Neuro Physiology - Nerves, Action Potentials, and the NMJ Flashcards
- PB_BK_65 Neuronal structure and function - PB_BK_66 Resting membrane potential, action potentials, conduction, synaptic mechanisms, actions of neurotransmitters - PB_BK_74 Sense: receptors, nociception, proprioception, sight, taste, smell, hearing, balance, touch, temperature
What is the resting membrane potential?
The steady state voltage across the cell membrane at rest, normally -70mV.
Determined by:
Ions present and their concentrations
Membrane permeability to these ions (100x more permeable to K than Na, causing it to leak down its gradient)
Ion pumps that alter these gradients (Na-K ATPase 3Na out for every 2K in)
Negatively charged phosplate and protein ions also contribute to the potential (Donan effect)
Draw and explain an action potential in a peripheral nerve
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The spontaneous depolarisation of any excitable cell as a result of a stimulus, such as ligand binding or voltage gated channel opening, split into four phases.
Phase 1: Resting potential of -70mV rises towards threshold potential of -55mV
Phase 2: All-or-nothing action potential, voltage gated Na channels open, membrane potential of +30mV
Phase 3: Na channels close, K channels open, causing rapid repolarisation
Phase 4: Temporary hyperpolarisation before the NaKATPase pump restores resting potential
What are the types of refractory period in nerve cells?
Absolute: The duration of time after an action potential, where another action potential cannot be conducted, no matter the stimulus applied.
During this time, the membrane ptoential is more positvie than the threshold
Relative: Where a second action potential could be transmitted but it would need to be supramaximal. This occurs during the period of hyperpolariation (Phase 4)
What is the effect of hypokalaemia on the action potential?
Potassium is primarily intracellular, and hypokalaemia can be categorised into acute or chronic.
Acute: Extracellular potassium decreases, causing an increased concentration gradient - cell becomes hyperpolarised and less excitable, with reduced conductivity, explaining symptom of muscle weakness.
Chronic: Intracellular K has time to redistrible and restore the correct gradient, so muscle weakness isn’t seen
What are the different types of nerve fibres?
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Aα 12-20 / 80-120 / Motor & Sensory (Propriocemption)
Aβ 5 / 30-70-12 / Sensory (Touch & pressure)
Aγ 3-6 / 15-30 / Motor to muscle spindles
Aδ 2-5 / 12-30 / Sensory (Pain, touch & temperature)
B < 3 / 3-15 / Autonomic (Preganglionic)
C 0.4-1.3 / 0.5-25 / Autonomic (Post-ganglionic) & Sensory (Pain, temperature)
Diameter (um) / Velocity (m/s) / Function
Myelinated fibres demonstrate saltatory conduction where the action potential jumps from one node of Ranvier to the next
What is the Nernst equation?
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It calculates the theoretical resting membrane potential for a particular ion.
E = - (RT/zF) * ln([in]/[out])
Eg: For Potassium
-(8.314 * 310.15 / (+1) * 93,485) * ln (150/4.5) =-0.09V (90mV)
E: Theoretical resting membrane potential
R: Gas Constant
T: Absolute Temperature
z: Ion Valency
F: Faraday Constant
natural log of intra/extra -cellular concentration
Think Nernst equation
What is the Goldman Equation?
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In essence, the Nernst equation applied to all the relevant ions acting across the membrane at the same time. Dermines the resting membrane potential.
E = (RT/F) * ln ( (P(K+) * [K+]ₒ + P(Na+) * [Na+]ₒ + P(Cl-) * [Cl-]ᵢ) / (P(K+) * [K+]ᵢ + P(Na+) * [Na+]ᵢ + P(Cl-) * [Cl-]ₒ) )
E: Theoretical resting membrane potential
R: Gas Constant
T: Absolute Temperature
F: Faraday Constant
ln: natural log
P = Membrane permeability to a particular ion
[ ] = Intra/Extracellular concentration of a particular ion
Explain the Gibbs-Donnan effect
Relates to the behaviour of charged particles across a semi-permeable membrane
Particles move down a concentration gradient until the electrochemical potential opposing it increases sufficiently to produce a balanced equilibrium
This is the equilibrium potential, and can be deduced using the Nernst equation
Describe the Neuro-Muscular Junction
A chemical junction between the motor neurone and the muscle.
Each muscle fibre receives a single axon from a Aα neurone.
Post synaptic membrane is folded, peaks having acetylcholine receptors, troughs containing acetylcholinesterase
ACh is produced from acetyl-coA and choline, and stored in presynaptic vesicles (~10,000 molecules per vesicle), some deeper in the neurone, some near the post-synaptic membrane in ‘active’ zones.
Depolarisation opens voltage gated calcium channels, releasing approximately 2 million molecules of ACh.