Neuromuscular structure and function Flashcards
Why do neuronal cells have a neg resting membrane potential?
- Potassium has the greatest intracellular potential(K+)
- Na+ greater extracellular potential (Na+)
- 70 mv
- Active transport and diffusion processes control the resting membrane potential
- AT has the biggest influence
3 Na+ in, 2 K+ out changes membrane potential
Explain the basis of resting membrane potential
- In all cells, Na+ and K+ are constantly pumped across the cell membrane by Na+, K+, - ATPase
- Maintains:
- High Na+ conc in the ECF and low Na+ conc in the ICF
- High K+ conc in thr ICF and low K+ conc in the ECF
- Constant diffusion of Na+ into the cell by:
- open K+ channels that are always open (leaky)
- When a cell is at rest, the pumping of the Na+, K+, -ATPase = the diffusion of Na+ and K+
Describe what happens during an Action Potential
1.) Na+/K+ ion pump active maintaining resting potential (-70mV)
2.Stimulus causes some Na+ channels to open allowing some Na+ ions into axon
3.Membrane potential is less neg as Na+ ion diffuse into axon (-55mV) : threshold is reasched
4.All Na+ ion channels open = rapid influx of Na+ ions
5. All Na+ channels close at +40mV
6. All K+ channels open
7. Rapid efflux of K+ ions - electrical charge inside axon falls as K+ ions move out so axon membrane starts to be repolarised back to original -70mV
8. K+ ions channel remain open = hyper-polarisation
9. K+ ions channels close at -80/90mV
10. Na+/ K+ ion pump allows membrane potential to go from hyper-polarised back to resting potential of -70mV
How are motorneruons activated?
- Iontropic mechanism
- Neuromodulation
What is the iontropic mechanism?
- Generate synaptic currents
- Initiate action potential
What is neuromodulation?
- Modification of the voltage/ ligand-gated channels
- can result in a lowering of activation threshold
What are important neuromodulators in the motor system?
- Serotonin (5-HT)
- Norepinephrine (NE) are important neuromodulators in the motor system
What happens when an action potential arrives at an axon terminal?
- Voltage gated Ca2+ channels open
- Ca2+ enters the presynaptic neuron
- Ca2+ signals to neurotransmitter vesicles
- Vescivles move to the membrane and dock
- Neurotransmitters released via exocytosis
- Neurotransmitters bind to receptors
- Signal initiated in postsynaptic cell
What ACH release at the NMJ dependent on?
- depolarisation of the presynaptic membrane of the motor neurone
- Depolarisation results in Ca2+ ion influx via voltage-dependent Ca2+ channels
- Ca2+ ions promote fusiion of the ACh vesicles with the presynaptic membrane
- Activation of nAChRs by ACh (2 molecules per receptor) leads to depolarisation of the muscle fibre membrane- via net influx of Na+ ions
- Release of a single vesicle of ACh results in a miniature end-plate potential whereas release of several causes an end plate potential or EPP
What is the relationship between T tubules and the SR?
- T tubules are deep inviginations of the muscle cell membrane and are placed at the junction of the A bands and the I bands
- They provide a mechanism for changes in membrane potential to be communicated right to the inners of the muscle fibre
- In striated muscle, each T tubule comes into close apposition with SR at several different levels
- When the membrane on the T tubule is depolarised, this triggers release of calcium from the SR
- T tubules and SR allow calcium conc in the sarcoplasm to rise in the area where they are needed