5.1.5b animal responses Flashcards

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1
Q

what are the two fundamental components of the nervous system?

A

Central nervous system and Peripheral nervous system

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2
Q

what is the Central nervous system?

A

Brain + Spinal cord
many relay neurones
the coordination centre, controlling the whole nervous system

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3
Q

what is the peripheral nervous system?

A

nerves (sensory and/or motor)
allows for communication between sensory recpetors, then CNS and effectors

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4
Q

what part of the nervous system is the somatic nervous system and autonomic nervous system apart of?

A

The peripheral nervous system

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5
Q

what is the PNS organised into?

A

Somatic nervous system
autonomic nervous system

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6
Q

what is the Somatic nervous system?

A

motor neurones that transmit action potentials from the CNS to the skeletal muscles.

consciously controlled or unconsciously controlled

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7
Q

what is the autonomic nervous system?

A

motor neurones that transmit action potentials from the CNS to the viscera (internal organs)

unconscious control only

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8
Q

what makes up he autonomic nervous system?

A

sympathetic and parasympathetic nervous systems

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9
Q

what makes up the sympathetic and parasympathetic nervous systems

A

Autonomic nervous system

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10
Q

when is the sympathetic nervous system active, and what does it coordinate, what is the neurotransmitter?

A

active in waking hours

coordinates the fight or flight response

noradrenaline

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11
Q

when is the parasympathetic nervous system active, and what does it coordinate, what is the neurotransmitter?

A

most active during sleep

coordinates rest and digest functions

Acetylcholine

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12
Q

Draw a diagram summarising the organisation of the mammalian nervous system

A
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13
Q

Label this :)

A
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14
Q

what is the function of the meninges?

A

Provides cushioning for the brain

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15
Q

what are the roles of the cerebro-spinal fluid?

A

Shock absorbtion

Absorbs excess heat energy + carries it away cooling the brain

Provides O2, glucose… to neurones and cells and removes waste CO2

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16
Q

What is the folded section of the cerebrum called?

A

Cerbebral cortex

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17
Q

what is the function of the cerebrum?

A

‘higher’ brain functions, including reasoning, problemsolving,

logic, speech;

initiation of consciously‐controlled movements;

memory;

personality.

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18
Q

what is the function of the cerebellum?

A

unconscious control of learned sequences of muscle contraction, e.g. during walking, cycling, driving, writing, producing a tennis serve etc;

control of posture and balance.

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19
Q

what is the function of the medulla oblongata (brain stem)?

A

unconscious control of basic body functions, e.g. breathing rate, heart rate, swallowing, peristalsis.

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20
Q

what is the function of the hypothalamus?

A

control of many aspects of homeostasis, e.g. contains thermoreceptors and osmoreceptors and is the coordination centre for both thermoregulation and osmoregulation

also controls hormone secretions from the pituitary gland (located just beneath it).

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21
Q

what is the function of the pituitary gland?

A

the ‘master endocrine gland;’ (secretes tropic hormones which control the release of other hormones)

secretes many hormones, including ADH [posterior pituitary] and growth hormone [anterior pituitary]

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22
Q

what is the definition of a reflex action?

A

A rapid, automatic response to a stimulus.

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23
Q

what part of the brain is used in a reflex action?

A

unconcious part of the brain

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24
Q

where does the neuronal pathways pass through in a reflex action?

A

simple neuronal pathways

two or three neurones

reflex pass through the CNS

spinal cord = spinal reflex

unconcious part of the brain = cranial reflex

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25
Q

why do we have reflex actions?

A

to increase out adaptive (survival) value

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26
Q

give two examples of reflexes with obvious adaptive value

A

Pupil constriction in response to bright light – decreases amount of bright light reaching the retina and hence decreases retinal damage

Withdrawing hand rapidly in response to touching a hot object – decreases length of skin contact time with object and hence decreases skin damage via burning

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27
Q

Example: Knee Jerk Reflex

Type of reflex:

Stimulus:

Receptor:

Neuronal pathway:

Effector:

Response:

Adaptive value:

A

Type of reflex: Spinal reflex

Stimulus: Stretching of the patella tendon

Receptor: Proprioceptors within the patella tendon

Neuronal pathway: Receptor → sensory neurone → synapse → relay neurone within the
spinal cord → synapse → motor neurone → effector

Effector: Skeletal muscle

Response: Lower part of leg jerks upwards

Adaptive value: Plays a role in balance during walking

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28
Q

Example: The blinking reflex

Type of reflex:

Stimulus:

Receptor:

Neuronal pathway:

Effector:

Response:

Adaptive value:

A

Type of reflex: Cranial reflex

Stimulus: Various - ie sudden exposure to bright light

Receptor: Photoreceptors in the retina of the eye

Neuronal pathway: → sensory neurone → synapse → relay neurone within an unconscious part of the brain → synapse → motor neurone → effector

Effector: Skeletal muscle

Response: Both eyelids close rapidly, i.e. blinking occurs

Adaptive value: Protective role, decreasing the chance or extent of mechanical damage to the eyeball or of photodamage to the retina

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29
Q

What two systems must work synergistically to controll the heart rate?

A

Nervous system and endocrine system

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30
Q

what is a typical resting heart trate? What happens to this during fight or flight and exercise?

A

70bmp

During exercise and during a fight or flight response, heart rate is increased in order to deliver oxygen and glucose to muscles at a higher rate and to remove more carbon dioxide and lactic acid

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31
Q

what neuronal components are relevant when controlling the heart rate?

6 separate things

A

Chemoreceptors – receptors sensitive to the pH of the blood plasma are located in the walls of the aorta, walls of the carotid artery (in the neck) and within the medulla oblongata;
oIf carbon dioxide levels increase (e.g. due to higher rate of respiration during exercise), more carbon dioxide reacts with water to form carbonic acid, which dissociates into H+ (and HCO3‐), lowering the pH;
o If carbon dioxide levels decrease (e.g. due to lower rate of respiration during rest), less carbon dioxide reacts with water to form carbonic acid, raising the pH

Baroreceptors – receptors sensitive to changes in blood pressure are located in the walls of the aorta, walls of the carotid artery and walls of the vena cava

Sensory neurones – these transmit electrical impulses from the chemoreceptors and baroreceptors to the medulla oblongata

Medulla oblongata – this is the part of the brain acting as the coordination centre for control of heart rate, with increases and decreases initiated by different regions of the medulla:

Centre for increasing heart rate – connected to the SAN of the heart by motor
neurones of the sympathetic nervous system, bundled together in the accelerator nerve (releases noradrenaline at the SAN)
o Centre for decreasing heart rate – connected to the SAN of the heart by motor neurones of the parasympathetic nervous system, bundled together in the vagus nerve (releases acetylcholine at the SAN)

Autonomic (sympathetic or parasympathetic) motor neurones (in the accelerator or vagus nerves, respectively) – these transmit electrical impulses from the medullaoblongata to the SAN

Sino‐atrial node (SAN; t he pacemaker) – this is the relevant effector, stimulated to increase or decrease the frequency with which it in itiates the electrical impulses that trigger the start of each cardiac cycle.

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32
Q

how do we increase our heart rate during exercise or a fight or flight response (neuronal)

5 steps

A
  1. Chemoreceptors in walls of aorta and carotid arteries detect that blood pH is too low and/or baroreceptors detect that blood pressure is too low
  2. Electrical impulses sent via sensory neurones to the centre for increasing heart rate in the medulla oblongata
  3. The medulla sends electrical impulses via sympathetic motor neurones in the accelerator nerve to the SAN (pacemaker) of the heart
  4. SAN initiates more frequent electrical impulses, so more cardiac cycles occur per minute, i.e. heart rate increases
  5. Blood pressure increases and, because flow rate of blood also increases, more carbon dioxide is excreted via the lungs, causing blood pH to rise: negative feedback withrespect to both these variables has occurred.
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33
Q

how do we decrease our heart rate during rest and sleep?

5 steps

A
  1. Chemoreceptors in walls of aorta and carotid arteries detect that blood pH is too high and/or baroreceptors detect that blood pressure is too high
  2. Electrical impulses sent via sensory neurones to the centre for decreasing heart rate in the medulla oblongata
  3. The medulla sends electrical impulses via parasympathetic motor neurones in the vagus nerve to the SAN (pacemaker) of the heart
  4. SAN initiates less frequent electrical impulses, so fewer cardiac cycles occur per minute, i.e. heart rate decreases
  5. Blood pressure decreases and, because flow rate of blood also decreases, less carbon dioxide is excreted via the lungs, causing blood pH to fall: negative feedback with respect to both these variables has occurred.
34
Q

how do we increase our heart rate during exercise or a fight or flight response (hormonal)

3 steps

A
  1. The hypothalamus, via motor neurones of the sympathetic nervous system, stimulates the adrenal medulla to secrete more adrenaline and noradrenaline directly into the blood
  2. These hormones bind to complementary receptors in the plasma membranes of cardiac muscle fibres in the SAN of the heart
  3. The consequence is that the SAN generates electrical impulses more frequently, so that new cardiac cycles are initiated more often and hence the heart rate increases.
35
Q

how do we decrease our heart rate during rest and sleep? (hormonal)

3 steps

A
  1. The hypothalamus does not transmit as many electrical impulses via sympathetic motor neurones to stimulate the adrenal medulla, so less adrenaline and noradrenaline are secreted into the blood
  2. Not as many adrenaline and noradrenaline hormones bind to complementary receptors in the plasma membranes of cardiac muscle fibres in the SAN of the heart
  3. The consequence is that the SAN generates electrical impulses less frequently, so that new cardiac cycles are initiated less often and hence the heart rate decreases.
36
Q

what is the fight or flight response?

A

A response the perception of a threat.

its prepare the body for self defence or for rapid escape

37
Q

How does the nervous system and endocrine system work synergistically to bring about the fight or flight
response?

7 steps

A
  1. The initial detection of the threat involves sensory receptors which detect environmental stimuli, e.g. the photoreceptors in the retina of the eye which give visual perception
  2. These receptors send electrical impulses via sensory neurones to the sensory areas of the cerebral cortex in the brain
  3. Electrical impulses are transmitted via relay neurones to association areas of the cerebral cortex, where a decision is reached about whether the sensory inputs suggest the presence of a threat to survival
  4. If so, electrical impulses are sent via relay neurones to the hypothalamus, which activates the sympathetic nervous system
  5. Sympathetic motor neurones (which secrete noradrenaline as the neurotransmitter at their NMJs) stimulate numerous body organs as detailed below
  6. Stimulation of the adrenal medulla by sympathetic motor neurones results in increased adrenaline and noradrenaline release directly into the blood
  7. These hormones act synergistically with the direct stimulation of organs by sympathetic motor neurones: the hormones bind to receptors in the plasma membranes of target cells and trigger the responses detailed below
38
Q

what occurs under stimulation by the sympathetic nervous system and/or increased adrenaline levels?

8 points

A

Increased breathing rate and tidal volume, i.e. faster and deeper breathing – creates steeper concentration gradients for O2 and CO2 so that rates of O2 uptake and CO2 excretion increase, supporting a higher rate of aerobic respiration in the body cells

Dilation of bronchi and bronchioles due to relaxation of circular smooth muscle and contraction of longitudinal smooth muscle in their walls – this decreases resistance to airflow so that both inspiration and expiration require less effort

Stimulation of the SAN resulting in increased heart rate and increased force of contraction of cardiac muscle (giving increased stroke volume) – the cardiac output, blood pressure and flow rate of blood all increase, delivering oxygen and glucose more rapidly to skeletal muscles (supporting a higher respiration rate) and carrying away more waste CO2 and lactic acid

Peripheral vasoconstriction in arterioles leading to skin capillaries, resulting in decreased blood flow to skin surface – means that more blood flow can be diverted to skeletal muscles, liver and brain

Increased glycogenolysis in the liver and increased release of glucose from liver cells into the blood, so blood glucose concentration rises – more glucose is available to skeletal muscles and the brain for respiration

Decreased digestive functions, including decreased secretion of pancreatic juice by exocrine tissues in the pancreas and decreased peristalsis of smooth muscle in the gut walls – more blood flow and more energy available to skeletal muscles and brain

Dilation of pupils due to relaxation of circular smooth muscle and contraction of radial smooth muscle in the iris – allows more light to reach the retina and hence improved quality of vision

Increased alertness and decreased threshold for perception of environmental stimuli – allows early detection of threats in the surroundings

39
Q

Are adrenaline molecules polar or non-polar? What does this mean for hormonal communication?

A

Non-polar

they cannot freely pass through the phospholipid bilayer of a plasma membrane

receptors embedded in the plasma membrane - hormone can bind to the receptor without having to enter the cell .

glycoprotein w/ binding site that is complementary in shape to adrenaline

40
Q

Following the release of adrenaline into the blood from the adrenal medulla, what is the sequence of events that occur?

A
  1. When the adrenaline hormone binds to the complementary binding site of its specific receptor (located in the plasma membrane of the target cells), there is a change in the 3D shape of the receptor
  2. This causes activation of an enzyme called adenylyl cyclase, which is located on the cytoplasmic (inner) surface of the plasma membrane
  3. Adenylyl cyclase catalyses the synthesis of cAMP (cyclic adenosine monophosphate)
  4. As cAMP concentration rises in the cytoplasm, it starts binding to proteins that havean allosteric site of the appropriate complementary shape
  5. This activates the proteins (by causing a change in their 3D shape), including some that act as protein kinase enzymes
  6. The activated protein kinase enzymes catalyse the phosphorylation (attachment of aphosphate group) of other proteins, activating these proteins (including otherenzymes)
  7. In this way, there is a change in the metabolism of the target cell, as enzymes that were previously inactive have been activated by the binding of cAMP or by phosphorylation. For example, in liver cells, glycogen phosphorylase is activated, which catalyses the hydrolysis of glycogen to glucose (i.e. glycogenolysis).
41
Q

what would we describe the adrenaline hormone as?

A

first messenger

42
Q

what would we describe cAMP as?

A

second messenger

43
Q

what is the role of the adrenal-cortical system?

A
  • *hypothalamus also activates the adrenalcortical system (alongside the sympathetic nervous system), which will begin to coordinate responses to ongoing stress, as follows:**
    1. In response to the perception of threat, the hypothalamus releases CRF (corticotropinreleasing factor)
  1. CRF stimulates the pituitary gland to secrete ACTH (adrenocorticotropic hormone, also called corticotropin) directly into the blood
  2. ACTH binds to receptors on cells in the adrenal cortex, triggering release of many hormones, including the glucocorticoid stress hormone, cortisol
  3. Cortisol and the other hormones released by the adrenal cortex coordinate responses to ongoing stress, e.g. changes in the types of respiratory substrate used preferentially by body cells.
44
Q

what are the three types of muscle we have?

A

skeletal, smooth and cardiac

45
Q

Muscle type: Skeletal

Location and function:

Can contraction be consciously controlled:

Nervous system control:

Shape of cells/fibres:

Appearance of cells/fibres:

Number of nuclei per fibre:

Membranes form intercalated discs, with gap junctions present?:

Contraction speed:

Fatigue:

A

Location and function: Attached to the bones - contraction exerts a pulling force which causes a bone to move

Can contraction be consciously controlled: Yes

Nervous system control: Somatic (acetylcholine at the NMJ)

Shape of cells/fibres: Cylindrical

Appearance of cells/fibres: Striated (overlapping actin and myosin filaments)

Number of nuclei per fibre: Multinucleate

Membranes form intercalated discs, with gap junctions present?: No

Contraction speed: fast

Fatigue: Fatigues rapidly

46
Q

Muslce type: Smooth

Location and function:

Can contraction be consciously controlled:

Nervous system control:

Shape of cells/fibres:

Appearance of cells/fibres:

Number of nuclei per fibre:

Membranes form intercalated discs, with gap junctions present?:

Contraction speed:

Fatigue:

A

Location and function: Multiple - ie arteries, iris and stomach wall

Can contraction be consciously controlled: No

Nervous system control: Autonomic (noadrenaline or acetlycholine at NMJ)

Shape of cells/fibres: spindle-shaped

Appearance of cells/fibres: Non‐striated(no regular pattern in the overlapping actin and myosin filaments)

Number of nuclei per fibre: Mononucleate

Membranes form intercalated discs, with gap junctions present?: No

Contraction speed: Slow

Fatigue: Fatigues slowly

47
Q

Muscle type: Cardiac

Location and function:

Can contraction be consciously controlled:

Nervous system control:

Shape of cells/fibres:

Appearance of cells/fibres:

Number of nuclei per fibre:

Membranes form intercalated discs, with gap junctions present?:

Contraction speed:

Fatigue:

A

Location and function: walls of the atria and ventricles in the heart - atirial wall push blood into ventricles. Ventricular walls push blood into arteries

Can contraction be consciously controlled: No

Nervous system control: myogenic - initiate its own contractions without stimulation by motor neurones due to the SAN. heart rate can be increased by the sympathetic motor neurones of the accelerator nerve (noradrenaline) or heart rate can be increased by the sympathetic motor neurones decreased by the
parasympathetic motor neurones of the vagus nerve (acetylcholine)

Shape of cells/fibres: Branched

Appearance of cells/fibres: Semi‐striated,

Number of nuclei per fibre: Mononucleate

Membranes form intercalated discs, with gap junctions present?: Yes - enabling action potentials to be transmitted from one cell directly to the next.

Contraction speed: fast

Fatigue: Never fatigues

48
Q

what two prefixes relate to muscle?

A

myo- and sarco-

49
Q

what are myofibrils made up of?

A

actin, myosin, tropomyosin and troponin

50
Q

what is the plasma membrane of a muscle fibre called?

A

sarcolemma

51
Q

what is heavily present in a sarcolemma?

A

large numbers of ion channels and carrier proteins

52
Q

what are T-tubules?

A

where the sarcolemma folds inwards to form a tubular structure that penetrates into the fibre

53
Q

what is the function of T-tubules?

A

transmit action potentials

54
Q

what is the specialised form of endoplasmic retuculum closely associated with the T-tubules?

A

sarcoplasmic reticulum

55
Q

what does the lumen of the sarcoplasmic reticulum contain?

A

store of Ca2+ ions, needed in the NMJ

56
Q

Can the membrane of the sarcoplasmic reticulum depolarise?

A

Yes it can, the membrane contains voltage-gated Ca2+ channels

facilitated diffusion of Ca2+ out of the SR

Active transport of Ca2+ into the SR

57
Q

What is the cytoplasm in a mucle fibre refferd as?

A

Sarcoplasm

58
Q

how many mitochondria are in the sarcoplasm of a muscle fibre?

A

very large number of mitochondria, which provide ATP for the contraction mechanism

59
Q

what does sarcoplasm contain?

A

lots of mitochndira

The enzymes needed for areboic respiration

60
Q

what is a sarcomere?

A

repeating sections

identical.

smallest unit of muscle structure capable of shortening during contraction

61
Q

draw and label a sarcomere

A
62
Q

what is the thick filament made of?

A

Myosin

63
Q

what is the thin filament made of?

A

actin

64
Q

what is the Thick myosin filament of a sarcomere?

A

bundle of many myosin proteins, each of which has a globular head group that projects outwards from the filament and is capable of binding to actin

65
Q

what is the thin actin filament of the sarcomere?

A

made up of individual globular actin proteins which have formed a helical polymer; two other proteins – troponin and tropomyosin – associate with the actin proteins, blocking the binding sites that myosin heads could attach to

66
Q

what is the A band of the sarcomere?

A

denotes the region of the sarcomere that is occupied by the full length of the thick myosin filaments; the A band is of fixed length, i.e. does not change length during contraction;

67
Q

what is the H band of the sarcomere?

A

denotes the region of the sarcomere that is occupied by thick myosin filaments only, i.e. the region of myosin that is NOT overlapping with any actin; the H band gets narrower during contraction, as the degree of overlap of actin and myosin increases, leaving less myosin that is not overlapping with actin.

68
Q

what is the I band in the sarcomere?

A

denotes the region of the sarcomere that is occupied by thin actin filaments only, i.e. the region of actin that is NOT overlapping with any myosin; the I band gets narrower during contraction, as the degree of overlap of actin and myosin increases, leaving less actin that is not overlapping with myosin

69
Q

in the sarcomere, which part shortens, and which part stay the same?

A

I band shortens

A band stays the same

70
Q

what is generates and the I band shortens?

A

contraction of the muscle tissue occurs, and a force is generated that pulls a bone into a new position

71
Q

what is a neuromuscular junction?

A

A specialised form of synapse, found where the end of a motor neurone (the motor end‐plate) meets a muscle fibre

72
Q

what is the role of an NMJ?

A

allow stimulation of the muscle fibre – triggering its contraction – following the arrival of an action potential at the end of the motor neurone

73
Q

Most NMJs are cholinergic, what does this mean?

A

they use acetylcholine molecules as the neurotransmitter

74
Q

Dont need to learn all 21 steps, but what are they overall?

A
  1. The arrival of an action potential at the motor end‐plate of the motor neurone results in depolarisation of its plasma membrane;
  2. Voltage‐gated calcium ion channels in this plasma membrane open;
  3. Calcium ions move by facilitated diffusion into the motor neurone through these open channels;
  4. The calcium ions bind to synaptic vesicles in the cytoplasm, which contain the acetylcholine (ACh) neurotransmitter molecules;
  5. This triggers the vesicles to move towards the pre‐synaptic membrane – the vesicles attach to microtubules (via motor proteins), which act as tracks directing the movement, using energy from ATP hydrolysis;
  6. The vesicle membranes fuse with the pre‐synaptic membrane, resulting in the release of ACh molecules into the synaptic cleft by exocytosis;
  7. The ACh molecules diffuse across the cleft;
  8. The ACh molecules bind to glycoprotein receptors with binding sites of complementary shape, located in the post‐synaptic membrane, i.e. the sarcolemma of the muscle fibre;
  9. The binding of ACh to a receptor triggers a change in the 3D shape of the receptor, resulting in the opening of a sodium ion channel (called a neurotransmitter‐gated sodium ion channel) that is part of the same glycoprotein;
  10. Sodium ions move by facilitated diffusion into the sarcoplasm of the muscle fibre through these open channels, depolarising the post‐synaptic membrane (sarcolemma);
  11. If the threshold potential is exceeded (due to sufficient movement of positivelycharged sodium ions into the muscle fibre), more sodium ion channels open: these are voltage‐gated sodium ion channels;
  12. Now, more sodium ions can enter the muscle fibre as the membrane is now more permeable to sodium ions – this is a positive feedback step (as the entry of some sodium ions has triggered the entry of even more sodium ions);
  13. The post‐synaptic membrane (sarcolemma) is further depolarised and a full‐strength action potential has been triggered;
  14. The action potential is now transmitted via the sarcolemma in both directions along
    the whole length of the muscle fibre;
  15. To prevent continuous inappropriate stimulation of the muscle fibre, the enzyme acetylcholinesterase (ACE) breaks down the acetylcholine that is attached to the receptors (resulting in the sodium ion channels returning to their closed state);
  16. The breakdown products of ACh are choline and ethanoic acid: these are reabsorbed by the motor neurone and are recycled to produce new ACh molecules (in a process that requires energy from ATP);
  17. Meanwhile the action potential that was generated not only spreads via the sarcolemma but also penetrates into the muscle fibre, due to depolarisation of the membranes of the T tubules;
  18. This leads to depolarisation of the membranes of the sarcoplasmic reticulum (SR);
  19. Depolarisation of the SR membranes causes their voltage‐gated calcium ion channels to open; meanwhile similar channels in the sarcolemma also open;
  20. Calcium ions move by facilitated diffusion from the lumen of the SR into the sarcoplasm through these open channels; further Ca2+ ions enter the sarcoplasm from the tissue fluid outside the fibre, through the open channels in the sarcolemma;
  21. As the Ca2+ concentration of the sarcoplasm rises, Ca2+ ions begin to bind to troponin protein, causing a change in troponin’s 3D shape. The sliding filament mechanism is now activated
75
Q

what events at the NMJ trigger the sliding filament theory?

A
  1. An action potential arrives at the end of a motor neurone.
  2. The motor neurone releases acetylcholine at the NMJ, then the ACh diffuses across the cleft and binds to complementary receptors in the sarcolemma of the muscle fibre, triggering depolarisation of the sarcolemma.
  3. The resulting action potential spreads via the sarcolemma, T‐tubules and the membranes of the SR;
  4. Voltage‐gated calcium ion channels in both the SR membranes and the sarcolemma open; Ca2+ ions now enter the sarcoplasm from the stores in the SR and from outside the muscle fibre, causing an increase in the Ca2+ concentration of the sarcoplasm.
76
Q

what is it that causes the sliding filament theory to be activated?

A

It is the rise in the Ca2+ concentration of the sarcoplasm that now causes the sliding filament mechanism to be activated.

77
Q

what are the 11 steps of the sliding filament mechanism?

A
  1. Ca2+ ions bind to troponin protein, causing a change in troponin’s 3D shape;
  2. As troponin changes shape it causes a distortion and change in position of the adjacent protein, tropomyosin (which was blocking the binding sites on actin where myosin heads can potentially bind);
  3. Tropomyosin proteins, having been pushed into a different shape and position by troponin, now no longer blocks the binding sites on actin; therefore, myosin heads now bind to their binding sites on actin;
  4. The ‘power stroke’ occurs: the myosin heads tilt (bend), pulling the actin filaments further past the myosin filaments, increasing the degree of overlap of the filaments;
  5. This increased degree of overlap of actin and myosin filaments means that each sarcomere in each myofibril becomes shorter, and hence each myofibril shortens;
  6. An ATP molecule now attaches to each myosin head, causing all the myosin heads to
    simultaneously detach from their binding sites on actin
  7. The ATP is hydrolysed to ADP and Pi (as the myosin heads have ATPase enzyme activity), with the energy released being used to reset the angle of each myosin head so it is ready to bind further along the actin in the next cycle;
  8. As long as the Ca2+ concentration of the sarcoplasm remains high enough, the above sequence of events will keep repeating, with the myosin heads detaching and then reattaching further along the actin filaments in each subsequent cycle;
  9. Thus, all sarcomeres in each myofibril – and hence the myofibrils themselves – become shorter and shorter as the mechanism repeats;
  10. The shortening of myofibrils causes the muscle fibres containing these myofibrils to shorten;
  11. All muscle fibres in a region of muscle tissue are likely to shorten simultaneously, creating a contraction force strong enough to pull on the bone that the muscle is attached to (via its tendon). Hence, the bone is pull into a different position, i.e. movement takes place.
78
Q

what are the 9 steps causing the sliding filament mechanism to stop?

A
  1. Action potentials no longer arrive at the NMJ, hence the motor neurone no longer releases ACh into the cleft
  2. Meanwhile the enzyme ACE breaks down any ACh already bound to the receptors on the sarcolemma;
  3. Now that the receptors no longer have ACh bound, the neurotransmitter‐gated Na+ ion channels (that are part of these receptor proteins) close
  4. The sarcolemma repolarises, mainly via the activity of Na+/K+ pumps
  5. The voltage‐gated Ca2+ ion channels in the sarcolemma and SR membranes close, so no further Ca2+ ions enter the sarcoplasm
  6. Ca2+ ion pumps (i.e. carrier proteins) in the sarcolemma and SR membranes actively transport Ca2+ ions out of the sarcoplasm in to the tissue fluid and back into storage within the SR lumen
  7. As the Ca2+ ion concentration in the sarcoplasm decreases, Ca2+ ions now detach from troponin proteins, resulting in these proteins changing back to their original 3D shape;
  8. As troponin changes shape, this in turn allows tropomyosin to return to its original shape and position, blocking the binding sites on actin where myosin heads can potentially bind
  9. It is now impossible for the myosin heads to attach to actin, hence no power strokes can occur and no shortening of sarcomeres, myofibrils and muscle fibres will take place – the muscle tissue can no longer generate a pulling force on a bone.
79
Q

what are the roles of ATP in the motor neurone at the NMJ?

A

o Maintaining (and later re‐establishing) the resting potential across the plasma membrane of the motor neurone, specifically the operation of Na+/K+ pumps

o Protein synthesis to make Na+/K+ pumps, calcium ion channels etc;

o Synthesis of acetylcholine;

o Formation of synaptic (secretory) vesicles containing acetylcholine;

o Movement of synaptic vesicles, attached via motor proteins, on tracks made of microtubules towards the pre‐synaptic membrane

o Exocytosis to release the acetylcholine into the cleft of the NMJ;

o Active transport of Ca2+ back out of the motor neurone to re‐establish its
concentration gradient.

80
Q

what are the roles of ATP in the muscle fibres?

A

o maintaining (and later re‐establishing) the resting potential across the sarcolemma,specifically the operation of Na+/K+ pumps;

o protein synthesis to make Na+/K+ pumps, calcium ion channels, actin, myosin, tropomyosin, troponin etc;

o in the sliding filament mechanism: ATP binds to the myosin head, then beinghydrolysed to cause the myosin head to detach from actin, allowing the head to reattach further along;

o active transport of Ca2+ out of the sarcoplasm back into the SR (or out of the cell), to end contraction and re‐establish the Ca2+ concentration gradient.