Lecture notes
physiology
- Module
- Physiology
- Institution
- The University Of Huddersfield (UoH)
Lecture notes of 8 pages for the course physiology at UoH (physiology lectures)
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PhysiologyResting membrane potential
- Ions move down a electrochemical gradient (concentration and charge
gradient)
- Examples of primary active transport have ‘ATPase’ in its name.
- Co transporter moves ions in one direction only if all ions are present like
the NaK2Cl.
- To measure RMP you take one electrode inside the cell and one touching
the membrane and measure in millivolts.
- Three reasons why charge exists: membrane is selectively permeable,
NaK ATPase pump and an unequal distribution of ions (ECF has a different
composition to the outside)
- RMP is -70 mv in reference to inside of the cell.
- Polarised = membrane is at rest and is at -70 mv in reference to ICF
- Depolarised = reduction in charge, goes to -30mv becomes more positive
- Hypolarised = increase in charge goes to -90mv becomes more negative
- At RMP the membrane is not excited so no AP created
- Equilibrium reached when there no net flux of ions
- RMP is closer to equilibrium of potassium as membrane more permeable
to potassium
- At rest more sodium ions are outside of cells than the inside and a greater
concentration of potassium on inside to outside. This is due to the pump.
- Exact value of RMP depends on movement of potassium ions back out of
the cell through ion channels, more K ions open so K has greater
permeability.
- Cells that can change the RMP are excitable cells like the muscle and
nerve cells.
- Two ways to change the MP: graded potential (small changes in
membrane potential about up to 15 mv, they decrease as you move
down.) action potential (big changes in MP like up to 100 mv,
propagated(spreads) without decreasing, reversal of RMP)
- Ion channels are the fastest to move ions across a channel they are: pores
in cell membrane, selectively permeable and passive (electrochemical
gradient).
- Axons can be 1M in length.
- AP results in opening and closing of voltage gated ion channels and
membrane becomes positively charged briefly.
- Cell membrane depolarises at axon hillock above threshold potential so Na
channels open and Na ions rapidly enter the channel causing the
membrane to be briefly positive. K channels open slowly so K leaves the
cell slowly.
- Voltage rises to 40 mv and Na channels close K channels remain open so
membrane becomes more negative, repolarisation. As lots of K ions leave
the cells the membrane becomes hyperpolarised, so this results in
refractory period. Membrane goes back to rest as NaK pump restores ions
- Absolute and relative (Second AP)
- K channels have one gate closed at RMP and opens slowly at D
- Na channels have two gates both have to open for Na to enter cell,
Activation closed at RMP and opens quickly in response to D. Inactivation
open at RMP and closed slowly
- All or none law is that when stimulus is too low no AP generated and when
stimulus above threshold AP generated.
, - Two types of AP propagation
- Continuous conduction: conducted in unmylelinated fibres, spreads along
whole membrane
- Saltatory conduction: rapid conduction in myelinated fibers. Impulse jumps
over sections of fibers covered in myelin. 50x faster.
Synapses
- Junction synapse is between two neurones
- Neuromuscular synapse is between a neurone and muscle
- Synaptic delay is 2 ms (everything slowed down at the synapse)
- It allows integration of information
- AP reaches end of axon terminal, calcium gates open, vesicles fuse with
presynaptic membrane releasing NT into synaptic cleft. NT bind with
receptors on postsynaptic cells that are ligand gated ions causing change
in membrane potential. After NT reabsorbed into first neurone and
restored in vesicles.
- EPSP: NT bind to non-specific ligand channel and causes influx of sodium
and efflux of potassium. depolarisation brings post synaptic closer to
threshold. AP more likely to fire. Binding of NT means Na and K diffuse in
e.g. ACH and Glutamate.
- IPSP: NT bind to specific ligand channel. Influx of sodium or efflux of
potassium. hyperpolarisation brings threshold further away. K or Cl ligand
gated ion channels open. E.g. Gaba or glycine
- Temporary summation: multiple EPSP from 1 synapse
- Spatial summation: single EPSP from 2> synapse
- Drug actions can alter the release of NT, change NT interactions with post
S receptor.
- Cocaine: blocks reuptake of dopamine
- Tetanus toxin: prevents release of GABA affects skeletal muscles muscles
can’t relax
- Neuromodulation: neurones can be influenced by environment aswell.
- Presynaptic inhibition: So inhibitory NT can enter the synaptic knob
causing calcium channels to be closed. It will affect the neurone
- Presynaptic Faciliation: serotonin released more calcium channels open,
enhances effect of NT.
-
Skeletal muscle
- The reason why we can move our joint sis because the muscles go over
the joints
- Muscles extend and contract rather than pull and push.
- They generate heat when they contract, stabilise joints and maintain
posture
- Muscles made out of elongated cells called muscle fibers, use ATP to
generate force during contractions.
- Muscles have contractile proteins called actin and myosin these are
organised into filaments which interact with each other to cause muscles
to shorten. Skeletal muscles are striated as they are stripy as A and M are
arranged in regular patterns
- Whole muscle made out of bundles of muscle fibers which then contains
hundreds of myofibrils which has parallel arrangements of A and M which
causes muscle to contract
- Myosin consists of 2 long polypeptide each ending with globular head.
They are arranged parallel so it forms thick filaments. Myosin heads stick
out
- Actin is a double helix so thin filament and has tropomyosin around it.
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