Lecture 5: Signal Propagation and Transmission

Propagation within a neuron

The way an electrical signal travels along an axon by triggering the same voltage change in each neighbouring part of the cell membrane.

Trigger zone of axon hillock → axon terminal.

Two methods of action potential propagation

1. Continuous conduction

2. Saltatory conduction

Continuous conduction involves:

Step-by-step depolarization and repolarization of adjacent sections of the plasma membrane.

Where does continuous conduction occur in?

Unmyelinated axons and muscle fibers

Steps of continuous conduction

1. Stimulus moves the RMP to threshold, causing voltage-gated Na+ channels to open to generate an action potential.

2. Na+ influx causes the adjacent membrane segment to depolarize until threshold, propagating the action potential along the membrane as a wave of depolarization.

3. Repolarization occurs, caused by inactivation of voltage-gated Na+ channels and opening of voltage-gated K+ channels.

4. The area behind the depolarized membrane is briefly refractory.

What causes repolarization after the depolarization wave?

1. Closing of voltage-gated Na+ channels.

2. Opening of voltage-gated K+ channels.

Saltatory conduction involves:

The action potential leaping from one unmyelinated segment (myelin sheath gaps/nodes of Ranvier) of the axon to the next.

Why is saltatory conduction more efficient?

The entire membrane does not need to depolarize (skips myelinated sections since its insulating nature blocks charged ions).

Voltage-gated ion channels are concentrated at the nodes.

Steps of saltatory conduction

1. Stimulus move RMP to threshold, opening voltage-gated Na+ channels to generate an action potential.

2. Na+ influx creates ionic currents that travel from one node to the next. Each nose reaches threshold and generates another action potential.

3. Depolarization of each node is followed by repolarization.

4. Each node becomes briefly refractory.

Refractory period

Short period after action potential when a neuron/muscle cell cannot easily generate another electrical signal.

Absolute refractory period

First phase of refractory period; no new action potential can occur no matter how strong the stimulus is.

Relative refractory period

Second phase of refractory period; a neuron/muscle cell can fire again but only in response to a stronger-than-normal stimulus.

What is the importance of the refractory period?

1. Ensures one-way propagation → prevents unorganized communication).

2. Keeps action potentials as separate events → allows info to be coded by action potential frequency rather than amplitude, since all action potentials have about the same amplitude.

3. Allows time for recovery → re-establish ionic gradients while limit amount of ATP required to restore these gradient.

Refractory membrane

Segment of neuron/muscle cell that temporarily cannot respond to a new stimulus while recovering from a previous action potential.

What is greater stimulus intensity measured by in action potentials?

Higher action potential frequency (amplitude is irrelevant, unlike graded potentials).

Three factors that increase nerve conduction speed

1. More myelination

2. Larger axon diameter (less internal resistance to ion flow)

3. Higher temperature

What is saltatory conduction used for?

Fast actions and long pathways

Ex: motor reflexes; somatic senses like sharp pain, touch, pressure, body position.

What is continuous conduction used for?

Slow, generalized processes and internal regulation.

Ex: GI tract movement during digestion, dull pain, temperature sensations.

Synapse

Region where neuron-neuron or neuron-effector cell (muscle/gland) communication occurs.

Presynaptic cell

Carries the impulse toward the synapse.

Post synpatic cell

Receives the signal from the presynpatic cell and carries the impulse away from the synapse.

Three types of neuron-to-neuron synapses

1. Axodendritic (axon-dendrite); most common

2. Axosomatic: (axon-soma)

3. Axo-axonal (axon-another axon)

Two types of synpases

1. Electrical

2. Chemical

Electrical synapses

Action potentials are conducted directly between adjacent cells through gap junctions.

Faster than chemical synapses.

Gap junctions

Specialized intercellular channels that allow ions to flow directly from one cell to another, providing almost instantaneous transmission of signal.

Present in electrical synapses.

Where in the body do electrical synapses occur?

Visceral smooth muscle (GI tract), cardiac muscle (myocardium), nervous system (brain, spinal cord)

Synaptic cleft

Small space separating cells.

Present in chemical synapses.

Chemical synapses

Electrical impulses in the presynaptic cell release a neurotransmitter (chemical messenger) that travels across the synaptic cleft to the postsynaptic cell, where the NT binds to a receptor on its membrane to produce a graded potential.

If the postsynaptic potential reaches threshold → action potential.

Why is there a chemical synaptic delay?

Neurotransmitter release and receptor activation take time, so there is a delay of ~0.5 ms between arrival of the impulse at the presynaptic cell and generation of an action potential in the postsynaptic cell.

Steps for chemical synaptic transmission

1. Action potential arrives at axon terminal in the presynaptic cell.

2. Voltage-gated Ca²⁺ channels open, allowing Ca²⁺ to enter.

3. Ca²⁺ causes fusion of NT-containing vesicles with the synaptic end bulb.

4. NT is released into the synaptic cleft and diffuses across it.

5. NT binds to ligand-gated ion channels on the postsynaptic membrane, opening the channels.

6. Ions flow and create a postsynaptic potential (graded potential). If it reaches threshold → action potential.

Excitatory postsynaptic potential (EPSP)

Graded potential that moves the cell closer to threshold through a small depolarization. If enough EPSPs are summed → action potential.

Caused by Na+ channels opening → Na+ enters the cell.

Inhibitory postsynaptic potential (IPSP)

Graded potential that moves the cell further from threshold through a small hyperpolarization. Can cancel out an EPSP.

Caused by K+ channels opening → K+ leaves the cell; Cl- channels opening → Cl- enters the cell.

Two types of neurotransmitter receptors

1. Ionotropic

2. Metabotropic

Ionototropic receptor

Type of ligand-gated ion channel that opens when an NT binds to it.

Metabotropic receptor

Have an NT binding site but are not ion channels themselves.

Instead, they are connected to an ion channel through a G-protein, which opens/closes the channel through second messengers.

G-protein

Opens/closes ion channels connected to metabotropic receptors through second messengers.

Second messenger

Small intracellular molecules that relay/amplify signals from cell-surface receptors to target proteins inside the cell.

Three methods of neurotransmitter removal

1. Diffusion → NT diffuses away from synapse.

2. Enzymatic degradation → enzymes break down or inactivate the NT

   • Ex: acetylcholinesterase breaks down acetylcholine; monoamine oxidase degrades epinephrine, norepinephrine, and dopamine into inactive forms.

3. Uptake by cells → NT is actively transported back into the cell, where they can be recycled and released again.

   • SSRIs block serotonin re-uptake → increase serotoning in synaptic cleft.

Neurotransmitter

Substance that transmits signals across a synapse.

Two major classes of neurotransmitters

1. Small-molecule neurotransmitters

2. Neuropeptides

Small-molecule neurotransmitters

Fast-acting chemical messengers synthesized locally in the nerve terminal.

Neuropeptides

NTs made of amino acids that bind to metabotropic receptors, and can also function as endocrine hormones.

Acetylcholine

Small-molecule neurotransmitter

Released by many PNS neurons for muscle contraction and autonomic regulation.

Can also be released by some CNS neurons for memory/cognition.

Amino acids (as neurotransmitters)

Small-molecule neurotransmitters in the CNS

• Aspartate → excitatory

• Glutamate → excitatory

• GABA → inhibitory

• Glycine → inhibitory

Biogenic amines

Small-molecule neurotransmitters containing an amino functional group (R—NH₂).

• Epinephrine (adrenaline) → fight or flight, SNS activity

• Norepinephrine (noradrenaline) → arousal, wakefulness, SNS activity

• Dopamine → pleasure/reward, addiction

• Serotonin → sleep, mood, appetite

• Histamine → wakefulness, attention

Purines

Small molecule neurotransmitters in the CNS and PNS.

Adenosine, ATP, ADP, and AMP are excitatory.

Nitric oxide (NO)

Lipid-soluble, excitatory small molecule neurotransmitters produced in brain and spinal cord.

Learning/memory; promotes vasodilation and inhibits blood clotting.

Substance P

Neuropeptide involved in pain signalling.

Enkephalins and endorphins

Neuropeptide that functions as an analgesic (painkiller) by blocking the release of Substance P.

Cholecystokinin (CCK)

Neuropeptide found in brain and small intestine. Regulates feeding and GI function → “stop eating” signal

Oxytocin

Neuropeptide released from the pituitary gland.

Bonding, sexual pleasure, uterine contractions, milk let-down.