The Neuron Flashcards
Structure of Neuron
Neuron is made up of three parts:
- Nerve cell body
- Dendrite
- Axon.
Nerve cell body is also known as soma or perikaryon. It is irregular in shape. Like any other cell, it is constituted by a mass of cytoplasm called neuroplasm, which is covered by a cell membrane. The cytoplasm contains a large nucleus, Nissl bodies, neurofibrils, mitochondria
and Golgi apparatus. Nissl bodies and neurofibrils are found only in nerve cell and not in other cells.
Each neuron has one nucleus, which is centrally placed in the nerve cell body. Nucleus has one or two prominent nucleoli. Nucleus does not contain centrosome. that is, the nerve cell has lost the power of division
Nissl bodies or Nissl granules are small basophilic granules found in cytoplasm of neurons and are named after the discoverer. These bodies are present in
soma and dendrite but not in axon and axon hillock.
Nissl bodies are called tigroid substances, since these bodies are responsible for tigroid or spotted appearance of soma after suitable staining.
- Nissl bodies are membranous organelles containing ribosomes. So, these bodies are concerned with
synthesis of proteins in the neurons. Proteins formed in soma are transported to the axon by axonal flow.
Number of Nissl bodies varies with the condition of the nerve. During fatigue or injury of the neuron, these bodies fragment and disappear by a process called chromatolysis. Granules reappear after recovery from fatigue or after regeneration of nerve fibers.
Neurofibrils are thread-like structures present in the form of network in the soma and the nerve processes.
Presence of neurofibrils is another characteristic feature of the neurons. The neurofibrils consist of microfilaments and microtubules.
Mitochondria are present in soma and in axon. As in other cells, here also mitochondria form the powerhouse
of the nerve cell, where ATP is produced
Golgi apparatus of nerve cell body is similar to that of other cells. It is concerned with processing and packing of proteins into granules
2) Dendrite is the branched process of neuron and it is branched repeatedly. Dendrite may be present or absent. If present, it may be one or many in number. Dendrite has Nissl granules and neurofibrils. Dendrite transmits impulses towards the nerve cell body. Usually, the dendrite is shorter than axon.
3) Axon is the longer process of nerve cell. Each neuron has only one axon. Axon arises from axon hillock of the
nerve cell body and it is devoid of Nissl granules. Axon extends for a long distance away from the nerve cell
body. Length of longest axon is about 1 meter. Axon transmits impulses away from the nerve cell
body.
Axon has a long central core of cytoplasm called axoplasm. Axoplasm is covered by the tubular sheath-
like membrane called axolemma. Axoplasm along with axolemma is called the axis
cylinder of the nerve fiber
classification of neurons/nerve fibres
- Depending upon structure
- myelinated
- non myelinated - Depending upon distribution
- somatic
- visceral or autonomic - Depending upon origin
- cranial
- spinal - Depending upon function
- sensory
- motor - Depending upon secretion of neurotransmitter
- adrenergic - noradrenaline
- cholinergic - acetylcholine - Depending upon diameter and conduction of impulse
(ErlangerGasser classification)
- 3 types on the basis of diameter and velocity of conduction of impulse
i. Type A nerve fibers
ii. Type B nerve fibers
iii. Type C nerve fibers.
Among these fibers, type A nerve fibers are the thickest fibers and type C nerve fibers are the thinnest fibers.
Type C fibers are also known as Type
IV fibers.
Except type C fibers, all the nerve fibers are myelinated
Type A nerve fibers are divided into four types:
a. Type A alpha or Type I nerve fibers
b. Type A beta or Type II nerve fibers
c. Type A gamma nerve fibers
d. Type A delta or Type III nerve fibers.
- velocity of conduction is directly proportional to the thickness of the nerve fiber. type A alpha fibers are the fastest.
Properties of nerve fibres
1) Excitability
The property of a living cell to respond to a change in the environment.
When a nerve fiber is stimulated, based on the strength of stimulus, two types of response develop:
1. Action potential or nerve impulse:
Action potential develops in a nerve fiber when it is stimulated by a stimulus with adequate strength. Adequate strength of stimulus, necessary for producing the action potential in a nerve fiber is known as threshold or minimal stimulus. Action potential is propagative in nature.
- Electrotonic potential or local potential:
When the stimulus with subliminal strength is applied, only electrotonic potential develops and the action
potential does not develop. Electrotonic potential is non-propagative.
2) Conductivity
Conductivity is the ability of nerve fibers to transmit the impulse from the area of stimulation to the other areas. Action potential is transmitted through the nerve fiber as nerve impulse. Normally in the body, the action potential is transmitted through the nerve fiber in only one direction.
However, in experimental conditions
when, the nerve is stimulated, the action potential travels through the nerve fiber in either direction.
3) Refractory Period
Refractory period is the period at which the nerve does not give any response to a stimulus.
Refractory period is of two types:
1. Absolute Refractory Period:
Absolute refractory period is the period during which the nerve does not respond to any second stimulus, no matter how strong it is.
- From when the firing level is reached till when one third of repolarization is completed.
- Relative Refractory Period
It is the period, during the action potential where the nerve can
respond to a second stimulus, provided it is greater than threshold stimulus.
- Rest of the repolarization and hyperpolarization
4) Summation
When one subthreshold stimulus is applied, it does not produce any response in the nerve fiber because, the subthreshold stimulus is very weak. However, if two or more subthreshold stimuli are applied within a short interval of about 0.5 millisecond, the response is produced. It is because the subthreshold stimuli are summed up together to become strong enough to produce the response.
This phenomenon is known as summation.
5) Adaptation
While stimulating a nerve fiber continuously, the excitability of the nerve fiber is greater in the beginning. Later
the response decreases slowly and finally the nerve fiber does not show any response at all. This phenomenon
is known as adaptation or accommodation.
Continuous depolarization inactivates the sodium pump and increases the
efflux of potassium ions.
6) Infatigability
Nerve fiber does not get fatigued, even if it is stimulated continuously for a long time.
7) All or none law
All-or-none law states that when a nerve is stimulated by a stimulus it gives maximum response or does not
give response at all
saltatory conduction
Saltatory condition is the mode of transmission of an impulse in which the impulse jumps from one node of Ranvier to the next . It is seen in case of myelinated nerve fibers .
Mechanism of transmission :-
The myelinated nerves are covered by myelin sheath deposited by Schwann Cells . It contains the lipid Sphingomyelin, which acts as insulator and prevents the flow of ions across the membrane.
Thus action potential is generated only at the nodes of Ranvier and impulse jumps from one node to the next. This is called Saltatory Conduction
That is, electrical current flows through the surrounding ECF outside the myelin sheath as well as through the axoplasm inside the axon from node to node.
Significance of saltatory conduction :-
- It increase the velocity of transmission of an impulse 5-50 times. Therefore conduction is faster in myelinated than in unmyelinated fibres.
- It conserves the energy for the axon because ions flow only at the nodes of Ranvier, therefore less energy is required to reestablish concentrations of Na+ and K+ ions across the membrane.
- The process of repolarisation becomes faster (permitting transmission of more impulses) because very few ions are transferred out of fibres during depolarization.
Action potential
Action potential is a rapid, reversible and conductive change of the membrane potential after the cell is stimulated adequately.
Action potential occurs in two phases:
- Depolarization
- Repolarization.
Depolarization:
Depolarization starts after the latent period. Initially, it is very slow and the muscle is depolarized for about 15 mV
Firing level and depolarization
After the initial slow depolarization for 15 mV, the rate of depolarization increases suddenly. The
point at which, the depolarization increases suddenly is called firing level.
Overshoot
From firing level, the curve reaches isoelectric potential (zero potential) rapidly and then shoots up (overshoots)
beyond the zero potential (isoelectric base) up to +30 mV. It is called overshoot.
Repolarization:
When depolarization is completed (+30 mV), the repolarization starts. Initially, the repolarization occurs rapidly and then it becomes slow.
Spike potential
Rapid rise in depolarization and the rapid fall in repolarization are together called spike potential. It lasts for 0.4 millisecond.
After depolarization or negative after potential:
Rapid fall in repolarization is followed by a slow repolarization. It is called after depolarization or negative after potential. Its duration is 2 to 4 milliseconds.
After hyperpolarization or positive after potential:
After reaching the resting level (–90 mV), it becomes more negative beyond resting level. This is called after
hyperpolarization or positive after potential. This lasts for more than 50 milliseconds. After this, the normal
resting membrane potential is restored slowly.
Ionic Basis:
Under-resting condition nerve fibre has got resting membrane potential of −90 mV. This is called polarized state. At the site of threshold stimulus the membrane permeability for sodium increases.
Sodium ions diffuse from extracellular fluid into the fibre. This increases the voltage at the site.
Change in voltage to threshold level initiates positive feedback cycle for opening of more and more number of voltage-gated sodium channels, due to which permeability of membrane for sodium increases to 5000 times as compared to that at resting level.
This allows entry of more positive charges into the fibre (in the form of sodium ions) than the number leaving the fibre (in the form of potassium ions).
Diffusion of large number of sodium ions to the interior of the fibre causes development of positivity inside the fibre (reversal potential) and negativity outside the fibre. This is known as depolarization. At this time, potential at the site rises abruptly from −90 mV to +55 mV in a short period of time
After depolarization, returning of membrane potential of the fibre back to the resting level is known as repolarization. When fibre is depolarized its potential rises from −90 mV to + 55 mV. At the same time, sodium channels are closed and potassium channels open up. So now nerve membrane is more permeable to potassium ions.
More number of potassium ions diffuse from interior of the fibre to exterior than the number of sodium ions diffusing in. This brings the potential of the fibre back to resting level rapidly
Unlike the Na+ channels, the K+ channels remain open for longer duration. These channels remain opened for few more milliseconds after completion of repolarization. It causes efflux of more number of K+ producing more negativity inside. It is the cause for hyperpolarization.
wallerian Degeneration
Augustus Waller first described the changes that occured when axons were physically separated from their cell bodies.
After the nerve is sectioned the nerve degenerates. The various functional and morphological changes that occur in the part of the nerve distal to the injury are called Wallerian degeneration.
Though nerve continues to conduct impulses for three days (after third day ability to conduct impulses is deteriorated and after fifth day nerve fails to conduct any impulse), morphological changes start appearing in about 24 hours.
Various changes are as follows:
- Axis cylinder along the whole length breaks into short lengths.
- Myelin sheath disintegrates into fat droplets in 8 to 10 days
- Macrophages from endoneurium invade the degenerating myelin sheath and axis cylinder.
- Macrophages phagocytoze the debris formed by remnants of myelin sheath and axis cylinder. They also secrete certain enzymes which aid in the destruction of myelin sheath. Thus only empty endoneural tubes remain.
Degenerating fibre can be stained with Marchi’s stain. It appears black after staining (between 8 and 21 days after injury).
Strength Duration Curve and Functional assessment of nerve damage.
e graph that demonstrates the
exact relationship between the strength and the duration
of a stimulus. So, it is also called the strength-duration
curve
Rheobase is the minimum strength (voltage) of stimulus,
that can elicit a biological response
Utilization time is the duration for which a stimulus of rheobase strength needs to be applied for in order to elicit a biological response.
Chronaxie is the duration that a stimulus twice the strength of rheobase needs to be applied for in order to elicit a biological response.
Importance of chronaxie
Measurement of chronaxie determines the excitability of the tissues. It is used to compare the excitability in different tissues. Longer the chronaxie, lesser is the excitability.
Myasthenia gravis
Myasthenia gravis is an autoimmune disease which occurs in about 1 in every 20,000 persons.
- Affected muscles are paralysed because of inability of neuromuscular junction to transmit the signals from nerve to the muscle fibres.
Pathologically, antibodies are produced against proteins of acetylcholine-gated channels.
This causes reduction in number of subneural clefts. The magnitude of end plate potential developed is mostly too weak to initiate opening of voltage gated sodium channels and thus muscle fiber depolarization does not occur. if the disease is intense enough the patient may die of respiratory failure as a result of severe weakness of the respiratory muscles.
the disease can usually be suppressed for hours by administering neostigmine or some other anticholinesterase drug that allows larger than normal amounts of ach to accumulate in the synaptic space. within minutes some of these people can begin to function normally until a new dose if required a few hours later.
Clinical features:-There is extreme weakness and fatigability (Myasthenia-muscle weakness, gravis - grave). There is drooping of eyelids, dysphagia, nasal regurgitation of food (due to paralysis of palatal muscles) and inability to carry out sustained movements.
Lambert Eaton Syndrome
In this syndrome, antibodies act against the voltage gated calcium channels in the terminal bouton of the axon.
As a result once the action potential reaches the nerve terminal calcium does not enter the nerve terminal and the subsequent events of neuromuscular transmission do not occur.
As a result there is reduced ach release from the nerve terminal and muscle contraction is impaired.
Patients with this syndrome have muscle weakness — the lower limbs are affected more than upper limbs.
- most often associated with lung cancers and with other autoimmune diseases
Excitation - Contraction Coupling
Excitation-contraction coupling refers to the sequence of events by which an action potential in the plasma membrane of a muscle fibre leads to cross-bridge activity by increasing cytosolic calcium concentration.
Stages of excitation-contraction coupling
• When a muscle is excited (stimulated) by the impulses passing through motor nerve and neuromuscular junction, action potential is generated in the muscle fiber.
• Action potential spreads over sarcolemma and also into the muscle fiber through the ‘T’ tubules. The ‘T’
tubules are responsible for the rapid spread of action potential into the muscle fiber.
• When the action potential reaches the cisternae of ‘L’ tubules, these cisternae are excited. Now, the calcium ions stored in the cisternae are released into the sarcoplasm
• The calcium ions from the sarcoplasm move towards the actin filaments to produce the contraction.
• Ca binds to troponin C
• Conformational change in tropomyosin
• Exposure of the binding sites on actin
• Myosin head binds to active site
• Power stroke — muscle shortening
Thus, the calcium ion forms the link or coupling material between the excitation and the contraction of muscle. Hence, the calcium ions are said to form the
basis of excitation-contraction coupling.
Sarcomere
Sarcomere is the fundamental contractile unit of the muscle fi bre.
The muscle fibre contains a large number of myofibrils formed of muscle filaments or myofilaments.
Myofilaments are of two types—myosin filaments and actin filaments.
Myosin filaments are thick, about 1,500 in number. Actin filaments are thin, around 3000 in number. These filaments lie side by side. They partially interdigitate forming alternate dark and light bands. The light band contains only actin filaments and is termed ‘I’ band, because it is isotropic to polarized light. The dark band contains myosin filaments as well as ends of actin filaments overlapping the myosin filament. This
band is termed ‘A’ band because it is anisotropic to polarized light. There are small projections from the sides of myosin filament which are called cross bridges. They protrude from the surfaces of myosin filaments along the entire extent of filament except in the centre.
At regular intervals, Z discs or Z membranes composed of filamentous proteins divide the entire muscle into sarcomeres as they pass across the muscle fibre. The portion of myofibril (or whole muscle) which lies between two successive Z membranes is termed sarcomere. In a sarcomere, actin filaments are attached to Z membranes and they overlap the myosin filaments present in the centre of the sarcomere. When the length of sarcomere is two microns, actin filaments completely cover the myosin filaments and begin to overlap each other
Sarcotubular system
Sarcotubular system:-
Sarcotubular system is a system of membranous structures in the form of vesicles and tubules in the sarco plasm of the muscle fiber. It surrounds the myofibrils embedded in the sarcoplasm.
Forms the basis of excitation contraction coupling. It consist of
1.Transverse or T tubules :-Ttubules or transverse tubules are narrow tubules
formed by the invagination of the sarcolemma. These tubules penetrate all the way from one side of the muscle fiber to an another side. That is, these tubules penetrate the muscle cell through and through. Because of their origin from sarcolemma, the T tubules open to the exterior of the muscle cell. Therefore, the ECF runs through their lumen.
function: T tubules are responsible for rapid transmission of impulse in the form of action potential from sarcolemma to the myofibrils.
2.Longitudinal L tubules:-These are parts of sarcoplasmic (Endoplasmic) Reticulum and are arranged longitudinally situated between the myofibrils. At either ends they have dilatations called ‘Terminal cisternae’.
The L Tubules store large quantity Ca ions and protein called cal-sequestrin facilitates the storage. L tubules also contains voltage gated Ca ++ channels and calcium pumps.
Each pair of terminal cisternae is in close contact with Ttubule. The Ttubule along with the cisternae on either side is called the triad of skeletal muscle.
Function: L tubules store a large quantity of calcium ions. When action potential reaches the cisternae of L tubule, the calcium ions are released into the sarcoplasm
Sliding Filament Theory
Contraction of skeletal muscle involves 2 types of proteins –
A. Contractile proteins called Actin and Myosin.
B. Regulatory proteins called Tropomyosin and Troponin.
Myosin:
Each myosin filament consists of about 200 myosin molecules
- made up of 6 polypeptide chains ; 2 heavy chains and 4 light chains.
At one end, the heavy chains are coiled around each other forming a double helix or ’tail’.
At the other end, the heavy chains project outwards and are folded at the tip to from a globular 'head'. Each head of myosin molecule also has (a) 2. Light chains, (b) ATP binding site and (c) ATPase activity.
The projecting part of heavy chain called ‘arm’ which together with head forms ‘crossbridge’
Actin:
Actin present in muscles is a globular
protein called G actin
such G actin molecules are
Polymerized to form F actin strands.
Two such F actin strands wind around
each other to form actin filament
There is one active site on each G actin molecule to which head of myosin molecules bind.
Tropomyosin:-
Is an elongated ribbon like molecule Many such tropomyosin molecules are polymerized to form tropomyosin strands which are situated in the groove
between two F actin, strands loosely attached to them.
In the resting state, tropomyosin strands physically cover the active sites on actin filament and prevent interaction between actin and myosin.
Troponin:- Is a globular protein molecule attached to each tropomyosin molecule.
It is made up of 3 sub unit:
• Troponin T which binds with tropomyosin,
• troponin I which has strong affinity for actin and
• troponin C which is attached to calcium ions.
Mechanism:
1) Arrival of impulse at nerve terminals
2) NM transmission
3) Excitation - contraction coupling
4) Release of Ca ions
5) Binding of Ca2+ to Troponin C
6) Conformational changes in Tropomyosin
7) Opening of binding sites of actin
8) With the helo of atp upward movement of myosin heads and its binding to actin
9) Cross bridge formation and power stroke
10) As myosin heads bind at the cross bridges detach from actin.
For detachment of myosin heads ATP is necessary
Hence this mechanism is called ‘walk along theory ‘ or ‘Retchet Theory’ of muscle contraction.
- A band does not change
- H band decreases and eventually disappears
- I band also decreases in size
Rigor Mortis
Several hours after death all the muscles of the body go into a state of contracture called rigor mortis i.e the muscles contract and become rigid even without action potentials. this rigidity results from loss of all the atp which is required to cause separation of the cross bridges from the actin filaments during the Relaxation process.
The muscles remain in rigor until the muscle proteins deteriorate about 15-25 hours later, which presumably results from autolysis caused by enzymes released by the lysosomes. all these events occur more rapidly at higher temperatures
Heat Rigor
muscle undergoes shortening when it is exposed to heat for instance, at around 50°C or greater during which there is coagulation of muscle proteins.
This is readily demonstrated in isolated muscle preparations and is called heat rigor
