Speeding Up the Action Potential, the Neuromuscular Junction, and CNS Synapses

Flashcards covering action potential conduction velocity, axonal anatomy, myelination, nerve fibre types, compound action potentials, the neuromuscular junction, and central nervous system synapses based on Dr Catriona Cunningham's lectures.

What is the typical conduction velocity of an unmyelinated axon propagating an action potential?

Approximately $1\,\text{m/s}$.

What are the two primary evolutionary mechanisms used to speed up action potential conduction velocity?

1. Increasing axon diameter (large axons)\n2. Myelination.

How does increasing axon diameter increase conduction velocity?

Axial resistance is lower, allowing electric current to flow more easily down a large axon than a small one, which allows $\text{Na}^+$ channels to be spaced further apart along the membrane.

Which organisms are noted for using large-diameter axons to increase conduction velocity, and what is the approximate diameter of the squid giant axon in the medial posterior mantle nerve?

Squid, fish, and earthworms use large axons; the squid giant axon in the medial posterior mantle nerve has a diameter of approximately $1\,\text{mm}$.

Which glial cells are responsible for myelination in the peripheral nervous system (PNS) versus the central nervous system (CNS)?

Schwann cells myelinate axons in the PNS, whereas oligodendrocytes myelinate axons in the CNS.

How does myelination affect membrane resistance and membrane capacitance?

It causes increased membrane resistance (less current leaks out through the membrane) and decreased membrane capacitance (less current is wasted charging up the membrane).

What is saltatory conduction?

The mechanism where an action potential spreads passively from node of Ranvier to node of Ranvier along a myelinated axon and still reaches threshold at each successive node.

What are two prominent demyelinating diseases of the CNS and PNS, respectively?

Multiple sclerosis in the CNS and Guillain-Barré syndrome in the PNS.

What are the physiological consequences of demyelination on axonal electrical properties and action potential propagation?

Demyelination causes decreased membrane resistance (more current leaks out) and increased membrane capacitance (more current is wasted charging the membrane), leading to conduction failure.

What are the anatomy, conduction velocity, and primary functions of $\text{A}\alpha$ nerve fibres?

They are the largest myelinated fibres, conduct at $70\text{--}120\,\text{m/s}$, and function in proprioception and somatic motor neurons.

What are the anatomy, conduction velocity, and primary functions of $\text{A}\beta$ nerve fibres?

They are large myelinated fibres conducting at $30\text{--}70\,\text{m/s}$, and they mediate touch and pressure.

What are the anatomy, conduction velocity, and primary functions of $\text{A}\gamma$ nerve fibres?

They are small myelinated fibres conducting at $15\text{--}30\,\text{m/s}$, functioning as motor neurons of muscle spindles.

What are the anatomy, conduction velocity, and primary functions of $\text{A}\delta$ nerve fibres?

They are the smallest myelinated fibres, conduct at $12\text{--}30\,\text{m/s}$, and mediate touch, cold, and \"fast\" pain.

What are the anatomy, conduction velocity, and primary functions of C nerve fibres?

They are unmyelinated fibres, conduct at $0.5\text{--}2\,\text{m/s}$, and mediate warmth and \"slow\" pain.

What is a compound action potential, and why does its extracellular recording show multiple distinct peaks?

It is an extracellular recording from a whole nerve (a bundle of axons); it displays multiple peaks because the different fibre types ($\text{A}\alpha, \text{A}\beta, \text{A}\gamma, \text{A}\delta, \text{C}$) conduct at different velocities, meaning the fastest conducted action potentials arrive first at the recording electrode.

How does an extracellular recording of a compound action potential compare to an intracellular action potential recording?

Extracellular recordings place electrodes outside axons relative to earth, detecting small individual action potentials that sum together into large waves; intracellular recordings insert a microelectrode through the membrane relative to the outside of the single cell.

What diagnostic information do nerve conduction studies provide, and what clinical conditions can they help identify?

They record compound action potentials to assess conduction velocity and amplitude, aiding in the diagnosis of Guillain-Barré syndrome, neuropathy, and carpal tunnel syndrome.

What neurotransmitter and receptor type mediate transmission at the neuromuscular junction?

Acetylcholine (ACh) and nicotinic acetylcholine receptors (ligand-gated $\text{Na}^+/\text{K}^+$ channels).

What triggers acetylcholine release from vesicles into the synaptic cleft at the motor axon terminal?

An action potential depolarises the presynaptic terminal, opening voltage-gated $\text{Ca}^{2+}$ channels and causing $\text{Ca}^{2+}$ influx, which drives $\text{Ca}^{2+}$-dependent exocytosis.

What is the end plate potential (EPP) at the neuromuscular junction, and what is its typical amplitude?

The EPP is a graded potential evoked in the post-junctional sarcolemma by the opening of nicotinic ligand-gated channels, typically having a very large amplitude of around $40\,\text{mV}$.

What anatomical feature of the skeletal muscle end plate facilitates triggering an action potential?

Post-junctional folds, which place high concentrations of voltage-gated $\text{Na}^+$ channels very close to where the end plate potential is evoked.

What is meant by the \"high safety factor\" of the neuromuscular junction?

The end plate potential is very large ($\sim 40\,\text{mV}$), always exceeding the threshold needed to activate voltage-gated $\text{Na}^+$ channels and fire a muscle action potential without requiring synaptic integration.

How is acetylcholine removed from the synaptic cleft at the neuromuscular junction?

It is degraded enzymatically by acetylcholinesterase.

Which amine and amino acid neurotransmitters are commonly found in the central nervous system?

Amines include acetylcholine, adrenaline, noradrenaline, dopamine, serotonin (5HT), and histamine; amino acids include glutamate, GABA, and glycine.

Which peptide, purine, and gas transmitters are found in the central nervous system?

Peptides: endorphins, cholecystokinin, substance P; Purines: ATP, adenosine; Gases: nitric oxide.

How do fast and slow postsynaptic potentials differ in the central nervous system?

Fast potentials (EPSPs and IPSPs) are mediated by ionotropic chemically gated ion channels, whereas slow potentials are mediated by metabotropic G protein-coupled receptors activating second messenger cascades.

What is the typical amplitude of a single postsynaptic potential in the CNS, and what functional capacity does this enable?

They are generally small ($\sim 1\,\text{mV}$), which enables complex synaptic integration (spatial and temporal summation) to decide whether threshold is reached.

What are the three anatomical arrangements of synapses between neurons in the CNS?

Axo-dendritic, axo-somatic, and axo-axonic synapses.

What is the difference between divergence and convergence in neural circuits?

Divergence occurs when one neuron makes synaptic connections onto multiple postsynaptic neurons; convergence occurs when multiple presynaptic neurons synapse onto a single postsynaptic neuron.

How does feedback inhibition work in a neural circuit?

When an action potential is fired, an axon collateral branch activates an inhibitory interneuron, which releases inhibitory neurotransmitter onto the initial neuron to hyperpolarise it and prevent repeated firing.

What is synaptic plasticity, and what are two primary examples?

Activity-dependent changes in the strength of synapses; examples include long-term potentiation (LTP) and long-term depression (LTD).