Slide 1
Independent work on the subject: “Physiology of the central nervous system” Completed by: student gr. P1-11 =))Slide 2
Hippocampus Hippocampal limbic circle of Peipetz. The role of the hippocampus in the mechanisms of memory formation and learning. Subject:
Slide 3
The hippocampus (from ancient Greek ἱππόκαμπος - seahorse) is part of the limbic system of the brain (olfactory brain).
Slide 4
Slide 5
Anatomy of the hippocampus The hippocampus is a paired structure located in the medial temporal lobes of the hemispheres. The right and left hippocampi are connected by commissural nerve fibers passing through the commissure of the fornix. The hippocampi form the medial walls of the inferior horns of the lateral ventricles, located in the thickness of the cerebral hemispheres, extend to the most anterior sections of the inferior horns of the lateral ventricle and end with thickenings divided by small grooves into separate tubercles - the toes of the seahorse. On the medial side, the hippocampal fimbria, which is a continuation of the peduncle of the telencephalon, is fused with the hippocampus. The choroid plexuses of the lateral ventricles are adjacent to the fimbriae of the hippocampus.
Slide 6
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Hippocampal limbic circle of Peipets James Peipets Neurologist, MD (1883 - 1958) Created and scientifically confirmed the original theory of the “circulation of emotions” in the deep structures of the brain, including the limbic system. The “Papetz Circle” creates the emotional tone of our psyche and is responsible for the quality of emotions, including emotions of pleasure, happiness, anger and aggression.
Slide 8
Limbic system. The limbic system has the shape of a ring and is located on the border of the neocortex and the brain stem. In functional terms, the limbic system is understood as the unification of various structures of the telencephalon, diencephalon and midbrain, providing emotional and motivational components of behavior and the integration of visceral functions of the body. In the evolutionary aspect, the limbic system was formed in the process of complicating the forms of behavior of the organism, the transition from rigid, genetically programmed forms of behavior to plastic ones, based on learning and memory. Structural and functional organization of the limbic system. olfactory bulb, cingulate gyrus, parahippocampal gyrus, dentate gyrus, hippocampus, amygdala, hypothalamus, mammillary body, mammillary bodies.
Slide 9
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The most important cyclic formation of the limbic system is the Peipets circle. It starts from the hippocampus through the fornix to the mamillary bodies, then to the anterior nuclei of the thalamus, then to the cingulate gyrus and through the parahippocampal gyrus back to the hippocampus. Moving along this circuit, excitement creates long-term emotional states and “tickles the nerves,” running through the centers of fear and aggression, pleasure and disgust. This circle plays a large role in the formation of emotions, learning and memory.
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Slide 13
The hippocampus and its associated posterior frontal cortex are responsible for memory and learning. These formations carry out the transition of short-term memory to long-term memory. Damage to the hippocampus leads to disruption of the assimilation of new information and the formation of intermediate and long-term memory. The function of memory formation and learning is associated primarily with the Peipetz circle.
Slide 14
There are two hypotheses. According to one of them, the hippocampus has an indirect effect on learning mechanisms by regulating wakefulness, directed attention, and emotional and motivational arousal. According to the second hypothesis, which has received widespread recognition in recent years, the hippocampus is directly related to the mechanisms of encoding and classification of material, its temporal organization, i.e., the regulatory function of the hippocampus contributes to the intensification and prolongation of this process and, probably, protects memory traces from interfering influences, in As a result, optimal conditions are created for the consolidation of these traces into long-term memory. The hippocampal formation is of particular importance in the early stages of learning and conditioned reflex activity. During the development of food conditioned reflexes to sound, short-latency neuronal responses were recorded in the hippocampus, and long-latency responses were recorded in the temporal cortex. It was in the hippocampus and septum that neurons were found whose activity changed only when paired stimuli were presented. The hippocampus is the first point of convergence of conditioned and unconditioned stimuli.
TOPIC: CENTRAL NERVOUS SYSTEM (CNS) PLAN: 1. The role of the CNS in the integrative, adaptive activity of the body. 2. Neuron - as a structural and functional unit of the central nervous system. 3. Synapses, structure, functions. 4. Reflex principle of regulation of functions. 5. History of the development of reflex theory. 6.Methods for studying the central nervous system.
The central nervous system carries out: 1. Individual adaptation of the body to the external environment. 2. Integrative and coordinating functions. 3. Forms goal-oriented behavior. 4. Performs analysis and synthesis of received stimuli. 5. Forms a flow of efferent impulses. 6. Maintains the tone of body systems. The modern concept of the central nervous system is based on the neural theory.
The central nervous system is a collection of nerve cells or neurons. Neuron. Sizes from 3 to 130 microns. All neurons, regardless of size, consist of: 1. Body (soma). 2. Axon dendritic processes Structural and functional elements of the central nervous system. The cluster of neuron bodies makes up the gray matter of the central nervous system, and the cluster of processes makes up the white matter.
Each cell element performs a specific function: The neuron body contains various intracellular organelles and ensures the life of the cell. The body membrane is covered with synapses, therefore it perceives and integrates impulses coming from other neurons. Axon (long process) - conducts a nerve impulse from the body of a nerve cell and to the periphery or to other neurons. Dendrites (short, branching) - perceive irritations and communicate between nerve cells.
1. Depending on the number of processes, they are distinguished: - unipolar - one process (in the nuclei of the trigeminal nerve) - bipolar - one axon and one dendrite - multipolar - several dendrites and one axon 2. In functional terms: - afferent or receptor - (perceive signals from receptors and carried to the central nervous system) - intercalary - provide communication between afferent and efferent neurons. - efferent - conduct impulses from the central nervous system to the periphery. They are of 2 types: motor neurons and efferent neurons of the ANS - excitatory - inhibitory CLASSIFICATION OF NEURONS
The relationship between neurons is carried out through synapses. 1. Presynaptic membrane 2. Synaptic cleft 3. Postsynaptic membrane with receptors. Receptors: cholinergic receptors (M and N cholinergic receptors), adrenergic receptors - α and β Axonal hillock (axon extension)
CLASSIFICATION OF SYNAPSES: 1. By location: - axoaxonal - axodendritic - neuromuscular - dendrodendritic - axosomatic 2. By the nature of the action: excitatory and inhibitory. 3. By signal transmission method: - electrical - chemical - mixed
The transmission of excitation in chemical synapses occurs due to mediators, which are of 2 types - excitatory and inhibitory. Exciting agents - acetylcholine, adrenaline, serotonin, dopamine. Inhibitory – gamma-aminobutyric acid (GABA), glycine, histamine, β-alanine, etc. Mechanism of excitation transmission in chemical synapses
The mechanism of excitation transmission in the excitatory synapse (chemical synapse): impulse, nerve ending into synaptic plaques, depolarization of the presynaptic membrane (input of Ca++ and output of transmitters), neurotransmitters, synaptic cleft, postsynaptic membrane (interaction with receptors), generation of EPSP AP.
1. In chemical synapses, excitation is transmitted using mediators. 2. Chemical synapses have one-way conduction of excitation. 3.Fatigue (depletion of neurotransmitter reserves). 4.Low lability imp/sec. 5. Summation of excitation 6. Blazing a path 7. Synaptic delay (0.2-0.5 m/s). 8. Selective sensitivity to pharmacological and biological substances. 9.Chemical synapses are sensitive to temperature changes. 10. There is trace depolarization at chemical synapses. PHYSIOLOGICAL PROPERTIES OF CHEMICAL SYNAPSES
REFLECTOR PRINCIPLE OF REGULATION OF FUNCTION The activity of the body is a natural reflex reaction to a stimulus. In the development of reflex theory, the following periods are distinguished: 1. Descartes (16th century) 2. Sechenovsky 3. Pavlovsky 4. Modern, neurocybernetic.
METHODS OF RESEARCH OF THE CNS 1. Extirpation (removal: partial, complete) 2. Irritation (electrical, chemical) 3. Radioisotope 4. Modeling (physical, mathematical, conceptual) 5. EEG (registration of electrical potentials) 6. Stereotactic technique. 7. Development of conditioned reflexes 8. Computed tomography 9. Pathological method
Multimedia support for lectures on “Fundamentals of neurophysiology and GND” General physiology of the central nervous system and excitable tissues
Basic manifestations of vital activity Physiological rest Physiological activity Irritation Excitation Inhibition
Types of biological reactions Irritation is a change in structure or function under the influence of an external stimulus. Excitation is a change in the electrical state of the cell membrane, leading to a change in the function of a living cell.
Structure of biomembranes The membrane consists of a double layer of phospholipid molecules, covered on the inside with a layer of protein molecules, and on the outside with a layer of protein molecules and mucopolysaccharides. The cell membrane has very thin channels (pores) with a diameter of several angstroms. Through these channels, molecules of water and other substances, as well as ions with a diameter corresponding to the size of the pores, enter and leave the cell. Various charged groups are fixed on the structural elements of the membrane, which gives the channel walls a particular charge. The membrane is much less permeable to anions than to cations.
Resting potential Between the outer surface of the cell and its protoplasm at rest there is a potential difference of the order of 60-90 mV. The surface of the cell is charged electropositively with respect to protoplasm. This potential difference is called the membrane potential, or resting potential. Its accurate measurement is possible only with the help of intracellular microelectrodes. According to the Hodgkin-Huxley membrane-ion theory, bioelectric potentials are caused by the unequal concentration of K+, Na+, Cl- ions inside and outside the cell, and the different permeability of the surface membrane for them.
Mechanism of MP formation At rest, the membrane of nerve fibers is approximately 25 times more permeable to K ions than to Na + ions, and when excited, sodium permeability is approximately 20 times higher than potassium. Of great importance for the occurrence of membrane potential is the concentration gradient of ions on both sides of the membrane. It has been shown that the cytoplasm of nerve and muscle cells contains 30-59 times more K + ions, but 8-10 times less Na + ions and 50 times less Cl - ions than the extracellular fluid. The value of the resting potential of nerve cells is determined by the ratio of positively charged K + ions, diffusing per unit time from the cell outward along the concentration gradient, and positively charged Na + ions, diffusing along the concentration gradient in the opposite direction.
Distribution of ions on both sides of the cell membrane Na + K +A – Na +K + rest excitation
Na. Na ++ -K-K ++ - - membrane pump 2 Na +3K + ATP -ase
Action potential If a section of a nerve or muscle fiber is exposed to a sufficiently strong stimulus (for example, a jolt of electric current), excitation occurs in that section, one of the most important manifestations of which is a rapid oscillation of the MP, called an action potential (AP)
Action potential In AP, it is customary to distinguish between its peak (the so-called spike) and trace potentials. The PD peak has an ascending and descending phase. Before the ascending phase, a more or less pronounced so-called local potential, or local response. Since the initial polarization of the membrane disappears during the ascending phase, it is called the depolarization phase; accordingly, the descending phase, during which membrane polarization returns to its original level, is called the repolarization phase. The duration of the AP peak in nerve and skeletal muscle fibers varies within 0.4-5.0 ms. In this case, the repolarization phase is always longer.
The main condition for the occurrence of AP and spreading excitation is that the membrane potential must become equal to or less than the critical level of depolarization (Eo<= Eк)
CONDITION OF SODIUM OUTPUT CHANNELS A L A D E P O L A R I S A T I O N S R E P O L A R I S A T I O N
Excitability parameters 1. Excitability threshold 2. Useful time 3. Critical slope 4. Lability
Threshold of stimulation The minimum value of stimulus strength (electric current) required to reduce the membrane charge from the resting level (Eo) to the critical level (Eo) is called the threshold stimulus. Threshold of irritation E p = Eo - Ek Subthreshold stimulus is less powerful than threshold Above-threshold stimulus is stronger than threshold
The threshold strength of any stimulus, within certain limits, is inversely related to its duration. The curve obtained in such experiments is called the “force-duration curve.” From this curve it follows that a current below a certain minimum value or voltage does not cause excitation, no matter how long it lasts. The minimum current strength that can cause excitation is called rheobase. The shortest time during which an irritating stimulus must act is called useful time. Increasing the current leads to a shortening of the minimum stimulation time, but not indefinitely. With very short stimuli, the force-time curve becomes parallel to the coordinate axis. This means that with such short-term irritations, excitation does not occur, no matter how great the strength of irritation.
LAW "STRENGTH IS DURATION"
Determining useful time is practically difficult, since the point of useful time is located on a section of the curve that turns into parallel. Therefore, it is proposed to use the useful time of two rheobases - chronaxy. Chronaximetry has become widespread both experimentally and clinically for diagnosing damage to motor nerve fibers.
LAW "STRENGTH IS DURATION"
The threshold value for irritation of a nerve or muscle depends not only on the duration of the stimulus, but also on the steepness of the increase in its strength. The irritation threshold has the smallest value for rectangular current impulses, characterized by the fastest possible increase in current. When the slope of the current increase decreases below a certain minimum value (the so-called critical slope), the PD does not occur at all, no matter to what final strength the current increases. The phenomenon of adaptation of excitable tissue to a slowly increasing stimulus is called accommodation.
The “all or nothing” law According to this law, under threshold stimuli they do not cause excitation (“nothing”), but with threshold stimuli, excitation immediately acquires a maximum value (“all”), and no longer increases with further intensification of the stimulus.
lability The maximum number of impulses that excitable tissue is capable of reproducing in accordance with the frequency of stimulation nerve - over 100 Hz muscle - about 50 Hz
Laws of excitation conduction Law of physiological continuity; Law of bilateral conduction; Law of isolated conduction.
The location where the axon originates from the nerve cell body (axon hillock) is of greatest importance in the excitation of the neuron. This is the trigger zone of the neuron; it is here that excitation occurs most easily. In this area for 50-100 microns. the axon does not have a myelin sheath, therefore the axon hillock and the initial segment of the axon have the lowest irritation threshold (dendrite - 100 mV, soma - 30 mV, axon hillock - 10 mV). Dendrites also play a role in the excitation of a neuron. They have 15 times more synapses than the soma, so PDs passing along the dendrites to the soma can easily depolarize the soma and cause a volley of impulses along the axon.
Features of neuronal metabolism High consumption of O 2. Complete hypoxia for 5-6 minutes leads to the death of cortical cells. Ability for alternative routes of exchange. The ability to create large reserves of substances. A nerve cell lives only with glia. Ability to regenerate processes (0.5-4 microns/day).
Classification of neurons Afferent, sensitive Associative, intercalary Efferent, effector, motor receptor muscle
Afferent stimulation is carried out along fibers that differ in the degree of myelination and, therefore, in the speed of impulse conduction. Type A fibers are well myelinated and conduct excitations at speeds of up to 130-150 m/s. They provide tactile, kinesthetic, as well as rapid pain sensations. Type B fibers have a thin myelin sheath and a smaller overall diameter, which also leads to a lower impulse conduction speed - 3-14 m/s. They are components of the autonomic nervous system and do not participate in the work of the skin-kinesthetic analyzer, but can conduct some of the temperature and secondary pain stimuli. Type C fibers - without a myelin sheath, impulse conduction speed up to 2-3 m/s. They provide slow pain, temperature and pressure sensations. Usually this is vaguely differentiated information about the properties of the stimulus.
Synapse(s) is a specialized zone of contact between neurons or neurons and other excitable cells, ensuring the transfer of excitation with the preservation, change or disappearance of its information value.
Excitatory synapse – a synapse that excites the postsynaptic membrane; an excitatory postsynaptic potential (EPSP) arises in it and the excitation spreads further. An inhibitory synapse is a synapse on the postsynaptic membrane of which an inhibitory postsynaptic potential (IPSP) arises, and the excitation that comes to the synapse does not spread further.
Classification of synapses Based on location, neuromuscular and neuroneuronal synapses are distinguished, the latter in turn divided into axo-somatic, axo-axonal, axo-dendritic, dendro-somatic. According to the nature of the effect on the perceptive structure, synapses can be excitatory or inhibitory. According to the method of signal transmission, synapses are divided into electrical, chemical, and mixed.
Reflex arc Any reaction of the body in response to irritation of receptors when the external or internal environment changes and carried out through the central nervous system is called a reflex. Thanks to reflex activity, the body is able to quickly respond to environmental changes and adapt to these changes. Each reflex is carried out thanks to the activity of certain structural formations of the NS. The set of formations involved in the implementation of each reflex is called a reflex arc.
Principles of classification of reflexes 1. By origin - unconditional and conditional. Unconditioned reflexes are inherited, they are enshrined in the genetic code, and conditioned reflexes are created in the process of individual life on the basis of unconditioned ones. 2. According to biological significance → nutritional, sexual, defensive, orientation, locomotor, etc. 3. According to the location of the receptors → interoceptive, exteroceptive and proprioceptive. 4. By type of receptors → visual, auditory, gustatory, olfactory, pain, tactile. 5. According to the location of the center → spinal, bulbar, mesencephalic, diencephalic, cortical. 6. According to the duration of the response → phasic and tonic. 7. By the nature of the response → motor, secretory, vasomotor. 8. By belonging to the organ system → respiratory, cardiac, digestive, etc. 9. By the nature of the external manifestation of the reaction → flexion, blinking, vomiting, sucking, etc.
Reflex. Neuron. Synapse. The mechanism of excitation through the synapse
Prof. Mukhina I.V.
Lecture No. 6 Faculty of Medicine
CLASSIFICATION OF THE NERVOUS SYSTEM
Peripheral nervous system
Functions of the central nervous system:
1). Combination and coordination of all functions of tissues, organs and systems of the body.
2). Communication of the body with the external environment, regulation of body functions in accordance with its internal needs.
3). The basis of mental activity.
The main activity of the central nervous system is reflex
Rene Descartes (1596-1650) - pioneered the concept of reflex as a reflective activity;
Georg Prochaski (1749-1820);
THEM. Sechenov (1863) “Reflexes of the Brain,” in which he first proclaimed the thesis that all types of conscious and unconscious human life are reflex reactions.
A reflex (from Latin reflecto - reflection) is the body's response to irritation of receptors and carried out with the participation of the central nervous system.
The Sechenov-Pavlov reflex theory is based on three principles:
1. Structurality (the structural basis of the reflex is the reflex arc)
2. Determinism (principle cause-and-effect relationships). Not a single response of the body occurs without a reason.
3. Analysis and synthesis (any effect on the body is first analyzed and then summarized).
Morphologically consists of:
receptor formations, whose purpose is
V transformation of the energy of external stimuli (information)
V energy of a nerve impulse;
afferent (sensitive) neuron, conducts nerve impulses to the nerve center;
interneuron (interneuron) neuronor nerve center
representing the central part of the reflex arc;
efferent (motor) neuron, conducts the nerve impulse to the effector;
effector (working body),carrying out relevant activities.
The transmission of nerve impulses is carried out using neurotransmitters or neurotransmitters– chemical substances released by nerve endings in
chemical synapse
LEVELS OF STUDY OF CNS FUNCTIONING
Organism
Neuron structure and function
Dendrites
Functions of neurons:
1. Integrative;
2. Coordinating
3. Trophic
Purkinje cell |
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Dendrites |
Astrocyte |
(cerebellum) |
Pyramid |
|
Oligodendrocyte |
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cortical neuron |
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central nervous
systems
Lecture No. 2
for 2nd year students
Head department Shtanenko N.I.
Lecture outline:
Basic physiological propertiesnerve centers.
Features of distribution
excitation in the central nervous system
Braking
V
CNS.
Nature
braking. Types of braking.
Reflex coordination mechanisms
activities
The third level of coordination is carried out in the process of activity of nerve centers and their interaction
Nerve centers are formedcombining several local
networks and represent
complex of elements capable
carry out a certain reflex
or behavioral act.
.–
This
totality
neurons,
necessary for implementation
certain
reflex
or
regulation of a certain function.
M. Flourens (1842) and N. A. Mislavsky (1885) is a complex structural and functional
Union
nervous
cells,
located at different levels
CNS and those providing due to them
integrative activity regulation
integral adaptive functions
(eg respiratory center in the broad sense of the word)
Classification of nerve centers (according to a number of characteristics)
Localizations (cortical, subcortical,spinal);
Functions (respiratory,
vasomotor, heat generation);
Modalities of holistic
biological states (hunger, emotions, drives, etc.) Unilateral conduction of excitation
Synaptic delay - slowing down
conducting excitation through the center 1.5-2 ms
Irradiation (divergence)
Convergence (animation)
Circulation (reverberation)
The main properties of nerve centers are determined by the characteristics of their
structure and presence of interneuron synaptic connections.
Reflex arc
Synaptic conduction delay
period temporarily required for:1. excitation of receptors (receptors)
for conducting excitation impulses
along afferent fibers to the center;
3.
distribution
excitement
through
nerve centers;
4.
spreading
excitement
By
efferent fibers to the working organ;
2.
5. latent period of the working organ.
Reflex time Central reflex time
Reflex time(latency period of the reflex) is
time from the moment of irritation to the end
effect. In a monosynaptic reflex it reaches 20-25 ms. This
time is spent on excitation of receptors, conducting excitation along
afferent fibers, transmission of excitation from afferent neurons to
efferent (possibly through several intercalary ones), conducting excitation
along efferent fibers and transmission of excitation from the efferent nerve to
effector
Central
time
reflex–
This
the period of time during which a nerve impulse is transmitted
by brain structures. In the case of a monosynaptic reflex arc, it
is approximately 1.5-2 ms - this is the time required for transmission
excitations at one synapse. Thus, the central time of the reflex
indirectly indicates the number of synaptic transmissions taking place in
this reflex. Central time in polysynaptic reflexes
more than 3 ms. In general, polysynaptic reflexes are very widespread
distributed in the human body. Central reflex time
is the main component of the total reflex time.
Knee reflex
Examples of reflex arcsKnee reflex
Monosynaptic. IN
as a result of a sharp
sprains
proprioceptors
quadriceps
extension occurs
shins
(- defensive
Reflex time
0.0196-0.0238sec.
alpha motor neurons
proprioceptive
motor
unconditional)
But: even the simplest reflexes do not work separately.
(Here: interaction with the inhibitory circuit of the antagonist muscle)
Mechanism of propagation of excitation in the central nervous system
Types of convergence of excitation on one neuron
MultisensoryMultibiological
Sensory-biological
Phenomena of convergence and divergence in the central nervous system. The principle of “common final path”
REVERBERATION(circulation) Inertia
Summation:
sequential(temporary)
spatial
Transformation of arousal
(rhythm and frequency)
Post-tetanic potentiation
(post-activation)
Time summation
Spatial summation
Summation in the central nervous system
SequentialTemporary
summation
Spatial summation
Transformation of the rhythm of excitation
Rhythm transformation
Trigger propertiesaxon hillock
Threshold 30 mV
Threshold 10 mV
Neuron body
Ek
Eo
Axon hillock
Ek
Eo
"At a gun shot
neuron responds
machine gun fire"
Rhythm transformation
50A
50
A
?
50
IN
Phase relationships
incoming pulses
IN
A
100
IN
A
IN
(following
fall into
refractoriness
previous
Features of the propagation of excitation in the central nervous system
Central relief
A1
At
irritation A
get excited
2 neurons (1,2)
2
IN
3
4
5
At
irritation B
get excited
2 neurons (5, 6)
6
Cells
peripheral
borders
For irritation A + B
excited 6
neurons (1, 2, 3, 4, 5, 6)
Cells
central
parts
neural pool
Central occlusion
A1
When irritated A
excited 4
neuron (1,2,3,4)
2
3
When irritated B
excited 4
neuron (3, 4, 5, 6)
IN
4
5
6
Cells
central
parts
neural pool
BUT with combined stimulation A + B
4 neurons are excited (1, 2, 5, 6)
Occlusion phenomenon
3+3=64+4=8
Post-tetanic potentiation
Ca2+Ca2+
Reverb circuit
High sensitivity centersto a lack of oxygen and glucose
Selective sensitivity
to chemicals
Low lability and high fatigue
nerve centers
Tone of nerve centers
Plastic
Synaptic plasticity
This is a functional and morphological restructuringsynapse:
Increased plasticity: facilitation (presynaptic
nature, Ca++), potentiation (postsynaptic nature,
increased sensitivity of postsynaptic receptors Sensitization)
Decreased plasticity: depression (decreased
neurotransmitter stores in the presynaptic membrane)
– this is a mechanism for the development of habituation - habituation
Long-term forms of plasticity
Long-term potentiation - long-termstrengthening of synaptic transmission on
high-frequency irritation, may
continue for days and months. Characteristic for
all parts of the central nervous system (hippocampus, glutamatergic
synapses).
Long-term depression - long-term
weakening of synaptic transmission (low
intracellular Ca++ content) active independent
physiological process
caused by excitement and
aimed at weakening
cessation or prevention
other excitement
Braking
BrakingInhibition of nerve cells, centers -
parity in functionality
significance with excitement nervous
process.
But! Braking does not apply
it is “attached” to the synapses on which
inhibition occurs.
Inhibition controls excitation.
Braking functions
Limits the spread of excitation in the central nervous system, irradiation, reverberation, animation, etc.Coordinates functions, i.e. directs arousal
along certain pathways to certain nerves
centers
Braking performs a protective or protective function.
role by protecting nerve cells from excessive
excitement and exhaustion during action
super-strong and prolonged irritants
Central braking was discovered by I.M. Sechenov in 1863
Central inhibition in the central nervous system (Sechenovsky)
Sechenov braking
Classification of inhibition in the central nervous system
Electrical state of the membranehyperpolarizing
depolarizing
Relation to synapse
postsynaptic
presynaptic
Neuronal organization
progressive,
returnable,
lateral
Bioelectric activity of a neuron
Brake mediators -
Brake mediators GAMK (gamma-aminobutyric acid)Glycine
Taurine
The occurrence of IPSPs in response to afferent stimulation is obligatory
is associated with the inclusion in the inhibitory process of an additional link of the inhibitory interneuron, the axonal endings of which are distinguished
brake mediator.
Inhibitory postsynaptic potential IPSP
mv0
4
6
8
ms
- 70
- 74
HYPERPOLARIZATION
K+ Clֿ
TYPES OF BRAKING
P E R V I C H N O E:A) POSTSYNAPTIC
B) PRESYNAPTIC
SECONDARY:
A) PESSIMAL according to N. Vvedensky
B) TRACE (with trace hyperpolarization)
(Inhibition following excitation)
Ionic nature of postsynaptic inhibition
Postsynaptic inhibition (Latin post behind, after something + Greek sinapsis contact,connection) is a nervous process caused by the action of specific substances on the postsynaptic membrane
inhibitory mediators secreted by specialized presynaptic nerve endings.
The transmitter released by them changes the properties of the postsynaptic membrane, which causes suppression
the cell's ability to generate excitation. This results in a short-term increase
permeability of the postsynaptic membrane to K+ or CI- ions, causing a decrease in its input
electrical resistance and generation of inhibitory postsynaptic potential (IPSP).
POSTSYNAPTIC INHIBITION
TOCl
GABA
TPSP
Braking mechanisms
Decreased membrane excitability inas a result of hyperpolarization:
1. Release of potassium ions from the cell
2. Entry of chlorine ions into the cell
3. Reduced electrical density
current flowing through the axonal
mound as a result of activation
chlorine channels
Classification of species
I.Primary postsynaptic
braking:
a) Central (Sechenov) inhibition.
b) Cortical
c) Reciprocal inhibition
d) Return braking
e) Lateral inhibition
Towards:
Direct.
Returnable.
Lateral.
Reciprocal.
MS, MR – flexor and extensor motor neurons.
Diagram of direct postsynapticinhibition in a segment of the spinal cord.
MS, MR – motor neurons
flexor and extensor.
Step reflex
Examples of reflex arcsStep reflex
4- disinhibition
3
4
1
2
A. continuous
motor stimulation
CNS centers are broken down
for successive acts
excitement of the right and
left leg.
(reciprocal + reciprocal
oh braking)
B. motion control when
posture reflex
(reciprocal inhibition)
Reciprocal inhibition – at the level of spinal cord segments
INHIBITION IN THE CNS
BRAKINGReturn braking
by Renshaw
B - excitement
T - braking
In the central nervous system
Lateral
braking
Reversible (antidromic) inhibition
Recurrent postsynaptic inhibition (Greek: antidromeo to run in the opposite direction) - processregulation by nerve cells of the intensity of signals received by them according to the principle of negative feedback.
It lies in the fact that the axon collaterals of a nerve cell establish synaptic contacts with special
interneurons (Renshaw cells), whose role is to influence neurons converging on the cell,
sending these axon collaterals. According to this principle, motor neurons are inhibited.
Lateral inhibition
Synapses on a neuron
Presynaptic inhibition
It is carried out through special inhibitory interneurons.Its structural basis is axo-axonal synapses,
formed by the axon terminals of inhibitory interneurons and
axonal endings of excitatory neurons. PRESYNAPTIC
BRAKING
1 - axon of inhibitory neuron
2 - axon of excitatory neuron
3 - postsynaptic membrane
alpha moto neuron
Cl¯- channel
At the terminals of the presynaptic inhibitory
the axon releases a transmitter, which
causes depolarization of excitatory
endings
behind
check
increase
permeability of their membrane to CI-.
Depolarization
causes
decrease
amplitude of the action potential coming
into the excitatory axon terminal. IN
As a result, the process is inhibited
release of the neurotransmitter by excitatory
nervous
endings
And
decline
amplitudes
exciting
postsynaptic potential.
Characteristic feature
presynaptic depolarization is
slow development and long duration
(several hundred milliseconds), even after
single afferent impulse.
Presynaptic inhibition
Presynaptic inhibition primarily blocks weakasynchronous afferent signals and transmits stronger,
therefore, it serves as a mechanism for isolating, isolating more
intense afferent impulses from the general flow. It has
enormous adaptive significance for the body, since of all
afferent signals going to the nerve centers, the most prominent
the main ones, the most necessary for this particular time.
Thanks to this, the nerve centers, the nervous system as a whole, are freed
from processing less essential information
Afferent impulses from the flexor muscle with the help of Renshaw cells cause presynaptic inhibition on the afferent nerve, which under
Presynaptic inhibition circuitin a segment of the spinal cord.
Afferent
impulses from muscles
– flexor s
using cells
Renshaw is called
presynaptic
braking on
afferent nerve,
which fits
motor neuron
extensor
Examples of inhibition disorders in the central nervous system
IMPAIRMENT OF POSTSYNAPTIC INHIBITION:STRYCHNINE - BLOCKING OF RECEPTORS OF INHIBITORY SYNAPSES
TETANUS TOXIN - RELEASE DISORDER
BRAKE MEDIATOR
IMPAIRMENT OF PRESYNAPTIC INHIBITION:
PICROTOXIN - BLOCKING PRESYNAPTIC SYNAPSES
Strychnine and tetanus toxin have no effect on it.
Postsynaptic reentrant inhibition. Blocked by strychnine.
Presynaptic inhibition. Blocked by picrotoxin
Classification of species
Secondary braking is not associated withinhibitory structures is
consequence of previous
excitement.
a) Transcendent
b) Pessimal inhibition of Vvednsky
c) Parobiotic
d) Inhibition following excitation
Induction
By the nature of the influence:Positive - observed when braking is replaced
increased excitability around you.
Negative - if the focus of excitation is replaced by inhibition
By time:
Simultaneous Positive simultaneous induction
observed when inhibition immediately (simultaneously) creates a state
increased excitability around you.
Sequential When changing the braking process to
excitation – positive sequential induction
Registration of EPSPs and IPSPs
PRINCIPLES OF COORDINATION OF REFLEX ACTIVITY
1. RECIPROCITY2. COMMON FINAL PATH
(according to Sherrington)
3. DOMINANTS
4. SUBORDINATION OF NERVOUS CENTRAL DETERMINATION OF DOMINANT
(According to A.A. Ukhtomsky, 1931)
temporarily
dominant
hearth
excitement
V
central
nervous system, determining
current activity of the body
DOMINANT
-DEFINITION OF DOMINANCE
(According to A.A. Ukhtomsky, 1931)
temporarily
dominant
reflex
or
behavioral
Act,
which
transformed and directed
for a given time with other
equal conditions of work for others
reflex arcs, reflex
apparatus and behavior in general
DOMINANT
-PRINCIPLE OF DOMINANCE
Irritants
Nerve centers
Reflexes The main signs of a dominant
(according to A.A. Ukhtomsky)
1. Increased excitability of the dominant
center
2. Persistence of excitation in the dominant
center
3. The ability to summarize excitations,
thereby reinforcing your excitement
extraneous impulses
4. Ability to slow down other current
reflexes on a common final path
5. Inertia of the dominant center
6. Ability to disinhibit
Scheme of formation of dominant D - persistent excitation - grasping reflex in a frog (dominant), caused by the application of strychnine. All
DDominant formation scheme
D – persistent excitation of the grasping reflex
frogs (dominant),
caused by application
strychnine. All irritations in
points 1,2,3,4 do not give answers,
but only increase activity
neurons D.
