Stories that even very small structures in the brain perform important functions have not surprised anyone for a long time. But still, the realization that even smaller areas in the same structures also work differently and are responsible for many things is admirable. We have previously talked about the small but important hypothalamus and its numerous nuclei. Now it’s the turn to talk about the thalamus and its nuclei.
Thalamus. Credit: Wikimedia Commons
The thalamus, or, in other words, the visual thalamus, is a paired organ that is located between the anterior and middle sections of the brain and on the sides of the third ventricle. It is shaped like a chicken egg, 3-4 centimeters in size. Its anterior end is pointed and is sometimes called the “anterior tubercle”, and the rear end is thickened and is called the “cushion”. The thalamus is small, but occupies approximately 80% of the total volume of the diencephalon. In each of the thalami, internal, external, superior and inferior surfaces can be distinguished. The visual thalamus is associated with a large number of structures of the nervous system, including the hypothalamus, cerebellum, basal ganglia, hippocampus, cerebral cortex, and spinal cord.
The thalamus collects information from all the body's senses (except smell) and sends it to the cerebral cortex. It turns out that each sensory system has its own “representative” there - a special core. In essence, the thalamus can be imagined as a hub into which a lot of information is concentrated and then transmitted to the right recipients. It is interesting that, according to available information, not all the information that comes to the visual thalamus is sent to the cortex, but only some. The other part probably takes part in the formation of unconditioned and, possibly, conditioned reflexes.
In addition to collecting and distributing sensory information, the thalamus controls the cycles of sleep and wakefulness, is also involved in the process of memorization, and exercises conscious control over automatic movements. Regarding the latter, let us explain that this organ is the most important link in the system that provides control over our usual movements (running, walking, jumping, swimming). The thalamus also regulates consciousness because it connects the areas of the cortex that are responsible for perception with other parts of the brain and spinal cord.
As with the hypothalamus, the thalamus also has nuclei. These are clusters of nerve cells that form gray matter and have a specific function. The rest of the thalamus is filled with white matter.
Cores
Some scientists consider the term “nuclei” not entirely correct and within the structures that are so called they distinguish “subnuclei”. You can do this, or you can get by with larger structures. Therefore, we will talk about some clusters as “nuclei,” although perhaps it would be more correct to divide them into an even larger number. However, this article is not a textbook, and our goal is to simply and clearly talk about nuclei and groups of nuclei in general.
Thalamic nuclei
The group of anterior thalamic nuclei is designated in the figure as AN. They are thought to play a role in the control of wakefulness and are involved in learning and episodic memory. And they are also part of the limbic system.
The group of middle nuclei of the thalamus, or dorsomedial nucleus (MD in the figure) , occupies a fairly large volume of the thalamus and is important in the process of memorization, attention, planning, and abstract thinking. It is also involved when a person simultaneously performs many actions (the so-called multitasking, which we do not recommend to anyone). If the functioning of this nucleus is disrupted, a condition called “Korsakov's syndrome” occurs. A person stops remembering events of the present, but can more or less well reproduce memories of the past.
The ventral group of nuclei (VNG in the figure) consists of three nuclei. The first is the anterior ventral nucleus (VA), which is involved in the process of movement. It is often affected in Parkinson's disease. The second, the anterior lateral nucleus (VL), is involved in the coordination of movements and in the process of planning to make some kind of movement. It also plays a role in learning to move. This is relevant not only for small children, as you might immediately think, but also for adults who are learning to dance or swim. The third nucleus is the ventral posterior (VPL and VPM), an important part of the somatosensory system. It perceives information from touch, body position in space (or the “muscle sense” of proprioception), pain, taste, arousal, and even the urge to scratch.
The pulvinar nucleus (PUL in the picture) is responsible for visual attention. In humans, it occupies up to 40% of the thalamus, that is, it is one of the largest nuclei. If something goes wrong in it, then one-sided spatial neglect may appear - when a person’s brain does not react to what is shown from the side opposite to the affected one. For example, if there is a problem with the left side of this core, a person either does not see what is happening on the right, or cannot concentrate on what is happening. Another manifestation of a problem with the pulvinar nucleus may be attention deficit hyperactivity disorder.
The metathalamus (MTh in the figure) is represented by two formations: the paired medial geniculate bodies (MG in the figure), which play the role of the subcortical center of the auditory analyzer, and the lateral geniculate bodies (LG in the figure). The latter are exactly the same subcortical center, but this time for the visual analyzer. Both of these analyzers are connected to the centers of the corresponding analyzers in the cerebral cortex. It is believed that MGs can determine the intensity and duration of sound.
Thalamus as a putative biomarker of mental disorders
Features of thalamic morphology in various neuropsychiatric disorders can provide important information about the onset, progression and outcome of the disorder, as well as response to treatment. The maturation of the thalamus and cortex are closely linked, such that a thalamic abnormality in early neurodevelopment can impair normal cortical development (and vice versa), and, not surprisingly, pathology of the thalamus has been implicated in the neurobiology of schizophrenia. The thalamus (from the Greek word thalamos, used to refer to the innermost room, the storeroom) can be divided into dorsal and ventral divisions: the dorsal thalamus consists of nuclei that have reciprocal connections with the cerebral cortex and striatum, while the ventral thalamus does not usually send its projections into the cortex. In humans, the dorsal thalamus is a paired structure with a strategic central location between other subcortical structures and the cortex. Two separate dorsal thalami are located at the base of each cerebral hemisphere on either side of the third ventricle, respectively. The dorsal thalamus has anterior, medial, and lateral divisions defined by a curved sheet of myelinated fibers called the internal medullary lamina. These divisions are composed of different nuclei of the thalamus, and their division is based on cytoarchitecture, connectivity patterns and functionality, with these nuclei having many functions.
There are two types of neurons in the dorsal thalamic nuclei that can be distinguished by their morphology and chemoarchitecture: locally acting gamkergic interneurons and glutamatergic relay cells projecting beyond the thalamus. The physiological properties of thalamic relay nylons indicate that they may be subject to two main types of response modes that will determine the nature of the message conveyed to the cortex: the impulse response mode is thought to be used for signal detection, whereas the tonic response mode is thought to be used by the thalamus relay cells for more accurate signal analysis. It has been suggested that disruption of modulation processes (i.e., the transition from signal analysis to signal detection) may lead to aberrant saliency, such as that observed in schizophrenia.
The dorsal thalamic nuclei are thought to receive two types of afferent fibers that are classified as modulators, regardless of their origin (i.e., cortical or subcortical), and which can be identified based on their synaptic morphology and postsynaptic actions. In this sense, drivers are essentially those afferents to the thalamus that carry the message conveyed by the thalamocortical cells, whereas modulators are essentially the afferents to the thalamus that influence how that message is conveyed by those thalamocortical cells. Thalamic nuclei can be classified according to the afferents they receive. The primary (or primary) nuclei receive their drivers from a peripheral or subcortical structure and receive their modulators from pyramidal cells in layer VI of the ipsilateral cortex. In this circuit, visual, somatosensory, and auditory afferents send peripheral sensory information to the first-order nuclei of the thalamus. On the other hand, higher order nuclei (or associations) receive their drivers from pyramidal cells located in layer V of the ipsilateral cortex. In this scheme, higher order relays transmit messages from one cortical area to another, for example, regarding output to motor or premotor centers from a cortical area. Just as sensory information passes through first-order nuclei on the way to the cortex, so cortico-cortical information passes through higher-order nuclei (with direct cortico-cortical pathways providing some other function, for example, modulatory); which challenges the traditional view of cortico-cortical signaling. With respect to the response mode of relay cells in higher order nuclei, burst and tonic modes are thought to be used in a similar way: burst mode can be used to indicate a shift in output pattern in transtochostic cortico-cortical connectivity (from one cortical area to another ), and the tonic mode is then turned on by higher order relay cells to more reliably transmit information to another area of the cortex. It should be noted that research shows that higher order nuclei have more discontinuities than first order relays. Although limited, available evidence suggests that drivers for higher-order relays originate from several different cortical regions, suggesting that relays are likely to represent several different functions. At least half of the thalamus is involved in transtochastic cortico-cortical communication, implying that disruption of this type of signaling may affect higher cortical functions. The function of the thalamo - cortical inputs to the cortex (both in the first and higher order) may be to update the cortex in the latter upon motor commands.
Traditional imaging has depicted many of the afferent and efferent connections of the thalamus, including afferent connections for first-order nuclei, as well as topographically organized first- and higher-order thalamo-cortical and cortico-thalamic pathways. Trans-synaptic neurodegeneration has been noted as a mechanism of neurodegenerative disease, in which deafferentation from cortical neurons can lead to synaptic dysfunction and hence the spread of neuronal pathology throughout vulnerable neural networks. This may be one of the mechanisms that leads to subcortical pathology, such as neuronal loss in neurodegenerative diseases, as evidenced by striatal lesions in Huntington's disease (HD), frontotemporal dementia (FTD), and Alzheimer's disease (AD). Given the topographical connectivity of the thalamus to the cortex, one would predict that the thalamus could serve as a map of structural changes in cortical afferent pathways in various neurodegenerative diseases.
From a neural circuit perspective, there are a number of well-defined anatomical loops associated with the thalamus. For example, the frontal-striatal thalamo-cortical loop lines are thought to form the core network through which motor activity and behavior are mediated and may explain the similarities in behavioral changes between frontal cortical and subcortical disorders. The thalamus is a critical center in these networks. It is hypothesized that cortico-subcortical lesions in neurodegenerative disease processes may uncouple these circuits and this underlies manifest neuropsychiatric dysfunction such as the cognitive and behavioral impairments seen, for example, in FTLD. Likewise, dysfunction of the cerebellar locular pathways is also associated with neuropsychiatric disease. Disruption of neural circuits connecting the cortex, thalamus, and cerebellum may play a significant role in the pathogenesis of schizophrenia, suggesting that disruption of this circuit may be dependent on emotional and cognitive dysfunction.
With the exception of most olfactory inputs, all sensory tracts on their way to the cerebral cortex first pass through the dorsal thalamus. The function of the dorsal thalamus was thought not to be limited to transmitting information, and indeed it has been described as a "gateway" to the cortex. In terms of the current conceptualization of thalamic function, the thalamic relay is thought to function as an interlocking gate (rather than a multi-message integrator) with its component relay cells transmitting the message from their afferent movement (whether cortical or subcortical) to the cortex; signaling occurs in either pulsed or tonic modes, although with slight variations. It's not entirely clear what benefit persists when information is sent through the thalamus before it reaches the cortex. In conceptualizing the role of the thalamus in neuropsychiatric disorders, it is useful to consider failure of neural circuits associated with the thalamus rather than neuropsychiatric symptoms arising directly from the thalamus itself. The role of thalamic pathology in the disease state might then be considered a failure of its relay functions or a gating abnormality that acts on the messages it receives.
In schizophrenia, there is a volumetric deficit in the thalamus relative to brain size, and thalamic size has been shown to negatively correlate with the severity of schizophrenia symptoms. Thalamic volume deficits have been reported in first-episode psychosis, in patients poorly medicated for schizophrenia, and in those patients taking antipsychotic drugs, and there is conflicting evidence about whether thalamic volume increases with antipsychotic treatment.
If something breaks
As you may have noticed, the thalamus has a complex structure and its functions are varied, therefore, if one of its parts begins to work incorrectly, completely different symptoms may appear. And if changes occur in the functioning of the thalamus, this can affect the functioning of the entire organism as a whole. After all, he plays such an important role as a redistributor. For example, anterograde amnesia may begin, in which a person forgets events that occurred after the onset of the disease. At the same time, the memory of what preceded the onset of symptoms remains intact. Another rare disorder affecting the thalamus was first described in 1979. This is "fatal familial insomnia." If a certain mutation has occurred in the PRPN gene, amyloid plaques begin to accumulate in the area of the thalamus that regulates sleep. Due to the improper functioning of this department, a person stops sleeping. A mutation in a gene is transmitted through the pedigree, which is why the name contains the word “family.” Known in only about 40 families worldwide and owned by 100 people. There is another type, this is “sporadic fatal insomnia,” which also has no special treatment, and the cause of which is also the malfunction of the thalamus.
To treat some diseases that affect the thalamus, electrodes are used that are implanted in the brain and can stimulate a certain part of it. For example, it is used to relieve symptoms of Parkinson's disease. The method is invasive and changes electrical activity, therefore magnetic resonance imaging is contraindicated for patients with such stimulators. But stimulation can be stopped at any time and the electrodes can be removed. A more drastic solution is surgical intervention, when certain areas of the thalamus are deliberately destroyed - thalamotomy. It is used to treat tremors in Parkinson's disease.
Text: Nadezhda Potapova
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