ISBN
978-3-00-064888-5
Monograph of Dr. rer. nat. Andreas Heinrich Malczan
The principles of action of the amygdala and the limbic system presented in this and the following chapters are mainly based on the structural investigations that can be found in the publications of Asla Pitkänen and Maria Pikkarainen on the projection paths of the different amygdala nuclei in [71] and [72], but also in the work of Aggleton [76] and Saunders on the amygdala. Without this preliminary work, the description of the presumed functioning of the neuronal circuitry of the amygdala and its subnuclei in this monograph would never have been possible.
An important early form of analysis of the Bilateria, the Chordata and the vertebrates consisted of motion analysis. For example, movements could be seen, smelled or even heard.
Why was motion detection so important?
With the development of the most different mouth tools - beginning for example with the rasp tongue, refined by the transformation of gills to jaws and the use of animal food, there was a new danger: the predator. Animals themselves became prey.
Prey animals and predators could move actively. Anyone who saw, smelled, heard, felt or even electrosensitively detected movement had a clear advantage. They found their prey more easily and could avoid predators.
One prerequisite was the creation of an image of the environment. Receptors formed surfaces - such as the retina of the eye, or the tactile receptors of the body surface, but also the olfactory surface of the nasal mucosa - and the excitation of these receptors created a signal image of the environment in this surface. This signal image was transmitted via various - mainly geometrically acting - transformations directly to the existing body images of the neural tube and the cortex and could interact with them. In particular, it could influence the body image of the muscle spindle signals and trigger suitable movements. Prey could be recognized and eaten, predators could be avoided.
The created images of the environment could in turn contain images of the most diverse objects. The detection of a movement of these objects required two images whose creation time differed from each other. If the two images were combined in a differential image, whereby the signals of one image were exciting, but those of the other were inhibiting, all motionless objects disappeared in the differential image. The objects that had moved in the meantime remained. The difference signals and their strength were a measure of the strength of the movement with respect to the size of the object and the object speed. In the amygdala such difference images were generated. The formation of motion-detecting difference images for analog signals has already been described.
It would go beyond the scope of this monograph if we were to analyze all types of motion-detecting differential imaging in the amygdala. We will limit ourselves here to the visual difference imaging that allowed us to detect movements of visual objects. A basic prerequisite for this was created by the early rope ladder system, which was present on both sides of the body. The visual differential imaging in the amygdala was therefore initially monocular.
As already explained in chapter 3.13., complementary signal classes were developed in the visual system, where one signal class was on-type and the other off-type. The reason was the signal inversion at the band synapses of the responsible retinal receptors.
The amygdala system was able to implement visual motion detection for both the visual on-signals and the off-signals at a very early stage.
For this purpose, both signal classes were first sent from the amygdala to the dopaminergic mean value centre, which in this case was the area tegmentalis centralis. There the switch to dopamine took place. The rear projection towards the origin of the signals ended at the GABAergic neurons of the central amygdala. As with the matrix neurons, these had the dopamine receptor D2, so that there was a neuron population of GABAergic neurons in the central amygdala which were inhibited by the dopaminergic signals.
A residual excitation was only left because these neurons received a tonic excitation from the mean nucleus of the amygdala, i.e. the magnocellular nucleus of the amygdala. The inhibition of this mean excitation caused a signal inversion. Therefore, this population of neurons became inversion neurons.
Due to the signal inversion every on-signal became an off-signal. It was now inhibiting. So it could become the inhibiting component of the time sensitive difference mapping. It reached the basal amygdala subcore and docked the differential neurons there in a point-to-point projection.
The excitatory off-signal of the retina reached via the lateral amygdala and the basal amygdala also the initial nucleus, the basal auxiliary nucleus of the amygdala and also ended in a point-to-point connection to the associated differential neurons. This resulted in the time-sensitive differential mapping for the off-signal type, which detected the movement of dark objects, for example.
For the off-signal of the retina, the same applied analogously. It was time-delayed and transferred to the on-signal type, which was also inhibitory. The original excitatory output of the retina was superimposed on the inhibitory on-signal in the basal amygdala subcore, thus creating a time-sensitive differential image which, for example, detected the movement of bright objects.
If the on-off signal consisted of the colour signal red+/green- and the off signal of the complementary signal red-/green+, the movement of red and green objects could be detected independently of each other.
This enabled the amygdala to analyse the movements of objects whose images were provided by all visual receptors that were of the on-off type.
A delay and switch-over core was required for this, here the VTA. Furthermore, a mean nucleus was needed, in the amygdala this was the magnocellular basal nucleus. An inversion core was also needed, this was the central core of the amygdala. Finally, a difference nucleus was also needed for the difference mapping, this was provided by the basal sub nucleus of the amygdala.
The basal subcore of the amygdala is a descendant of the basal nucleus. It consists of excitatory projection neurons. The excitatory input comes from the input nucleus of the amygdala, which arrives in the lateral nucleus and reaches the basal side nucleus via the basal amygdala. On its way through the basal amygdala it is included in the averaging process of the magnocellular basal nucleus.
The inhibiting input reaches this core from two sources. Both the central amygdala and the medial amygdala project inhibitory input into the basal amygdala. The basal amygdala auxiliary nucleus is the differential nucleus of the amygdala system and serves to form differential images of the different modalities and thus to recognize movement and change.
The output of this nucleus is excitatory and contains in the early stage of the amygdala, among other things, the optical monocular differential mapping of the visual on-off signals (brightness/color) in a topologically well-ordered form.
If a signal type is present in the on-off variant, the formation of a time-sensitive differential image for motion detection for this modality in the amygdala takes place through the involvement of the VTA, the central amygdala, the magnocellular nucleus of the amygdala and the basal auxiliary nucleus of the amygdala.
At first, the signal projection takes place from the lateral amygdala on the one hand to the basal amygdala and on the other hand to the basal auxiliary nucleus of the amygdala, in both cases the signals were present in the excitatory form.
From the basal amygdala a point-to-point projection to the VTA is performed. In one neuron layer the on-signals arrive, in the adjacent one the off-signals. The retinotopia is preserved.
TheVTA acts as a delay and changeover core. After switching to dopamine, there is an inhibitory projection into the central core of the amygdala, the off-signals contact a layer of inhibitory neurons, the on-signals also. The retinotopia is also maintained here.
The neurons are inhibited by the dopaminergic signals of the VTA because they possess - like the matrix of the striatum - the dopamine receptor D2.
In addition, these neurons receive tonic mean excitation from the magnocellular basal nucleus of the amygdala. This leads to signal inversion.
The on signal becomes an off signal, the off signal becomes an on signal. Both types are inhibitory and form the inhibitory and time-delayed component of the differential mapping that occurs in the basal amygdala's secondary core. There, the inhibitory on-signal from the central amygdala is superimposed with the excitatory on-signal from the retina, so that all moving objects remain of signal type on. Likewise, the inhibitory off signal from the central amygdala is superimposed with the excitatory off signal from the retina, so that all moving objects of signal type off remain. All images are topologically accurate 1:1 images of the retinal signals.
Unmoving objects cancel each other out in the difference mapping and are invisible.
Since both the brightness signals and the colour signals of the red/green channel are present in an on and off variant, the amygdala can detect the movement of light, dark, red and green objects. In the differential images, the output neurons are (in principle) active exactly where movement was visually perceived. The output controls the motor neurons assigned to it and causes motor responses to visually perceived movements.
The output of the amygdala reached the hippocampus where it participated in the signal rotation. This made the images of all newly recognized objects permanently available, as they rotated in the limbic loop until new objects deleted them or deletion commands externally from time clocks or other systems reached the amygdala and interrupted the signal rotation.
Since the ascending signals of the VTA not only reached the amygdala but also (via collaterals) contacted the nucleus accumbens, they found their way into the basal ganglia system. They were treated as described in chapter 3.13. Finally, a differential mapping for these signal classes was also created in the thalamus.
The signals of the on-off signal types sent from the amygdala to the VTA also reached the nucleus accumbens from there. They ended at GABAergic shell neurons, which used the dopamine receptor D1 and were inhibited by dopamine. Since they also received tonic signals from the substantia nigra pars compacta and especially from the nucleus subthalamicus, they acted as inversion neurons. The inverted signals were inhibitory and reached the (ventral) thalamus, where they were type-correctly superimposed with the same signals that reached this thalamus in descending order from the amygdala. This made type-correct differential imaging possible, in which movements of the objects assigned to these signal types became visible. The difference image reached the cortex via the thalamus where it could be further evaluated.
But there was a huge difference. In the thalamus, these signals existed only for a short time, only for the moment the detected objects were moving. In the limbic system, the short-term output reached the hippocampus and began a signal rotation, quasi subconsciously. It reminded latently of the danger of the predator or the attraction of the food.
This signal rotation was of some importance for visual signals, especially for colored signals. The image did not disappear when you closed your eyes. Then these limbic signals in the thalamus could not be suppressed by the retinal signals just arriving by lateral neighbor inhibition, because the eyes had just been closed.
But also other signals remained quasi present in the subconscious through the signal rotation and were indirectly present. The limbic rotation system kept them alive in the subconscious.
The signals rotating in the limbic loop - which are also ordered retinotopically - finally reach the (visual) thalamus via the nucleus accumbens and produce so-called afterimages with closed eyes.
Monograph of Dr. rer. nat. Andreas Heinrich Malczan