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Notes - Biology 25-04-25

The document outlines the structure and function of neurons, detailing types such as sensory, relay, and motor neurons, along with the roles of myelination and action potentials in nerve impulse transmission. It explains the processes of depolarization and repolarization during action potentials, as well as the significance of synapses and neurotransmitters in communication between neurons. Additionally, it discusses how various drugs can influence synaptic activity, providing examples of their effects on the nervous system.

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CHANDANI SHARMA
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0% found this document useful (0 votes)
13 views11 pages

Notes - Biology 25-04-25

The document outlines the structure and function of neurons, detailing types such as sensory, relay, and motor neurons, along with the roles of myelination and action potentials in nerve impulse transmission. It explains the processes of depolarization and repolarization during action potentials, as well as the significance of synapses and neurotransmitters in communication between neurons. Additionally, it discusses how various drugs can influence synaptic activity, providing examples of their effects on the nervous system.

Uploaded by

CHANDANI SHARMA
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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8A.

1 – The Structure of Neurons

🔍 Learning Objectives
1.​ Know the structure and function of sensory, relay, and motor neurones,
including Schwann cells and myelination.​

2.​ Understand how the nervous system causes effectors to respond to stimuli.​

3.​ Understand how a nerve impulse (action potential) travels along an axon,
including changes in sodium and potassium ion permeability.​

🧠 The Nervous System – Overview


●​ The nervous system maintains homeostasis by coordinating rapid,
targeted responses to stimuli.​

●​ It uses neurones (nerve cells) to transmit electrical impulses from:​

○​ Receptors (detect changes)​

○​ To the CNS (processes info)​

○​ Then to effectors (muscles or glands that respond)​

🔗 Basic Structure of the Nervous System


●​ Composed of neurones, which carry impulses.​

●​ Divided into:​

○​ Central Nervous System (CNS): brain + spinal cord.​

○​ Peripheral Nervous System (PNS): all other nerves.​

🔍 Types of Nerves:
●​ Sensory Nerves: only sensory fibres.​
●​ Motor Nerves: only motor fibres.​

●​ Mixed Nerves: both sensory and motor fibres.​

🔌 Types of Neurones
1. Sensory Neurone

●​ Carries impulses from receptors → CNS.​

●​ Has a cell body off to the side of the axon.​

2. Relay (Connector) Neurone

●​ Found in CNS, connects sensory and motor neurones.​

●​ Also called bipolar neurones (2 fibres).​

3. Motor Neurone

●​ Carries impulses from CNS → effectors.​

●​ Cell body at one end, axon leads to muscle/gland.​

🧬 Structure of a Neurone
●​ Cell body: contains nucleus, mitochondria, rough ER, and ribosomes (for
neurotransmitter synthesis).​

●​ Dendrites: receive impulses from other neurones.​

●​ Axon: long fibre carrying impulses away from the cell body.​

●​ Dendron (in sensory neurones): carries impulses towards the cell body.​

●​ Synaptic bulbs: transmit impulses to the next cell.​

●​ Myelin sheath (formed by Schwann cells): speeds up impulse transmission


and protects axon.​
●​ Nodes of Ranvier: gaps between Schwann cells where impulses "jump"
(saltatory conduction).​

⚡ Myelinated vs Unmyelinated Fibres


●​ Myelinated fibres: faster impulse transmission (up to 120 m/s), found in
voluntary motor neurones.​

●​ Unmyelinated fibres: slower, found in autonomic neurones.​

●​ Invertebrates: lack myelin but may have giant axons for fast responses (e.g.,
squid).​

🧪 Investigating Nerve Impulses


●​ Early studies used external electrodes on whole nerves (limited accuracy).​

●​ Hodgkin and Huxley (1940s): Used internal microelectrodes in giant squid


axons.​

●​ Discovered the resting potential: ~–70 mV (more negative inside the axon).​

🔁 How Action Potentials Work


●​ Based on movement of Na⁺ (sodium) and K⁺ (potassium) ions through
membrane proteins.​

●​ Involves:​

○​ Depolarisation: Na⁺ enters → inside becomes positive.​

○​ Repolarisation: K⁺ exits → restores resting state.​

●​ Myelination causes saltatory conduction, boosting speed.​

Topic 8A.2 – How the Nervous System Works


💡 Learning Objective:
Understand how a nerve impulse (action potential) is conducted along an axon,
including changes in membrane permeability to sodium (Na⁺) and potassium (K⁺)
ions.

🔋 Resting Potential
At rest, the axon membrane is polarised – the inside is negative compared to the
outside. This difference is about -70 mV and is maintained by:

🧪 Sodium-Potassium Pump (Na⁺/K⁺ pump):


●​ 3 Na⁺ ions are pumped out of the axon.​

●​ 2 K⁺ ions are pumped in, using ATP.​

●​ This active transport creates ion gradients.​

⚠️ Membrane Permeability:
●​ Membrane is almost impermeable to Na⁺ → they stay outside.​

●​ Membrane is permeable to K⁺ → they leak out through potassium channels.​

●​ Result: More positive charge outside = polarised membrane.​

⚡ Action Potential (Impulse)


When a stimulus (e.g. light, sound, neurotransmitter) reaches a neurone:

1. Depolarisation:

●​ Voltage-gated Na⁺ channels open.​

●​ Na⁺ rushes in (down its electrochemical gradient).​

●​ Inside becomes positive (+40 mV) → action potential.​


2. Repolarisation:

●​ Na⁺ channels close.​

●​ Voltage-gated K⁺ channels open.​

●​ K⁺ rushes out, restoring negative inside.​

3. Hyperpolarisation:

●​ K⁺ channels stay open too long → inside becomes more negative than -70
mV.​

●​ Channels then close, and Na⁺/K⁺ pump restores resting potential.​

📉 Refractory Period
This is the recovery time of the axon:

●​ Absolute Refractory Period: No new action potential can happen – Na⁺


channels are inactivated.​

●​ Relative Refractory Period: A stronger-than-usual stimulus is needed – K⁺


channels are still open.​

🔁 Ensures one-way transmission of impulses and limits frequency (about


500–1000 impulses/sec).

🧠 All-or-Nothing Principle
●​ If the stimulus does not reach the threshold, no action potential occurs.​

●​ If the threshold is reached, the action potential is always the same size, no
matter how strong the stimulus.​

📉 Evidence from Poisons


●​ DNP (dinitrophenol) blocks ATP production → Na⁺/K⁺ pump fails → resting
potential is lost.​

●​ When DNP is washed away or ATP is added, the pump restarts → resting
potential is restored.​

●​ Confirms the role of ATP in maintaining the resting potential.​

🧪 Summary of Ionic Changes:


Phase Ion Channels Ion Movement Membrane
Open Potential
Resting K⁺ leak channels K⁺ out -70 mV
Depolarisation Na⁺ channels Na⁺ in +40 mV
Repolarisation K⁺ channels K⁺ out Falling to -70 mV
Hyperpolarisation K⁺ still open More K⁺ out < -70 mV
Recovery Na⁺/K⁺ pump Na⁺ out, K⁺ in Back to -70 mV
active (active)

—----------------------------------------------------------------------------------------------------------

8A.3 The Neurones in Action

Learning Objectives Summary:

1.​ Understand how the nervous system causes effectors to respond to stimuli.​

2.​ Explain the role of myelination in saltatory conduction.​

3.​ Describe the structure and function of synapses, including the role of
neurotransmitters like acetylcholine.​

1. Nerve Impulses and Action Potentials

●​ When a stimulus is detected, it can trigger an action potential (AP), an


electrical signal that travels along a neurone.​
●​ At resting potential, the outside of the axon is more positive than the inside
due to:​

○​ High Na⁺ (sodium) concentration outside​

○​ High K⁺ (potassium) concentration inside​

How the Action Potential Travels

●​ When an AP begins, voltage-gated sodium channels open, and Na⁺ ions


rush into the axon. This causes depolarisation.​

●​ Localised electrical currents (local circuits) are set up in the membrane,


causing nearby sodium channels to open.​

●​ This creates a positive feedback loop: depolarisation triggers more


depolarisation.​

●​ Behind the AP, potassium channels open and K⁺ ions leave, repolarising
the membrane. This is followed by a short hyperpolarisation.​

●​ Refractory period: Ensures AP only moves forward because sodium


channels cannot reopen immediately.​

2. Saltatory Conduction

In myelinated neurones, the axon is wrapped in a fatty myelin sheath, interrupted


at gaps called nodes of Ranvier.

How It Works:

●​ The AP jumps from node to node, speeding up the signal. This is called
saltatory conduction (from Latin saltare, to jump).​

●​ This allows faster conduction in thin fibres and enables compact, complex
nervous systems.

3. Synapses and Neurotransmission

●​ A synapse is the gap between two neurones (or a neurone and an effector).​
●​ Information is passed across this gap by chemical neurotransmitters.​

Synapse Structure (See Fig C):

●​ Presynaptic knob (axon terminal)​

●​ Synaptic cleft (gap)​

●​ Post-synaptic membrane (receives signal)​

●​ Vesicles contain neurotransmitter (e.g. acetylcholine)​

Steps of Transmission Across a Synapse:

1.​ AP arrives at presynaptic knob.​

2.​ Calcium ion channels open; Ca²⁺ enters the knob.​

3.​ Vesicles move to and fuse with the presynaptic membrane.​

4.​ Neurotransmitter (ACh) is released by exocytosis.​

5.​ ACh diffuses across the cleft and binds to receptors on the post-synaptic
membrane.​

6.​ This opens Na⁺ channels, leading to an excitatory post-synaptic potential


(EPSP).​

7.​ If the EPSP reaches threshold, a new action potential is triggered.​

8.​ Acetylcholinesterase breaks down ACh into acetate and choline, which are
recycled.​

Types of Synaptic Effects

●​ Excitatory (EPSP): Triggers depolarisation → new action potential.​

●​ Inhibitory (IPSP): Allows Cl⁻ or K⁺ to enter → more negative inside → inhibits


AP.​
Common Neurotransmitters
Neurotransmitter Found in Action Notes
Acetylcholine (ACh) Motor neurones, Usually Broken down by
parasympathetic excitatory acetylcholinesterase
system, CNS
Noradrenaline Sympathetic Can be Reabsorbed and recycled
(Norepinephrine) system, brain excitatory
or
inhibitory

8A.4 – The Effect of Drugs on the Nervous System

🔍 Learning Objectives
●​ Understand how drugs influence nerve impulse transmission.​

●​ Know examples: nicotine, lidocaine, cobra venom alpha toxin, L-DOPA


(Parkinson’s), and MDMA/ecstasy.​

🧠 How Drugs Affect Synapses


Drugs can either increase or decrease synaptic activity by acting at different points
in neurotransmission:

🚀 Ways to Increase Synaptic Response


1.​ Boost neurotransmitter production.​

2.​ Increase neurotransmitter release from vesicles.​

3.​ Mimic neurotransmitter and activate post-synaptic receptors (agonist).​

4.​ Prevent breakdown of neurotransmitter by enzymes.​

5.​ Block reuptake into the presynaptic knob, so more stays in the cleft.​
🛑 Ways to Decrease Synaptic Response
1.​ Block neurotransmitter synthesis.​

2.​ Cause neurotransmitter to leak and degrade before release.​

3.​ Prevent neurotransmitter release from vesicles.​

4.​ Block receptors on post-synaptic membrane (antagonist), so


neurotransmitters can’t bind.​

💊 Examples of Drug Effects


1. Nicotine

●​ Mimics acetylcholine (ACh) and binds to nicotinic receptors on the


post-synaptic membrane.​

●​ Triggers action potentials and causes:​

○​ 🔺 Increased heart rate and blood pressure​


○​ 😀 Dopamine release (pleasure sensation → addiction)​

●​ At low doses: acts as a stimulant.​

●​ At high doses: blocks ACh receptors → toxic and potentially fatal.​

●​ Used in nicotine patches to reduce cravings in smokers.​

2. Lidocaine

●​ A local anaesthetic used by dentists and in hospitals.​

●​ Blocks voltage-gated sodium (Na⁺) channels, preventing:​

○​ Sodium influx​

○​ Action potential initiation​

○​ → No pain signal transmission​


●​ Also used for heart arrhythmias: it stabilizes the membrane and prevents
extra action potentials in the heart’s pacemaker.​

3. Cobra Venom (Alpha-cobratoxin)

●​ Binds to acetylcholine receptors at neuromuscular junctions.​

●​ Blocks ACh from binding, so:​

○​ No muscle contraction​

○​ Leads to paralysis​

●​ Can be fatal if breathing muscles are paralyzed.​

●​ In very low doses, can relax airway muscles during severe asthma attacks
(rare, controlled medical use).​

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