation of associations also has a motor component. Motor learning ability belongs to it.

And it is above all the intellectual and motor short-term memory, which is represented by the magnocellular system of the brain.

It should not be forgotten that according to the author's theory, the magnocellular system is also responsible for the recursive resolution pyramid. From the original image of the world using sensors, the magnocellular system produces reduced images with lower resolution. These become - as will perhaps be shown later - the basis for the recognition of identical objects of different sizes. An object, viewed from different distances, is stored several times within this recursive system and its different sized images are later used for recognition. This is very important for orientation in space, for example.

Therefore, with the demise of the neurons in the nigrosomes, the cognitive abilities to recognize objects are partially lost, as is the ability to orientate in space and time.

Researchers need to clarify which circuitry causes the nigrosomal degenerations. One possibility would be the deterioration of the magnocellular signal flow. A demyelination of the axons of the large mean neurons of layer V would be a conceivable cause. The shrinking of the isolating myelin layer would greatly reduce the range of the mean value signals. Given the large spatial distance between the cerebral cortex and substantia nigra pars compacta, the attenuation would be too great, so that no action potential would be able to overcome this distance.

In this monograph the connections of the magno- and parvocellular system with the system of the amygdala are not presented due to time constraints. Nevertheless, these do exist. However, they are so extensive that a separate presentation is required. The reader is therefore put off until later. Those who cannot stand it out of curiosity can support the work of the author. There are many possibilities. Even the burden of the author's daily professional activity as a system administrator ties up a huge amount of possible resources. Here, those companies could act as sponsors who profit from the scientific results of this private research work without ever having invested anything in it. The translation of this monograph into English alone will cost the author a fortune. But printing by a printing house also costs a huge amount, without the author being able to benefit from it in any way. Until now, not even someone was willing to check this work for typing errors and correct spelling.

ISBN 978-3-00-037458-6
ISBN 978-3-00-042153-2

Monografie von Dr. rer. nat. Andreas Heinrich Malczan