black substance (SN listen)) is a basal ganglion structure located in the brain that plays an important role in reward and movement. black substance is Latin for "black substance", which reflects the fact that parts of the black substance appear darker than in neighboring areas, due to high level neuromelanin in dopaminergic neurons. It was discovered in 1784 by Vic d'Azire and Samuel Thomas Sömmering referred to this structure in 1791. Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta.
Although the substantia nigra appears as a continuous band in sections of the brain, anatomical studies have shown that it actually consists of two parts with very different connections and function: Pars compacta (SNPC) and Pars reticula (SNpr). This classification was first proposed in 1910. Sano pars compacta serves primarily as an output signal to the base ganglion circuit, supplying the striatum with dopamine. Pars reticulo, though, serves primarily as input, relaying signals from the basal ganglia to many other brain structures.
Compound
Scheme of the main components of the basal ganglia and their relationship
Pars geisia
Pars reticulio bears a strong structural and functional resemblance to the interior of the globus pallidus. The two are sometimes considered part of the same structure, separated by the white matter of the internal capsule. Like the globus pallidus, the neurons in Pars reticulata are mostly GABA.
Afferent connections
The main contribution to SNpr comes from the striatum. It is delivered via two routes known as direct and indirect routes. The direct pathway consists of axons from the middle spiny cells in the striatum, which project directly to Pars reticula. The indirect path consists of three links: a projection from the striated environment of spiny cells to the outer part of the pale ball; GABAergic projection from the globus pallidus to the hypothalamic nucleus and glutamatergic projection from the subthalamic nucleus to the parsa reticulum. Thus, activity in the striatum via the direct pathway has an inhibitory effect on neurons in (SNpr) but an excitatory effect via the indirect pathway. The direct and indirect pathways originate from different subsets of the striatal medial spiny cells: they are tightly intertwined but express Various types dopamine receptors, and also shows other neurochemical differences.
Efferent connections
Significant projections occur to the thalamus (ventral lateral and anterior ventral nuclei), colliculus, and other caudal nuclei from the nigrothalamic pathway, which use GABA as their neurotransmitter. In addition, these neurons form up to five collaterals that branch into both pars compacta and pars reticulla, likely modulating dopaminergic activity in pars compacta.
function
The substantia nigra is an important player in brain function, specifically in eye movement, motor planning, reward-seeking, learning, and addiction. Many of the substantia nigra's effects are mediated through the striatum. The dopaminergic substantia nigra is introduced into the striatum via the nigrostriatal pathway closely related to the striatum's function. The co-dependence between the striatum and the substantia nigra can be seen as follows: with the substantia nigra electrically stimulated, no movement occurs; however, the symptoms of nigral degeneration associated with Parkinson's disease is a bitter example of the effect of substantia nigra on movement. In addition to striatum-mediated functions, substantia nigra also serves as a major source of GABAergic inhibition to various brain targets.
Pars geisia
Pars compacta
The most prominent feature of pars compacts is engine control, although the role of the substantia nigra in engine management is indirect; electrical stimulation of the substantia nigra does not result in movement, due to the mediation of the striatum in the nigral influence of movement. Pars compacta sends excitatory input to the striatum via the D1 pathway, which excites and activates the striatum, resulting in the release of GABA on the globus pallidus to inhibit its inhibitory action on the thalamic nuclei. This causes the thalamocortical pathways to become excited and signal motor neurons in the cerebral cortex to allow movement initiation, which is absent in Parkinson's disease. However, the absence of pars compact neurons has a major impact on movement, as evidenced by the symptoms of Parkinson's disease. The engine role of pars compacts may include precise control motor, as has been confirmed in animal models with lesions in this area.
Pars compacta are actively involved in reflexes to stimuli. In primates, dopaminergic neurons increase activity in the nigrostriatal pathway when a new stimulus is presented. Dopaminergic activity decreases with repeated stimulus presentation. However, the behaviorally significant presentation stimulus (i.e. reward) continues to activate dopaminergic neurons in the substantia nigra pars compacta. Dopaminergic projections from the ventral tegmental area (lower part of the "midbrain" or midbrain) to the prefrontal cortex (mesocortical pathways) and into the nucleus accumbens (mesolimbic pathway - "meso" in reference to "of the mesencephalon" ... specifically, the ventral area tires) are involved in reward, pleasure, and addictive behaviors. Pars compacta is also important in spatial learning, observing one's environment and location in space. Lesions in the pars compacta lead to learning deficits in repeating similar movements, and some studies point to its involvement in a dorsal striate-dependent memory-based response system that functions relatively independently of the hippocampus, which is traditionally thought to promote spatial or episodic-like memory function.
Pars compacts also play a role in timing processing and are activated during playback time. Lesions in the Pars compacta result in a temporary deficit. Recently, Pars compacta has been suspected of regulating the sleep-wake cycle, consistent with symptoms such as insomnia and REM sleep disorders reported in patients with Parkinson's disease. However, partial dopamine deficiency that does not affect motor control can lead to disruption of the sleep-wake cycle, especially REM-like patterns of neural activity during wakefulness, especially in the hippocampus.
Clinical Significance
The substantia nigra is critical in the development of many diseases and syndromes, including parkinsonism and Parkinson's disease.
Parkinson's disease
Parkinson's disease is a neurodegenerative disease characterized, in part, by the death of dopaminergic neurons in the SNPC. The main symptoms of Parkinson's disease include tremor, akinesia, bradykinesia, and stiffness. Other symptoms include disturbances in posture, fatigue, sleep disturbances, and depressed mood.
The cause of dopaminergic neuron death in SNPC is unknown. However, some contributions to the specific sensitivity of dopaminergic neurons in pars compacta have been identified. On the one hand, dopaminergic neurons show abnormalities in the mitochondrial complex 1 , causing alpha-synuclein aggregation; this can lead to incorrect protein turnover and neuronal death. Secondly, dopaminergic neurons in pars compacta contain less calbindin than other dopaminergic neurons. Calbindin is a protein involved in calcium ion transport within cells, and excess calcium in cells is toxic. The Kalbindin theory explains the high cytotoxicity of Parkinson's in the substantia nigra compared to the ventral tegmentum. Regardless of the cause of neuronal death, the plasticity of Pars compacta is very reliable; Parkinson's symptoms do not appear until up to 50-80% of pars compacts of dopaminergic neurons have died. Much of this plasticity occurs at the neurochemical level; the dopamine transport systems are slowed down, allowing dopamine to linger for longer periods of time at the chemical synapses in the striatum.
Menke, Jbabdi, Miller, Matthews, and Zarya (2010) used the diffusion tensor, as well as T1 imaging, to estimate volumetric differences in SNPC and SNpr in participants with Parkinson's disease compared to healthy individuals. These researchers found that participants with Parkinson's disease consistently had less substantia nigra, specifically in SNpr. Because SNpr is connected to the posterior thalamus, ventral thalamus and, specifically, the motor cortex, and because participants with a report of Parkinson's disease having smaller SNprs (Menke, Jbabdi, Miller, Matthews, and Dawn, 2010), a small volume of this region may be responsible for the movement disorders found in patients with Parkinson's disease. This small volume may be responsible for weak and/or less controlled motor movements, which can lead to the tremors often experienced by those with Parkinson's disease.
Schizophrenia
Elevated levels of dopamine have long been implicated in the development of schizophrenia. However, much debate continues to this day around this dopamine hypothesis of schizophrenia. Despite controversy, dopamine antagonists remain the standard and successful treatment for schizophrenia. These antagonists include the first generation of (typical) antipsychotics such as butyrophenones, phenothiazines, and thioxanthenes. These drugs have largely been replaced by second generation (atypical antipsychotics) such as clozapine and paliperidone. It should be noted that, in general, these drugs do not act on dopamine-producing neurons per se, but on receptors on the postsynaptic neuron.
Other, non-pharmacological evidence in favor of the substantia nigra dopamine hypothesis includes structural changes in parse compacta, such as a decrease in synaptic terminal size. Other changes in the substantia nigra include increased expression of NMDA receptors in the substantia nigra as well as a decrease in Disbindin expression. An increase in NMDA receptors may indicate the involvement of glutamate-dopamine interactions in schizophrenia. Disbindin, which has been (controversially) associated with schizophrenia, may regulate dopamine release, and low expression of Disbindin in the substantia nigra may play an important role in the etiology of schizophrenia. Due to changes in the substantia nigra in the schizophrenic brain, it may eventually be possible to use special imaging techniques (such as neuromelanin-specific imaging) to detect physiological signs of schizophrenia in the substantia nigra.
Wooden chest syndrome
Shortly thereafter, MPTP was tested in animal models for its effectiveness in inducing Parkinson's disease (with success). MPTP induced akinesis, stiffness, and tremor in primates, and its neurotoxicity has been found to be very specific to the substantia nigra pars compacta. In other animals, such as rodents, Parkinson's induction of MPTP is incomplete or requires much higher and more frequent doses than in primates. Today, MPTP remains the most favored way to induce Parkinson's disease in animal models.
story
Additional images
Not a single animal suffers from this disease - you will not see a cat or a mouse with a trembling paw. And since the origins of the disease are unclear, there is no complete cure. You asked about the starting point, the very first "call" that marked trouble. Once, on the way to the country house, we stopped at the market. I remember choosing a melon, the seller suddenly became rude. My husband's hand suddenly trembled - and it has been trembling for 11 years. The hospital said, "Parkinson's disease." We opened medical books, reference books and made sure that such patients are long-lived and that this disease is incurable throughout the world."
There are not many specialists in Russia who are closely "familiar" with the disease, which has become a personal enemy for Margarita Vasilievna and her husband. Nikolai Nikolayevich YAKHNO is the head of the Clinic of Nervous Diseases of the I. Sechenov Moscow Medical Academy. He has been dealing with the problem of Parkinson's disease for many years.
- Nikolai Nikolaevich, this ailment in many respects remains a mystery to medical science. But lately it has received a lot of attention all over the world. What is the reason for this interest?
- Parkinson's disease is a fairly common disease. There are about four million such patients in the world, in Russia about 300 thousand people suffer from this disease. Indeed, in different countries the most active studies of the causes of the disease and the search for ways to treat it are being conducted. This is partly due to the fact that the proportion of older people in society is growing, which means that there are more and more patients with Parkinson's disease, because most often people get sick with Parkinson's disease over the age of 60 years.
Its study began at the beginning of the twentieth century. Then for the first time it was shown what happens with this disease. In the human brain there is a certain nucleus of nerve cells. It is called substantia nigra because it actually looks like a dark spot when cut. So, in Parkinson's disease, the number of these cells decreases dramatically. Why this happens is not fully understood. But there are ways to at least partially correct the defect. In the 1950s, it was discovered that this disease affects Chemical substance necessary for the full functioning of the brain: dopamine. The search began for a drug that could replace it. So the drug appeared: levodopa. When it was created, the newspapers wrote: "Insulin for parkinsonism found." It seemed that the situation is similar to the situation with diabetes - after all, insulin allows you to live with the disease for a very long time and relatively fully. Unfortunately, it soon became clear that this was not the case. First, like all drugs, levodopa has side effects. But most importantly, after a few years of using the drug, very serious complications can occur. The disease itself gives rise to a lot of suffering: both trembling of the hands, and slowness of movements, stiffness and pain, instability. When we prescribe the drug, the patient becomes much better. And a few years later he felt bad again, only "in a different way." And these complications are even more difficult to treat than the disease itself. What does it look like? The patient takes a pill - and can move normally. And in half an hour he is again "shackled". Such "switching on" and "switching off" motor abilities occurs many times during the day.
Listening to the professor, I tried to imagine what the life of a person suddenly deprived of the ability to move becomes. Margarita Vasilievna describes it this way:
- After examinations, it became clear that my husband had a brain area that is responsible for all movements, speech, swallowing. Only the thought is still clear. This disease pulls out of the usual life rapidly and, it seems, forever. At first, such a tremor appeared that the husband could not even sign - and was forced to quit his job. Then there was a gradual loss of the simplest life skills: putting a handkerchief in your pocket, fastening a button, tying your shoelaces, shaving - all this becomes impossible. For seven years, the husband had difficulty leaving the house five or six times. He was tormented by a tremor of all the muscles of his face, arms, legs (almost like "withdrawal" in drug addicts), it was difficult to walk and talk. All this drove me into such a depression that I did not want to live. And so - months, years... And now we are LIVING again. I get up at six in the morning - there is already light in his room: he sits and writes - he works. Once the husband realized that he was able to go out alone - that day he left and returned six times, he still could not believe in his happiness.
How did this miracle happen?
- A year and a half ago, we were lucky: my husband was in a group of patients who were taken for testing the Mirapex drug. At first, no one really believed in the success of the treatment. The doses given were very small. And about a week later, the husband suddenly began to smile, to joke. This was the beginning of his and our return to normal life.
The suffering patients and their relatives today are confident in the effectiveness of the new drug. Nikolai Nikolayevich Yakhno, like any serious scientist, prefers to be as careful as possible in his wording and not to add any emotions to his assessments.
- In addition to levodopa, we also use other drugs, including mirapex. The goal is either to delay the use of levodopa and its associated complications, or to reduce its dose. Unfortunately, in most patients, Parkinson's disease also provokes deep depression. So, the "substitutes" for levodopa, which we are talking about (they are called by the medical term "dopamine agonists"), help to partially relieve depression. Today we have reason to say that of all the dopamine agonists that we have, Mirapex is indeed the most effective and has the fewest side effects.
- Reviews of patients and their relatives about the drug are full of rave reviews. But if this medicine is not given to them at a discount or free of charge, there is practically no chance of acquiring it on their own - the price is too high. In your opinion, how justified are the requests of patients to include Mirapex in the list of subsidized medicines that are provided free of charge for health reasons?
- The logic here is quite simple. If there is no drug, it is difficult to provide a person with a full life. Levodopa improves the patient's condition, but may contribute to the development of complications. In fact, this new medicine, of course, is necessary for our patients for health reasons. Yes, it is quite expensive. But here, I think, a pharmaco-economic study is needed. It is necessary to calculate all the losses from the disability of patients, all the costs of caring for them, for disability benefits. And then it may well turn out that it is much more profitable to provide the patient with a drug, not to mention the moral side of the matter. Now a lot expensive drugs. But many of them can cut society's costs.
Little remains to be added to this opinion. A group of patients with Parkinson's disease turned to the Ministry of Health of the Russian Federation with a request for help in providing them with medicine, on which the future of these people literally depends. The Ministry of Health replied that, by law, these issues are under the jurisdiction of local authorities authorities. In this case, the decision of the issue depends on the Moscow Health Committee. From there, the patients received an explanation that the drug they were interested in was not used in city medical institutions, that it could be included in the "preferential" list of drugs dispensed to patients free of charge or at a discount only after appropriate tests were carried out on the basis of Moscow clinics. Perhaps I am unaware of some legal subtleties of the entire process of drug provision. But it seems strange that the authority of the clinic of nervous diseases, which is headed by N. Yakhno, and the clinical hospital named after S. Botkin, where the drug was also tested, is insufficient to resolve the issue of this drug. By the way, it has long been approved by all relevant authorities and is freely sold in Moscow pharmacies.
Margarita Vasilievna has her own view on the relationship between society and a sick person:
- My husband worked in civil aviation for forty-six years, he was a leading specialist in the industry. His pension is 900 rubles. And the cost of the drug for a month is about four and a half thousand rubles. Yes, treatment is expensive, but people are returning to work! By the way, Parkinson's disease often affects people of mental labor. As a rule, these are professionals with extensive experience. Are their knowledge, their qualifications worth nothing? And don't they deserve a decent pension? We are ready to spend all of it on buying a medicine that returns us to the joy of life. Understand, there was an absolutely helpless invalid, doomed to crawl along the long, hopeless tunnel of life. Now the medicine for him is like a door from a tunnel, there the star shines, there is a full-fledged life, as before, before the illness. And what now - to slam this door?
Today we offer you a story about a dark, but irreplaceable substance (or substance) of our brain.
black substance(or Substantia nigra) does not take up as much space as the white matter. It is located in the midbrain - one of the oldest structures in the center of the brain. Namely, hidden under its four mounds. To be completely precise, each of us has two Substantia nigra - on the left and on the right.
Midbrain. Animation from Life Science Databases(LSDB).
Cross section of the midbrain at the level of the quadrigemina. The black substance is shown in guess what color.
Despite the fact that in Substantia nigra, as well as in gray matter, there are bodies of neurons, it is much darker due to its “coloration” with neuromelanin (by the way, another form of this pigment - melanin - gives color to our eyes, skin and hair).
Neuromelanin monomer
In total, two layers are distinguished in the black substance: compact layer (pars compacta) and ventral layer (pars reticulata). Here it is necessary to clarify the word "ventral".
Physicians use two spatial antonyms: ventral and dorsal. "Ventral" means "abdominal". This does not mean at all that the ventral layer of the black substance is in the stomach. It is simply located more “in front” in the body. "Ventral" is the anterior, "dorsal" is the posterior (dorsal).
If we talk about the functionality of the layers, then the compact one is in some sense similar to a computer processor - it processes information and transmits it to the thalamus and quadrigemina of the midbrain, and the ventral one ensures the production of the neurotransmitter dopamine. The layers are arranged vertically, the pars compacta is located closer to the body axis than the pars reticulata.
Dopamine
Thanks to the black substance, we can move our eyes, perform small and precise movements, in particular, fingers, chew and swallow. And our body can carry out breathing, cardiac activity, keep blood vessels in good shape.
Violations of the work of the black substance lead to various diseases. There is a hypothesis that it is in him that the secret of schizophrenia lies. And Parkinson's disease, which we often write about on the portal, is caused precisely by a violation of the production of dopamine in the substantia nigra: it causes the death of neurons there.
Ecology of life. Cognitively: Today we offer you a story about, though black, but irreplaceable substance (or substance) of our brain.
Today we offer you a story about a dark, but irreplaceable substance (or substance) of our brain.
black substance(or Substantia nigra) does not take up as much space as the white matter. It is located in the midbrain - one of the oldest structures in the center of the brain. Namely, hidden under its four mounds. To be completely precise, each of us has two Substantia nigra - on the left and on the right.
Midbrain. Animation from Life Science Databases(LSDB).
Cross section of the midbrain at the level of the quadrigemina. The black substance is shown in guess what color.
Despite the fact that in Substantia nigra, as well as in gray matter, there are bodies of neurons, it is much darker due to its “coloration” with neuromelanin (by the way, another form of this pigment - melanin - gives color to our eyes, skin and hair).
Neuromelanin monomer
In total, two layers are distinguished in the black substance: compact layer (pars compacta) and ventral layer (pars reticulata). Here it is necessary to clarify the word "ventral".
Physicians use two spatial antonyms: ventral and dorsal. "Ventral" means "abdominal". This does not mean at all that the ventral layer of the black substance is in the stomach. It is simply located more “in front” in the body. "Ventral" is the anterior, "dorsal" is the posterior (dorsal).
If we talk about the functionality of the layers, then the compact one is in some sense similar to a computer processor - it processes information and transmits it to the thalamus and quadrigemina of the midbrain, and the ventral one ensures the production of the neurotransmitter dopamine. The layers are arranged vertically, the pars compacta is located closer to the body axis than the pars reticulata.
Dopamine
Thanks to the black substance, we can move our eyes, perform small and precise movements, in particular, fingers, chew and swallow. And our body can carry out breathing, cardiac activity, keep blood vessels in good shape.
Violations of the work of the black substance lead to various diseases. There is a hypothesis that it is in him that the secret of schizophrenia lies. And Parkinson's disease, which we often write about on the portal, is caused precisely by a violation of the production of dopamine in the substantia nigra: it causes the death of neurons there.
Histology of the black body of a patient with Parkinson's disease
Researchers even found a neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which, just like Parkinson's disease, destroys dopamine neurons, and now they are actively using it in mice to model the disease and looking for ways to treat it. published
midbrain comprises:
Mound of the quadrigemina,
red core,
black substance,
Seam core.
red core- provides skeletal muscle tone, redistribution of tone when changing posture. Just stretching is a powerful work of the brain and spinal cord, for which the red nucleus is responsible. The red core ensures the normal tone of our muscles. If the red nucleus is destroyed, decerebration rigidity occurs, while the tone sharply increases in some animals of the flexors, in others - of the extensors. And with absolute destruction, both tones increase at once, and it all depends on which muscles are stronger.
black substance– How is the excitation from one neuron transmitted to another neuron? Excitation occurs - this is a bioelectric process. He reached the end of the axon, where a chemical substance is released - a neurotransmitter. Each cell has its own mediator. The neurotransmitter is produced in the substantia nigra in nerve cells dopamine. When the substantia nigra is destroyed, Parkinson's disease occurs (fingers, head constantly tremble, or there is stiffness as a result of a constant signal going to the muscles) because there is not enough dopamine in the brain. The substantia nigra provides subtle instrumental movements of the fingers and influences all motor functions. The substantia nigra exerts an inhibitory effect on the motor cortex through the stripolidar system. In case of violation, it is impossible to perform fine operations and Parkinson's disease (stiffness, tremor) occurs.
Above - the anterior tubercles of the quadrigemina, and below - the posterior tubercles of the quadrigemina. We look with our eyes, but we see with the occipital cortex hemispheres where the visual field is located, where the image is formed. A nerve departs from the eye, passes through a series of subcortical formations, reaches the visual cortex, there is no visual cortex, and we will not see anything. Anterior colliculi is the primary visual area. With their participation, an orienting reaction to a visual signal occurs. The orienting response is “what is the response?” If the anterior tubercles of the quadrigemina are destroyed, vision will be preserved, but there will be no quick reaction to the visual signal.
Posterior tubercles of the quadrigemina This is the primary hearing area. With its participation, an orienting reaction to a sound signal occurs. If the posterior tubercles of the quadrigemina are destroyed, hearing will be preserved but there will be no orienting reaction.
Seam cores is the source of another mediator serotonin. This structure and this mediator takes part in the process of falling asleep. If the nuclei of the suture are destroyed, then the animal is in a constant state of wakefulness and quickly dies. In addition, serotonin is involved in learning with positive reinforcement (this is when a rat is given cheese). Serotonin provides such character traits as forgiveness, goodwill, in aggressive people there is a lack of serotonin in the brain.
12) Thalamus - a collector of afferent impulses. Specific and nonspecific nuclei of the thalamus. The thalamus is the center of pain sensitivity.
thalamus- visual tubercle. They were the first to discover in him a relation to visual impulses. It is a collector of afferent impulses, those that come from receptors. The thalamus receives signals from all receptors, except for the olfactory ones. Infa enters the thalamus from the cortex, from the cerebellum and from the basal ganglia. At the level of the thalamus, these signals are processed, only the most important information for a person at the moment is selected, which then enters the cortex. The thalamus consists of several dozen nuclei. The nuclei of the thalamus are divided into two groups: specific and nonspecific. Through specific nuclei of the thalamus, signals arrive strictly to certain areas of the cortex, for example, visual to the occipital, auditory to the temporal lobe. And through non-specific nuclei, information diffusely enters the entire cortex in order to increase its excitability in order to more clearly perceive specific information. They prepare the bp cortex for the perception of specific information. The highest center of pain sensitivity is the thalamus. The thalamus is the highest center of pain sensitivity. Pain is necessarily formed with the participation of the thalamus, and with the destruction of some nuclei of the thalamus, pain sensitivity is completely lost, with the destruction of other nuclei, barely tolerable pain occurs (for example, phantom pains are formed - pain in the missing limb).
13) Hypothalamo-pituitary system. The hypothalamus is the center of regulation of the endocrine system and motivations.
The hypothalamus and pituitary gland form a single hypothalamic-pituitary system.
Hypothalamus. The pituitary stalk departs from the hypothalamus, on which it hangs pituitary- the main endocrine gland. The pituitary gland regulates the work of other endocrine glands. The hypoplamus is connected to the pituitary gland by nerve pathways and blood vessels. The hypothalamus regulates the work of the pituitary gland, and through it the work of other endocrine glands. The pituitary gland is divided into adenohypophysis(glandular) and neurohypophysis. In the hypothalamus (this is not an endocrine gland, this is a part of the brain) there are neurosecretory cells in which hormones are secreted. This is a nerve cell, it can be excited, it can be inhibited, and at the same time hormones are secreted in it. An axon departs from it. And if these are hormones, they are released into the blood, and then it goes to the decision organs, that is, to the organ whose work it regulates. Two hormones:
- vasopressin - contributes to the preservation of water in the body, it acts on the kidneys, with its deficiency, dehydration occurs;
- oxytocin - is produced here, but in other cells, provides contraction of the uterus during childbirth.
Hormones are secreted in the hypothalamus and secreted by the pituitary gland. Thus, the hypothalamus is connected to the pituitary gland by neural pathways. On the other hand: nothing is produced in the neurohypophysis, hormones come here, but the adenohypophysis has its own glandular cells, where a number of important hormones are produced:
- ganadotropic hormone - regulates the work of the sex glands;
- thyroid-stimulating hormone - regulates the functioning of the thyroid gland;
- adrenocorticotropic - regulates the work of the adrenal cortex;
- somatotropic hormone, or growth hormone, - ensures the growth of bone tissue and the development of muscle tissue;
- melanotropic hormone - is responsible for pigmentation in fish and amphibians, in humans it affects the retina.
All hormones are synthesized from a precursor called pro-opiomelanocortin. synthesized big molecule, which is broken down by enzymes, and other hormones that are smaller in terms of the number of amino acids are released from it. Neuroendocrinology.
The hypothalamus contains neurosecretory cells. They produce hormones:
1) ADG (antidiuretic hormone regulates the amount of urine excreted)
2) oxytocin (provides contraction of the uterus during childbirth).
3) statins
4) liberals
5) thyroid-stimulating hormone affects the production of thyroid hormones (thyroxine, triiodothyronine)
Thyroliberin -> thyroid stimulating hormone -> thyroxine -> triiodothyronine.
The blood vessel enters the hypothalamus, where it branches into capillaries, then the capillaries gather and this vessel passes through the pituitary stalk, branches again in the glandular cells, exits the pituitary gland and carries with it all these hormones, which each go with the blood to its own gland. Why do we need this "wonderful vascular network"? There are nerve cells in the hypothalamus that terminate in the blood vessels of this wonderful vasculature. These cells produce statins And liberals - This neurohormones. Statins inhibit the production of hormones in the pituitary gland, and liberals reinforce it. If an excess of growth hormone causes gigantism, this can be stopped with samamatostatin. On the contrary: the dwarf is injected with samatoliberin. And apparently for any hormone there are such neurohormones, but they are not yet open. For example, thyroid, thyroxine is produced in it, and in order to regulate its production in the pituitary gland, thyrotropic hormone, and in order to control thyroid-stimulating hormone, thyreostatin was not found, but thyroliberin is used perfectly. Although these are hormones, they are produced in nerve cells, therefore, in addition to endocrine effects, they have a wide range of extra-endocrine functions. Thyreoliberin is called panactivin, because it improves mood, increases efficiency, normalizes blood pressure, accelerates healing in case of spinal cord injuries, it cannot be used alone for disorders in the thyroid gland.
Previously, the functions associated with neurosecretory cells and cells that produce neurofebtides have been considered.
The hypothalamus produces statins and liberins, which are included in the body's stress response. If the body is affected by some harmful factor, then the body must somehow respond - this is the stress reaction of the body. It cannot proceed without the participation of statins and liberins, which are produced in the hypothalamus. The hypothalamus is necessarily involved in the response to stress.
The next function of the hypothalamus is:
It contains nerve cells that are sensitive to steroid hormones, that is, sex hormones to both female and male sex hormones. This sensitivity provides the formation of the female or male type. The hypothalamus creates the conditions for motivating behavior according to the male or female type.
A very important function is thermoregulation, in the hypothalamus there are cells that are sensitive to blood temperature. Body temperature can change depending on environment. Blood flows through all the structures of the brain, but thermoreceptive cells that detect the slightest changes in temperature are found only in the hypothalamus. The hypothalamus turns on and organizes two body responses, either heat production or heat loss.
food motivation. Why does a person feel hungry?
The signal system is the level of glucose in the blood, it should be constant ~ 120 milligrams % - s.
There is a mechanism of self-regulation: if our blood glucose level decreases, liver glycogen begins to break down. On the other hand, glycogen stores are not enough. In the hypothalamus there are glucoreceptor cells, i.e. cells that register the level of glucose in the blood. Glucoreceptor cells form hunger centers in the hypothalamus. When the blood glucose level drops, these blood glucose-sensitive cells become excited, and a feeling of hunger occurs. At the level of the hypothalamus, only food motivation arises - a feeling of hunger, in order to search for food, the cerebral cortex must be connected, with its participation a true food reaction occurs.
The satiety center is also located in the hypothalamus, it inhibits the feeling of hunger, which prevents us from overeating. When the satiety center is destroyed, overeating occurs and, as a result, bulimia.
The hypothalamus also has a thirst center - osmoreceptive cells (osmotic pressure depends on the concentration of salts in the blood). Osmoreceptive cells register the level of salts in the blood. With an increase in salts in the blood, osmoreceptive cells are excited, and drinking motivation (reaction) occurs.
The hypothalamus is the highest center of regulation of the autonomic nervous system.
The anterior hypothalamus mainly regulates the parasympathetic nervous system, rear - sympathetic nervous system.
The hypothalamus provides only motivation and purposeful behavior of the cerebral cortex.
14) Neuron - structural features and functions. Differences between neurons and other cells. Glia, blood-brain barrier, cerebrospinal fluid.
I First, as we have already noted, in their diversity. Every nerve cell consists of a body - catfish and offshoots. Neurons are different:
1. by size (from 20 nm to 100 nm) and shape of the soma
2. by the number and degree of branching of short processes.
3. according to the structure, length and branching of axon endings (laterals)
4. by the number of spines
II Neurons also differ in functions:
A) perceiving information from the external environment
b) transmitting information to the periphery
V) processing and transmit information within the CNS,
G) exciting,
e) brake.
III Differ in chemical composition : a variety of proteins, lipids, enzymes are synthesized and, most importantly, - mediators .
WHY, WITH WHAT FEATURES IS IT RELATED TO?
This variety is defined high activity of the genetic apparatus neurons. During neuronal induction, under the influence of neuronal growth factor, NEW GENES are switched on in the cells of the ectoderm of the embryo, which are characteristic only for neurons. These genes provide the following features of neurons ( the most important properties):
A) The ability to perceive, process, store and reproduce information
B) DEEP SPECIALIZATION:
0. Synthesis of specific RNA;
1. No reduplication DNA.
2. Proportion of genes capable of transcriptions, make up in neurons 18-20%, and in some cells 40% (in other cells - 2-6%)
3. Ability to synthesize specific proteins (up to 100 in one cell)
4. The uniqueness of the lipid composition
C) Food Privilege => Level Dependence oxygen and glucose in blood.
Not a single tissue in the body is in such a dramatic dependence on the level of oxygen in the blood: 5-6 minutes of respiratory arrest and the most important structures of the brain die, and first of all - the cerebral cortex. A decrease in glucose levels below 0.11% or 80 mg% - hypoglycemia may occur and then coma.
And on the other hand, the brain is fenced off from the blood flow of the BBB. He does not let anything that could harm them into the cells. But, unfortunately, not all - many low-molecular toxic substances pass through the BBB. And pharmacologists always have a task: does this drug pass through the BBB? In some cases, this is necessary when it comes to diseases of the brain, in others it is indifferent to the patient if the drug does not damage nerve cells, and in still others this should be avoided. (NANOPARTICLES, ONCOLOGY).
Sympathetic NS is excited and stimulates the work of the adrenal medulla - the production of adrenaline; in the pancreas - glucagon - breaks down glycogen in the kidneys to glucose; glucocarticoids produced. in the adrenal cortex - provides gluconeogenesis - the formation of glucose from ...)
And yet, with all the variety of neurons, they can be divided into three groups: afferent, efferent and intercalary (intermediate).
15) Afferent neurons, their functions and structure. Receptors: structure, functions, formation of an afferent volley.
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