Biology (9610) | Nerve impulses and synaptic transmission

Study Notes: Nerve Impulses and Synaptic Transmission

Hello Biologists! Welcome to one of the most exciting and fast-paced areas of the "Control" section of the syllabus. This chapter is all about how your nervous system transmits information at incredible speed, allowing you to react instantly to the world around you.

Don't worry if the vocabulary (like depolarisation!) seems complicated at first. We will break down the process of nerve signalling into simple, step-by-step electrical and chemical events. Think of it as learning the language of the body's super-fast communication network!

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3.4.3.1 Nerve Impulses: The Electrical Signal

A nerve impulse is essentially an electrical signal travelling along the membrane of a neurone. Before we dive into the signal itself, let’s quickly look at the cell that carries it.

Structure of a Myelinated Motor Neurone

A motor neurone carries impulses from the central nervous system (CNS) to an effector (like a muscle or gland). It is typically myelinated, meaning it is insulated for speed.

• Axon: The long fibre that carries the impulse away from the cell body.
• Myelin Sheath: A fatty layer (made by Schwann cells) that wraps around the axon, acting like electrical tape on a wire. This insulation speeds up the transmission.
• Nodes of Ranvier: Tiny, unmyelinated gaps between the segments of the myelin sheath. These gaps are crucial for increasing speed.

The Resting Potential: Charging the Battery

Before a neurone sends an impulse, it sits in a resting state. The membrane is said to be polarised, meaning there is a potential difference (voltage) across it. This resting potential is usually around –70 mV (millivolts).

How the Resting Potential is Established:

The difference in charge is created and maintained by:

1. Sodium-Potassium Pumps: These are carrier proteins located in the neurone membrane. They actively transport ions using ATP (energy):
   • 3 Sodium ions (Na+) are pumped out of the axon.
   • 2 Potassium ions (K+) are pumped into the axon.
   (Quick Tip: "Na-Out, K-In" – remember there are more Na+ pumped out than K+ pumped in.)
2. Differential Membrane Permeability: At rest, the membrane is much more permeable to K+ ions than Na+ ions. K+ ions leak out easily down their concentration gradient.
3. Electrochemical Gradient: The combined effect of the pump and the leaking K+ ions means the inside of the axon becomes highly negative relative to the outside, setting up the resting potential.

Key Takeaway: The resting potential is negative inside due to the continuous active transport of more Na+ out than K+ in, combined with the leakage of K+ ions.

The Action Potential: Firing the Signal

An action potential is the rapid change in electrical potential across the membrane, resulting in a signal being transmitted. This is caused by the rapid opening and closing of voltage-gated ion channels.

Steps of the Action Potential:

1. Stimulation and Depolarisation:
   • A stimulus causes the membrane potential to rise above a certain level (the threshold potential, usually around -55 mV).
   • If the threshold is reached, voltage-gated Na+ channels open rapidly.
   • Na+ ions flood into the axon, driven by the strong electrochemical gradient. The inside becomes positive (up to +40 mV). This reversal of charge is called depolarisation.
2. Repolarisation:
   • At the peak of the action potential, the Na+ channels close and lock.
   • Voltage-gated K+ channels open (though they open more slowly than the Na+ channels).
   • K+ ions rush out of the axon, making the inside negative again. This process is called repolarisation.
3. Restoring the Resting Potential (Hyperpolarisation):
   • The K+ channels are slow to close, causing a brief period where the potential drops slightly lower than the resting potential (hyperpolarisation).
   • The Sodium-Potassium pump then works continuously to return the ion concentrations and the potential difference back to the stable resting potential of -70 mV.

Did you know? This entire sequence takes only a few milliseconds (thousandths of a second)!

The All-or-Nothing Principle

Nerve impulses obey the all-or-nothing principle. If a stimulus is strong enough to reach the threshold potential, an action potential will always be generated, and it will always have the same maximum voltage (amplitude), regardless of the stimulus strength. If the stimulus is too weak, no action potential is generated at all.

Think of it like flushing a toilet: pressing the handle harder doesn't make the water flow faster or fuller; once the threshold is reached, the flush is always the same size.

The Refractory Period: A Necessary Pause

The refractory period is a short time immediately after an action potential during which the neurone membrane cannot be stimulated to produce a second action potential. It occurs because the voltage-gated Na+ channels are closed and cannot be reopened for a short time.

Importance of the Refractory Period:

1. Discrete Impulses: It ensures that action potentials are separate, individual events. This means the signal doesn't merge into one continuous electrical buzz.
2. Limiting Frequency: It restricts the number of action potentials that can be transmitted per second, meaning the cell cannot fire too rapidly.
3. Unidirectionality (Crucial!): It ensures the impulse travels in only one direction (away from where it just fired) because the section of the axon behind the impulse is temporarily inactive.

Factors Affecting the Speed of Conduction

1. Myelination (Saltatory Conduction):

   In myelinated neurones, the electrical charge cannot flow across the membrane where the myelin sheath is present. Instead, the impulse "jumps" from one Node of Ranvier to the next. This jumping is called saltatory conduction. This dramatically increases speed (up to 100 m/s) compared to non-myelinated neurones (around 1 m/s).

2. Axon Diameter:

   A larger axon diameter results in faster conduction. A wider axon has less internal resistance to the flow of ions, allowing the depolarisation current to spread more quickly.

3. Temperature:

   Higher temperatures increase the rate of diffusion of ions and the rate of respiration (providing ATP for the Na+/K+ pumps), leading to faster conduction, up to a point where the proteins (like ion channels) begin to denature.

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3.4.3.2 Synaptic Transmission: The Chemical Relay

When an electrical impulse reaches the end of a neurone, it must jump across a gap to the next neurone or muscle cell. This gap and the structures around it form the synapse.

We focus on the cholinergic synapse, which uses the neurotransmitter acetylcholine (ACh). A neuromuscular junction is a specific type of cholinergic synapse connecting a motor neurone to a muscle cell.

Detailed Structure of a Cholinergic Synapse

• Presynaptic Membrane: The membrane of the neurone sending the impulse. Contains voltage-gated Ca2+ channels and synaptic vesicles filled with neurotransmitter (ACh).
• Synaptic Cleft: The small gap (20-30 nm) between the two neurones.
• Postsynaptic Membrane: The membrane of the receiving cell. Contains specific receptor proteins that bind to the neurotransmitter and Na+ ion channels.

The Process of Synaptic Transmission (Step-by-Step)

1. Action Potential Arrival: The electrical impulse reaches the synaptic knob (the end swelling of the presynaptic neurone).
2. Calcium Influx: The depolarisation causes voltage-gated Ca2+ channels in the presynaptic membrane to open. Ca2+ ions rush into the synaptic knob (down their concentration gradient).
3. Neurotransmitter Release: The influx of Ca2+ ions causes the synaptic vesicles, containing acetylcholine (ACh), to fuse with the presynaptic membrane. ACh is released into the synaptic cleft by exocytosis.
4. Binding and Depolarisation: ACh molecules diffuse across the cleft and bind to specific receptor proteins on the postsynaptic membrane. This binding causes Na+ channels to open.
5. Postsynaptic Potential: Na+ ions flow into the postsynaptic cell, causing a small depolarisation known as a postsynaptic potential (PSP). If enough PSPs occur to reach the threshold, a new action potential is generated in the postsynaptic neurone.
6. Neurotransmitter Breakdown: To prevent continuous stimulation, the enzyme acetylcholinesterase (AChE) breaks down ACh into acetyl and choline. These products are then reabsorbed by the presynaptic neurone to be recycled.

Key Takeaway: The synapse converts the electrical signal into a chemical signal (ACh) and then back into an electrical signal.

Properties of Synaptic Transmission

Unidirectionality

Synaptic transmission can only occur in one direction: from the presynaptic neurone to the postsynaptic cell.

Why? Because the neurotransmitter (ACh) is stored only in the presynaptic vesicles, and the specific receptor molecules are only present on the postsynaptic membrane.

Summation: Adding up the Signals

Often, a single postsynaptic potential (PSP) is not strong enough to reach the threshold for an action potential. However, the effect of multiple PSPs can be added together, a process called summation.

1. Temporal Summation (Time)

This occurs when a single presynaptic neurone releases neurotransmitter many times in quick succession. The effects of the individual release events overlap and combine to reach the threshold.

Analogy: Imagine a single tap dripping slowly. If you make it drip very quickly, the water level (the charge) in the postsynaptic cup rises until it overflows (reaching threshold).

2. Spatial Summation (Space)

This occurs when multiple different presynaptic neurones release neurotransmitter simultaneously onto the same postsynaptic neurone. The combined effect of these multiple inputs is sufficient to reach the threshold.

Analogy: Imagine three different taps dripping onto the same cup at the same time. The combined rate of flow causes the cup to overflow (reach threshold) much faster.

Inhibition by Inhibitory Synapses

Not all synapses are designed to excite the next cell. Inhibitory synapses make it *less* likely that the postsynaptic neurone will fire an action potential.

• They typically release neurotransmitters (like GABA) that bind to receptors which cause Cl- ion channels to open.
• Cl- ions rush into the postsynaptic cell, making the inside even more negative (hyperpolarisation), pushing the potential further away from the threshold.
• This acts as a "brake" on the system, giving the nervous system finer control over responses.

Predicting the Effects of Drugs and Toxins

Many drugs and toxins work by interfering with the delicate processes at the synapse. When studying this, focus on *where* the drug acts:

1. Mimic the Neurotransmitter: A drug may have a shape similar to ACh and bind to the postsynaptic receptors, activating them (acting as an agonist). This leads to continuous stimulation.
2. Block the Receptors: A toxin might block the postsynaptic receptors, preventing ACh from binding. This stops transmission entirely (leading to paralysis, e.g., curare).
3. Inhibit Enzyme Activity: A drug might inhibit the action of acetylcholinesterase (AChE). If ACh is not broken down, it stays in the cleft and continues to stimulate the postsynaptic membrane, leading to excessive nerve firing.
4. Prevent Neurotransmitter Release: Some toxins prevent the presynaptic release of the neurotransmitter (e.g., by interfering with Ca2+ influx). This stops transmission.

Understanding these four mechanisms allows you to predict the effect of any substance on the nervous system!

Chapter Summary: Key Takeaways

Nerve impulses are self-propagating electrical signals (action potentials) moving along a neurone, maintained by the Na+/K+ pump. Transmission speed is increased by myelination (saltatory conduction). At the synapse, the signal becomes chemical (neurotransmitters like ACh) and is governed by rules like unidirectionality and the need for summation to reach the threshold.