Control and Coordination in Mammals: The Nervous and Endocrine Systems

Hello future Biologists! Welcome to one of the most fascinating topics in A-Level Biology: how mammals, including you, manage to keep all their complex body systems running smoothly. Think of your body as a high-tech company: you need both super-fast instant messaging and slower, more reliable emails to coordinate everything. In biology, these are the nervous system (fast) and the endocrine system (slower, sustained).

This chapter will teach you the intricate dance between electrical signals (nerve impulses) and chemical signals (hormones) that keeps you coordinated, allows you to sense the world, and lets you run, jump, or even just breathe!

Key Takeaway from the Introduction

Coordination relies on two main systems:
1. The Nervous System (Electrical, rapid, short-term responses).
2. The Endocrine System (Chemical, slower, widespread, long-term regulation).

1. Comparing Nervous and Endocrine Systems (15.1.1, 15.1.2)

While both systems aim to coordinate the body, they achieve this goal in very different ways. Understanding their differences is essential for exam success.

Features of the Endocrine System (Hormonal Control)

The endocrine system uses chemical messengers called hormones.

  • Hormones are secreted by endocrine glands (e.g., pancreas, pituitary).
  • They are transported in the bloodstream (hence, slow speed).
  • They act on specific target cells that possess complementary receptors.
  • Examples: You have already studied the regulation of blood glucose by insulin and glucagon, and water potential control by ADH. These are classic examples of endocrine action (refer back to Topic 14 for details!).

Nervous System vs. Endocrine System: The Core Differences

Think of the nervous system as a phone line and the endocrine system as postal mail.

Feature Nervous System Endocrine System
Messenger Electrical impulses (Action Potentials) and Neurotransmitters Hormones (Chemicals)
Pathway Neurones (A specialized network) Bloodstream
Speed Very Rapid (milliseconds) Slower (seconds to hours)
Duration Short-lived, specific effects Longer-lasting, widespread effects
Target Area Highly localized (e.g., a single muscle fibre) Widespread (any cell with the right receptor)

Memory Aid: Nervous = Near and Now. Endocrine = Everywhere and Extended time.

2. The Nervous System: Structure and Transmission (15.1.3, 15.1.4, 15.1.6, 15.1.7, 15.1.8)

Types of Neurones (Nerve Cells)

Neurones are specialised cells that carry electrical signals (impulses).

There are three main types, forming a pathway from stimulus to response:

  1. Sensory Neurones:
    Function: Carry impulses from receptors (sense organs) to the Central Nervous System (CNS).
    Structure: Often have long dendrons and a cell body positioned partway along the axon.
  2. Intermediate Neurones (Relay Neurones):
    Function: Connect sensory neurones to motor neurones within the CNS (brain and spinal cord).
  3. Motor Neurones:
    Function: Carry impulses from the CNS to effectors (muscles or glands) to produce a response.
    Structure: Have long axons and cell bodies located at one end.

The Resting Potential (RP)

A neurone that is not transmitting an impulse is at its resting potential (RP).

  • The RP is typically about –70 mV (millivolts). This means the inside of the axon is 70 mV more negative than the outside.
  • This potential difference is maintained by the Sodium-Potassium Pump: a carrier protein in the axon membrane.
  • The pump actively transports 3 Na⁺ ions out for every 2 K⁺ ions in.
  • Result: The outside of the membrane has a net positive charge (more positive ions outside) and the inside has a net negative charge (fewer positive ions inside and the presence of negatively charged organic ions). The membrane is therefore polarised.

Generating the Action Potential (AP) (15.1.5)

A signal begins when a receptor detects a stimulus and generates a current. If this current is strong enough, it reaches the threshold potential (around -50 mV), triggering an AP.

Step-by-step: Action Potential (AP)

An AP is a rapid, temporary reversal of the membrane potential, which quickly restores itself.

Prerequisite: The Stimulus (e.g., Chemoreceptor in a Taste Bud)

When you eat something sweet, chemical molecules dissolve in the saliva and bind to chemoreceptor cells on your tongue. This binding causes a change in the membrane permeability of the sensory neurone linked to the chemoreceptor, leading to the influx of positive ions. This influx creates a generator potential. If the generator potential is strong enough to reach the threshold, an AP is fired.

The Three Events of the AP:

  1. Depolarisation (Rising Phase):
    Stimulus reaches threshold (-50 mV). Voltage-gated Na⁺ channels open rapidly. Na⁺ ions rush into the axon down their electrochemical gradient. The inside becomes positive (up to +40 mV). The membrane is now depolarised.
  2. Repolarisation (Falling Phase):
    At the peak (+40 mV), the Na⁺ channels inactivate. Now, the voltage-gated K⁺ channels open fully (these open more slowly). K⁺ ions rush out of the axon. The potential difference returns towards negative values.
  3. Hyperpolarisation (Refractory Period):
    K⁺ channels are slow to close, causing too many K⁺ ions to leave. The potential briefly drops below the RP (e.g., -85 mV). The membrane is hyperpolarised.
    The Na⁺/K⁺ pump then actively restores the balance, bringing the membrane back to -70 mV (Resting Potential).
Refractory Period (15.1.6, 15.1.8)

The short period during and immediately after the AP where the neurone cannot be excited again is the refractory period.

  • Importance: This ensures that impulses travel in one direction only (they can't flow backward) because the previous section of the axon is inactive.
  • It also ensures impulses are discrete (separate) and limits the maximum frequency (rate) at which impulses can be transmitted.

Transmission Speed: Saltatory Conduction (15.1.7)

In vertebrates, many axons are surrounded by a fatty layer called the myelin sheath, formed by Schwann cells.

  • The myelin sheath acts as an electrical insulator.
  • Gaps occur at regular intervals along the sheath, called Nodes of Ranvier.
  • In a myelinated neurone, the AP can only be generated at the Nodes of Ranvier, as these are the only points where voltage-gated Na⁺ channels are present.
  • The impulse 'jumps' from one node to the next. This is called saltatory conduction ("saltare" means to jump in Latin).
  • This jumping mechanism makes transmission much faster than in non-myelinated neurones (where the AP must propagate across the entire membrane surface).

Quick Review: Resting potential is maintained by the Na⁺/K⁺ pump. Action potential starts with rapid Na⁺ influx (depolarisation). Saltatory conduction means the signal jumps nodes, increasing speed.

3. Communication: The Cholinergic Synapse (15.1.9)

Neurones communicate with each other, or with effectors, across tiny gaps called synapses (or neuromuscular junctions, if the target is muscle).

Structure and Function of the Cholinergic Synapse

A cholinergic synapse uses the neurotransmitter acetylcholine (ACh).

Anatomy of the Synapse:
  • Presynaptic Membrane: The end of the sending neurone. Contains synaptic vesicles filled with ACh.
  • Synaptic Cleft: The small gap (about 20 nm) between the neurones.
  • Postsynaptic Membrane: The membrane of the receiving neurone or effector cell. Contains specific ACh receptors.
Step-by-step Synaptic Transmission (The Role of Calcium Ions):
  1. Arrival of AP: An action potential arrives at the presynaptic terminal.
  2. Calcium Influx: The depolarisation opens voltage-gated Calcium ion (Ca²⁺) channels on the presynaptic membrane. Ca²⁺ ions rush into the presynaptic knob.

    (Crucial Role: Without this Ca²⁺ influx, transmission stops!)

  3. Vesicle Fusion: The influx of Ca²⁺ causes the synaptic vesicles (containing ACh) to move toward and fuse with the presynaptic membrane.
  4. Neurotransmitter Release: Acetylcholine (ACh) is released by exocytosis into the synaptic cleft.
  5. Binding and Depolarisation: ACh diffuses across the cleft and binds to specific receptor proteins on the postsynaptic membrane. This binding causes ligand-gated Na⁺ channels to open.
  6. Postsynaptic Potential: Na⁺ ions rush into the postsynaptic cell, causing a postsynaptic potential (PSP). If this PSP reaches the threshold, a new Action Potential is generated in the receiving neurone.
  7. Clearance: Acetylcholinesterase (an enzyme) rapidly breaks down ACh in the cleft, ensuring the signal is short and discrete. The products are reabsorbed by the presynaptic neurone.

Did You Know? Synapses allow for integration. A single neurone may receive signals from thousands of synapses, allowing the CNS to make complex decisions by summing up excitatory and inhibitory signals.

4. Control of Muscular Contraction

The most powerful output of the nervous system is muscle contraction, carried out by effectors. We focus on striated muscle (skeletal muscle) which is responsible for voluntary movement.

Striated Muscle Ultrastructure (15.1.11)

Striated muscle tissue contains long, multi-nucleated cells called muscle fibres. The cytoplasm (sarcoplasm) contains many parallel bundles of contractile elements called myofibrils.

Myofibrils are made up of repeating units called sarcomeres. The striped (striated) appearance comes from the arrangement of two types of protein filaments:

  • Thick filaments: Made primarily of myosin.
  • Thin filaments: Made primarily of actin, along with regulatory proteins troponin and tropomyosin.
Key Sarcomere Regions (You Must Know These!)
  • Z-lines: Boundary discs separating one sarcomere from the next.
  • I-band: The light region, containing only thin (actin) filaments.
  • A-band: The dark region, corresponding to the length of the thick (myosin) filaments.
  • H-zone: The central part of the A-band, containing only thick (myosin) filaments.
  • M-line: The central point of the H-zone (and the sarcomere), anchoring the thick filaments.

Excitation-Contraction Coupling (The Trigger) (15.1.10)

How does a nerve impulse at the neuromuscular junction (NMJ) trigger the sarcomere to contract?

  1. Signal at NMJ: A motor neurone impulse arrives at the NMJ (a large synapse). ACh is released and binds to receptors on the muscle fibre membrane (sarcolemma).
  2. T-Tubule Activation: An AP is generated in the sarcolemma and rapidly spreads deep into the muscle fibre via a network of infoldings called the T-tubules (Transverse tubules).
  3. Calcium Release: The AP travelling through the T-tubules stimulates the adjacent sarcoplasmic reticulum (SR)—a specialised endoplasmic reticulum that stores Ca²⁺—to release large amounts of calcium ions (Ca²⁺) into the sarcoplasm.

Analogy: The SR is the bank vault holding the Ca²⁺. The T-tubule acts as the security alarm, triggering the vault to open.

The Sliding Filament Model (15.1.12)

Contraction occurs when the thin actin filaments slide past the thick myosin filaments, shortening the sarcomere. The filaments themselves do NOT shorten.

Roles of Troponin, Tropomyosin, Calcium, and ATP:
  1. The Blockade: In a relaxed muscle, the regulatory protein tropomyosin wraps around the actin filament, physically blocking the binding sites where myosin heads would attach.
  2. Ca²⁺ Role (The Key): When Ca²⁺ is released from the SR, it binds to troponin.
  3. Shifting the Tropomyosin: The binding of Ca²⁺ to troponin causes a conformational change that pulls the tropomyosin molecule away from the actin binding sites, exposing them.
  4. Myosin Head Attachment (Cross-Bridge Formation): The myosin heads (which are already energised by hydrolysing ATP) attach to the exposed binding sites on the actin, forming a cross-bridge.
  5. Power Stroke: The myosin head pivots (like rowing a boat), pulling the actin filament towards the M-line. ADP and Pi are released during this movement.
  6. ATP Role (Releasing the Head): A new molecule of ATP binds to the myosin head. This binding breaks the cross-bridge (myosin detaches from actin).
  7. Re-Energising: ATP is hydrolysed into ADP + Pi. The energy released re-cocks the myosin head, ready to form a new cross-bridge further along the actin filament.

This cycle repeats rapidly, causing the thin filaments to slide inwards, shortening the H-zone and I-band, and resulting in full muscle contraction. When the nervous impulse stops, Ca²⁺ is pumped back into the SR, and tropomyosin re-blocks the binding sites, causing relaxation.

Key Takeaway from Muscle Contraction:

The three main requirements for contraction are:
1. Nervous impulse (to release Ca²⁺).
2. Calcium ions (Ca²⁺) (to remove tropomyosin blockade).
3. ATP (for the power stroke and to detach the myosin head).