Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Systems > Nerve > Flashcards

Nerve Flashcards

1
Q

Junction between what is a neuromuscular junction
Other names for this junction .
It’s function

A

Motor neuron and a muscle fibre .neural membrane and sarcolemma , do not touch but apposed to each other
Names - Myoneural junction or motor end plate
Transmission of action potential from neuron to the muscle fibre .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Structure of the neuromuscular junction

A

Divided into 3 parts - presynaptic ,synaptic ,post synaptic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presynaptic portion (axon terminal )

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are motor neurons

A

Skeletal muscle fibres , have cell bodies in anterior horn of the spinal cord or in the brainstem.
Myelinated axons , largest diameter axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Schwann cells that cover terminals called

A

Teloglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Each terminal is expanded at its end to form a synaptic knob (terminal button )

A

Contains plenty of mitochondria ( indicates metabolic activity)and neurotransmitter vesicles.
Lies in groove (synaptic trough) in the surface of the muscle fiber but outside the muscle cell membrane .

The vesicles ,clustered around points, active zones .
Active zone membrane, dense bar contains numerous VG Ca2+ chammels . Medicate ACh release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Synaptic cleft , gap btw terminal button and ,uncle fiber

A

Width - 40-100nm
Muscle fiber covered by CT called basement membrane or basal lamina [consist collagen , glycoprotein , Extra matrix proteins ]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which part of synaptic cleft contains the enzyme Acetylcholine- esterase

A

Basement membrane , enzyme anchored to the collagen fibrils and secreted into membrane by presynaptic terminal and muscle fiber .

AChE rapidly hydrolyses ACh into acetate and choline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is quanta release

A

Process of release of neurotransmitter Quanta =Vesicle / multi molecular packet ACh ,
Witch each AP, presynaptic terminal discharges same mount of neurotransmitter
Quantum of neurotransmitter / quantal content / number of vesicle released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

End plate potential (EPP)

A

Amplitude of it is proportional to the amount of neurotransmitters released *****

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Presynaptic blockade of neuromuscular transmission

A

Events at pre synaptic axon terminal -impaired calcium influx causing decreased vesicle release
*botulinum toxins B , D F , G - inactivate synaptobrevin ( vesicle membrane protein that is required for binding and fusion of a ACh vesicle with the plasma membrane of the axon terminal .)
*A &B act on snap-25
*C breaks down syntaxin
*hemicholinium - inhibits choline uptake by terminal , result in depletion of ACh . Consequently EPP decreases and ap cannot be formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Major functions of anti- AChR antibodies in myasthenia gravies B

A

1.compete with ACh to bind to AChR , receptor blockade
2. Induce endocytosis of AChR
3. Damage post-synaptic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of myasthenia gravis

A
  • fatigue - normally repeated stimulation of motor nerve , amount of ACh released per action potential gradually decreases (presynaptic rundown ) but enough to generate an EPP well above threshold level .
    MG Patients = decremental response to repetitive nerve stimulation on EMG recording from affected muscle
  • women to men 3:2
  • weakness - Increases on prolonged use , better after rest /sleep
    *extraocular muscles and eyelids involved early course . Diplopia (double vision) and ptosis(eyelid drooping )
    *proximal limb muscles affected
    Resp muscle paralysis - death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment of myasthenia gravis

A

*Adminst AChE inhibitors (pyridostigmine , neostigmine)
Increase ACh at nmj
*thymectomy - reduces immune response by T cells .and improves condition
* immunosuppression - glucocorticoids, azathioprine . Inhibit immunological mech
*plasmapheresis -removes AChR antibodies from plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lambert- Eaton myasthenic syndrome caused due to

A

Presynaptic disorder of nmj due to production of antibodies against Vg Ca2+.
Decreased ions= impaired ACh release from nerve endings .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Etiological of myasthenia gravis

A

Decrease in number of AChR present on motor end plate due to production of circulating antibodies against R .
Post synaptic folds flattened or simplified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Symptoms and signs of lambert-Eaton myasthenia syndrome

A

Muscular weakness 1° in limb muscles
Incremental response to repetitive nerve stimulation as Ca level rises with each AP , prolonged contraction muscle strength increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is denervation hypersensitivity

A

When neuron is cut , distal axons degenerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are connective tissue layers around the muscle made up of

A

Collagen and elastin that helps transmit the force from the muscles to the bones . Muscles usually attached to bones by collagen fiber (tendon )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rigor mortis

A

Stiffening of muscle after death
Within 3 to 6 h of death , as ATP conc decreases in all cells.
Depletion of ATP fails to detach the cross bridge , therefore muscle remains in a state of contraction or rigidity.
Rigidity completes in 12 h
Disappears in 40 to 60 h due to disintegration and putrefaction of muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Thickness of thin :thick filament

A

1:2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

The structural unit of muscle in muscle fibre that is a

A

single skeletal muscle cell (myocyte)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The important functions of the sarcolemma

A
  1. Transmits the wave of depolarisation originating at the motor end plate over the entire cell surface to initiate contraction.
  2. Contributes to the parallel elastic resistance ( the resistance to stretch offered by all the connective tissue layers )
  3. It has no gap junctions or tight junctions, thereby pro- motes electrical separation between fibers.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Three types of muscle proteins in skeletal muscles

A

Contractile proteins : actin and myosin
Regulatory proteins : troponin and tropomyosin
Attachment proteins : Titian , nebulin, alpha actinin, , deaminase , myomesin , dystrophin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

A myosin filament is composed of

A

Two intertwined heavy chains
Two regulatory light chains
Two alkali (essential) light chains

26
Q

The three regions of myosin II

A

Two globular heads ,
Neck (hinge region )
Long tail

27
Q

The two binding sites of myosin head

A

One for actin and one for ATP(functions as ATPase by hydrolyzing ATP)

28
Q

The function of the two light chains of myosin head

A

Alkali light chain - stabilises the myosin head
regulatory light chain - regulates ATPase activity

29
Q

What are tropomyosin

A

Composed of two strands of polypeptides in an alpha helical config with length approx equal to sevenmm actin filament
S

30
Q

What is calmodulin

A

Small protein associated with Myosin light -chain kinase (MLCK)
MLCK - Ca++ calmodulin dependent protein kinase .

31
Q

Major events of smooth muscle contraction and relaxation

A
  1. Ca++ influx into the smooth muscle cell
    2.binding of ca++ with calmodulin-dependent MLCK
  2. Phosphorylation of myosin
    4.increased myosin ATPase activity
    5.myosin binds with actin resulting in cross bridge formation
    6.contraction of muscle
  3. Dephosphorylation of myosin by MLCP
    8.Latch- bridge state
    (Sustained contraction )
  4. slow relaxation
32
Q

RMP of skeletal muscle

A

-90 mV

33
Q

RMP of cardiac muscle

A

-80 mV

34
Q

RMP of smooth muscle

A

-55 mV
Unstable

35
Q

Missal granules or bodies

A

Basophilic granules composed of many thin , parallel arranged membrane bound cavities or cisternae which are covered by many minute particles consisting of ribose nucleo- proteins, i.e. RNA with protein

36
Q

Neurofibrillae

A

Fine threads 6-10nm in diameter and of variable length
Transverse the cytoplasmic matrix
Form a loose framework of fibrils in cytoplasm

37
Q

Muscle cell with poorly developed sarcoplasmic reticulum and no characteristic sarcotubular system

A

Smooth muscle

38
Q

Sarcotubular system is present A-I junction in

A

Skeletal muscle

39
Q

Sarcotubular system is present at ____ in cardiac muscle

A

At Z lines

40
Q

Length tension relationship in different muscles

A

Skeletal -maximum active tension at optimal length
Cardiac -same
Smooth - property of plasticity

41
Q

Excitation contraction coupling , slowest

A

Smooth muscle

42
Q

Muscle twitch duration of cardiac muscle

A

1 1/2 times the total duration of action potential

43
Q

Blood supply to each type of muscle

A

Skeletal- 3to 4 ml / 100gm
Cardiac - 80ml /100gm/min
Smooth - 1.4 ml /100gm /min

44
Q

Sliding filament theory ( ratchet theory)

A

The process by which the shortening of the contractile elements in the muscle is brought abt by sliding of actin filament over the thick (myosin ) filament . Sliding of filaments is brought about by the formation of cross bridges between the head of myosin and actin molecules

45
Q

When nerve fiber is sufficiently injured which part begins to die . What is the process called

A

The part proximal to it .
Wallerian Degeneration

46
Q

Nerve membrane in close approximation with the muscle membrane is called

A

Presynaptic membrane

47
Q

The muscle membrane in a NMJ is called

A

Post synaptic membrane

48
Q

The space between the 2 membranes in NMJ ,and what is it filled with

A

Synaptic cleft (50-100nm wide )
Filled with ECF

49
Q

What is found in high conc in the postsynaptic clefts and what is their function

A

An enzyme specific acetylcholinesterase , which destroys ACh

50
Q

Name of the many folds of muscle membrane on the post synaptic membrane and it’s function

A

Subneural cleft , increases surface area for the synaptic transmitters

51
Q

The axon terminal part of the axon has many __

A

Has many mitochondria (for the synthesis of ACh ]
also has many small pockets of chemical neurotransmitter ACh ( responsible for synaptic transmission)

52
Q

Synthesis of ACh

A

Within the mitochondria from choline in e presence of enzyme Choline Acetyl transferase ( choline acetylase )
Requires co-enzyme A ,ATP and glucose .
only choline not already present in the mitochondria or ready access to them

53
Q

Diagram of neuromuscular junction

A

Mitochondria
Synaptic vesicles
Voltage gated Ca2+ channels
Axon terminal
Pre synaptic membrane
Docking protein
Postsynaptic receptor
Neurotransmitter molecules released from fused vesicles

54
Q

Storage and release of NMJ

A

Temporarily stored in minute vesicles
Nerve impulses cause fusion of vesicles with membrane of terminal nerve fiber
by increasing permeability of ca++

55
Q

Function of ca++ in a NMJ

A

Ca++ in ECF helps in fusion by changing ionic composition thereby decreasing the flow of axoplasm so vesicles easily come in contact with the membrane .
Mg2+ decrease this process.
Amount of transmitter released is directly proportional to to Ca2+ influx

56
Q

Sequence of events during nerve impulse transmission.

A

1.MOTOR NERVE FIBER action potential
2. AXON TERMINAL opening of voltage gated calcium channels
3.entry of calcium ions from ECF
4. Opening of vesicles and release of ACh
5. SYNAPTIC CLEFT
passage of ACh
6.POSTSYNAPTIC MEMBRANE
binding of ACh with receptors and formation of ACh receptor complex
7.opening of ligand gated sodium channels
8.Entry of sodium ions from ECF
9. development of endplate potential
MUSCLE FIBER
10. generation of action potential
11. Excitation contraction coupling
12. Muscular contraction

57
Q

Toxins which blocks neurotransmitter release

A

a. d tubucurarine competes with ACh for same nicotinic receptors on the motor endplate.
b. Tetanus and botulinum neurotoxin-b cleaves VAMP

c. Botulinum neurotoxin-b cleave SNAP-25
(Tetanus cause spastic paralysis, botulinum cause flaccid paralysis).

58
Q

Drugs that stimulate nmj by inactivating acetylcholinesterase

A
  1. Neostigmine
  2. Physostigmine
  3. Diisopropyl fluorophoshate
59
Q

Define Excitation contraction coupling

A

Process by which depolarization of the muscle fiber initiates contraction

60
Q

Sequence of events in excitation contraction coupling

A

*steps in muscular contraction
1.stimulation of motor neuron
2.release of ACh into the synaptic cleft ,
Causing generation of end plate potential
3. Depolarization of muscle membrane by increasing its permeability of na+
4.generation of action potential in the muscle fiber
5.inward spread of
AP along the T-system
6. Spread of depolarization to terminal cistern with the release of Ca+ in myofibrils
7.increase of ca++ concentration in ICF by 2000 times
8. Muscle contraction

  • steps in muscle relaxation
    1. Few milliseconds after AP is over , SER begins to reaccumulate Ca++
    2. Ca++ ions are actively pumped by the Ca+- Mg+ ATPase pump
    In to the longitudinal portion of the reticulum to terminal cistern for storage
61
Q

Role of Ca++ in ECC , Muscle contraction

A

*Ca++ binds w/ troponin C causing tropomysoin to move laterally . Exposes binding site for myosin heads on the actin .
* activated prosthetic group of myosin filament which acts as enzyme (ATPase )

62
Q

Law that states length-tension relationship of cardiac muscle

A

Starlings law
Frank-starling law

Systems (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions