Week 2 Physiology - Body fluids and nerve transmission Flashcards
What is membrane potential?
Membrane potential results from separation of positive and negative charges across a membrane
What is the resting membrane potential in neurons?
-70mV, similar to equilibrium potential for K+
Define resting membrane potential?
Equilibrium between driving force for ions down concentration gradient versus electrical gradient
i.e. for K+, it is negative inside cell, so electrically these ions want to move into the cell, but chemically the concentration of K+ is very high intracellularly, so this also works against the net influx (versus the way that sodium moves into the cell during depolarisation, with both favouring electrical and chemical gradient inwards)
What is the chief mechanism by which K+ is kept at higher concentration inside cell versus Na+?
NaK ATPase
More open K+ channels at rest, allows greater permeability of K+ at rest, therefore K+ is prime determinant of membrane potential at rest
Describe movement of ions in an action potential?
- Opening of voltage gated Na+ channels
- Influx of Na+ into cell, reaches threshold potential, and membrane potential becomes positive –> generation of action potential, becomes closer to equilibrium potential for sodium (+60mv)
- Na+ channels rapidly close, and remain inactive
- Repolarisation is achieved by opening of K+ channels (voltage gated) causing K+ efflux and return to RMP
What effect does increased extracellular K+ have on membrane potential?
Decreased resting membrane potential, making it easier for threshold to be reached
What effect does decreased extracellular calcium have on excitability of nerve and muscle cells?
Increased excitability, by decreasing the amount of positive charge that is repelling inwards movement of Na+ into cell
What are the biggest to smallest categories of nerve fibres?
A - 5-20 micrometres
B - <3 micrometres
C - 0.3 -1.3 micrometres
What are type A nerve subdivisions, and what they are responsible for?
“There’s a guy balancing”.
“A touch screen pressure cooker”
“And a motor”
“But it’s so cold, it hurts”
Alpha = Proprioception, somatic motor 12-20 microns
Beta = Touch, pressure 5-12 microns
Delta = motor to muscle spindles 3-6 microns
Gamma = cold, pain, touch 2-5 microns
In regards to hypoxia, pressure, and local anaesthetic, what are the susceptibilities of different nerve fibres? Pneumonic order of HPA axis
“Band was shit, so they had to go:
BACk to their ABCs but Can’t Be Arsed”
Hypoxia: B –> A –> C
Pressure: A –> B –> C
Anaesthetic (local): C –> B –> A
How is a skeletal muscle organised?
Muscle = combined sum of organised muscle cells - called ‘muscle fibres’.
Muscle fibres span the length of the muscle, and are multinucleate cells, long and cylindrical.
Cell membrane = sarcolemma, cytoplasm = sarcoplasm
Each muscle fibre composed of myofibrils, divisible units of myofilaments - containing contractile proteins. These are organelles of the muscle fibre.
Each myofibril is surrounded by the sarcoplasmic reticulum, an organelle which sequesters calcium.
What are T tubules? What is their function?
Invaginations of the sarcolemma in which the extracellular fluid/space resides.
Role is the propagation of action potentials along the muscle fibre (allowing coordinated contraction of muscles.
What is the RMP of a muscle cell?
-90mV
What is the speed of conduction of muscle action potential?
5 m per second
Describe the structure of the contractile proteins of muscle cell:
Thick filament = myosin
Thin filament = actin
Myosin has ‘heads’ which bind to actin and allow cross-bridge formation.
Actin contains tropomyosin filaments, which are long windy molecules that wrap around the actin, as well as troponin (I and C).
What is the role of troponin I?
In resting state, bound to actin and tropomysin over sites where myosin heads interact with actin, preventing inadvertent interactions.
What is the role of troponin C?
Free Ca2+ (such as when action potential triggers voltage gated opening of SR) binds to troponin C, which causes weakening of troponin I interactions with actin - and exposure of actin binding sites to myosin
What are the events of a power stroke?
- At rest, myosin heads are bound to ADP
- When Ca2+ enters cell and binds troponin C, conformation change leads to myosin head binding to thin filament actin
- The myosin head rotate and move attached actin to shorten muscle fibre, forming ‘power stroke’
- At end of power stroke, ATP binds to now displaced site, and causes detachment from actin
- ATP is hydrolysed into ADP and inorganic phosphate, and this cycle continues as long as there is calcium in cell
How does muscle relaxation occur?
- Calcium is pumped back into the sarcoplasmic reticulum
- Calcium is released from troponin
- Actin and myosin cease to interact
What transport mechanism is responsible for calcium homeostasis in muscle cells?
SERCA
Sarcoplasmic or Endoplasmic Reticulum Ca2+ ATPase
Hydrolysis of ATP required (active process) –> both for contraction and relaxation (which is why rigor mortis occurs)
What’s the difference between isometric vs isotonic contraction?
Isometric = same length, maintaining posture
Isotonic = shortening of muscle against constant load (ie. movement of joints)
What is a sarcomere?
Repeating contractile unit of the myofibril, consisting of actin and myosin filaments which are anchored to Z discs. Myosin is fixed between the Z discs and does not move. Actin is anchored laterally to the Z discs, but have a free ending in the middle to allow movement along the myosin
What is the ‘A’ band in the sarcomere?
A band = dArk, consists of the length of sarcomere were myosin and actin overlap
What is the ‘I’ band in the sarcomere?
I band = lIght, consists of the area where actin is anchored to the Z discs and there is no overlap with myosin
What is the ‘H’ zone?
It is the slightly lighter area in the A band where there is no more actin overlapping with the myosin, causing a lighter appearance under microscopy
What’s the difference between type I and II muscle fibres?
Type I = slow, oxidative, small diameter, red
Type II (a and b) = fast, IIa = moderate oxidative, (red) IIb = low oxidative (white)
What is the RMP of cardiac muscle cells?
-90mV
What occurs in phase 0 of cardiac myocyte action potential?
Phase 0 = opening of voltage gated Na+ channels, rapid influx of Na+ to cause depolarisation of cell
What occurs in phase 1 of cardiac myocyte action potential?
Phase 1 = initial rapid repolarisation caused by closure of Na+ channels and opening of K+ channels
What occurs in phase 2 of cardiac myocyte action potential?
Phase 2 = plateau phase, slower but prolonged opening of voltage gated Ca2+ channels
What occurs in phase 3 of cardiac myocyte action potential?
Phase 3 = Final repolarisation brought about by closure of Ca2+ channels, and slow, delayed efflux of K+ through various K+ channels
What occurs in phase 4 of cardiac myocyte action potential?
Phase 4 = return to resting membrane potential
What phases constitute the absolute refractory period?
Phases 0-2 (and part of phase 3)
How does smooth muscle contraction differ to skeletal/cardiac?
No troponin in SM. Instead, myosin is phosphorylated to activate myosin ATPase.
Ca2+ binds to calmodulin, and the complex of these activates calmodulin dependent myosin light chain kinase. This then causes phosphorylation of myosin and increased myosin ATPase, which leads to binding of myosin to actin.
What are the sequence of events that occurs with transmission at a synapse?
1) Impulses arrive at presynaptic terminal, causing NT vesicles to fuse with membrane and contents released into synaptic cleft
2) Binding of NT to receptors on post-synaptic membrane, which cause fluctuations in membrane potential
What are the 3 kinds of synaptic vesicles, and what types of NT do they correspond to?
- Small, clear (ACh, glycine, GABA, glutamate)
- Small, dense (Catecholamines
- Large (neuropeptides)
Describe transmission of action potential at neuromuscular junction?
1) Impulses arrive at end of motor neuron, and voltage gated calcium channels open
2) Increased calcium entry into the nerve ending triggers exocytosis of of ACh containing vesicles
3) ACh binds to nicotinic receptors and increases Na+ conductance via voltage gated channels
4) Depolarisation travels along membrane with ongoing activation of voltage gated channels
**This depolarisation activates release of Ca2+ from SR and muscle contraction
