Biopsychology

PET Scans

Positron Emission Tomography (PET) measures metabolic activity in the brain.

How it works:

  • A radioactive isotope is injected into the bloodstream.

  • Active brain areas consume more energy and absorb more of the tracer.

  • The scan shows which brain regions are most active.

The Case of Kim Jong-Nam

In 2017, Kim Jong-nam was attacked at an airport in Kuala Lumpur when two women smeared VX nerve agent onto his face.

VX nerve agent:

  • Extremely potent chemical weapon.

  • As little as 10 mg can be lethal.

  • Causes severe paralysis within minutes.

  • Affects muscles involved in breathing and heart function.

  • Death usually occurs from respiratory failure (asphyxiation).

Kim Jong-Nam died approximately 15–20 minutes after exposure.

Neurons

Neurons are specialised cells that transmit information throughout the nervous system.

Sensory neurons (afferent):

  • Carry information from sensory receptors to the brain.

Motor neurons (efferent):

  • Carry commands from the brain to muscles and glands.

Interneurons:

  • Connect neurons within the brain and spinal cord.

  • Most common neuron type.

How Neurons Work

Resting Potential

At rest, a neuron is polarised:

  • Inside of cell = negative

  • Outside of cell = positive

  • Resting potential = approximately −70 mV

This occurs because:

  • More Na⁺ (sodium) ions are outside the cell.

  • More K⁺ (potassium) ions are inside the cell.

Depolarisation and Action Potentials

When stimulated:

  1. Sodium channels open.

  2. Na⁺ enters the neuron.

  3. The inside becomes less negative.

  4. If the neuron reaches approximately −60 mV (threshold), many more sodium channels open.

  5. Rapid influx of Na⁺ causes the inside of the neuron to become positive (+40 mV).

This electrical spike is called an action potential.

Repolarisation

After firing:

  1. Potassium channels open.

  2. K⁺ leaves the neuron.

  3. Sodium-potassium pumps restore original ion concentrations.

  4. Energy is required for this process.

Myelin Sheath

The myelin sheath surrounds the axon and acts as an insulator.

Function:

  • Speeds up transmission of action potentials.

  • Increases efficiency of neural communication.

Synaptic Communication

Neurons communicate at synapses.

Process
  1. Action potential reaches the axon terminal.

  2. Vesicles release neurotransmitters into the synaptic cleft.

  3. Neurotransmitters bind to receptors on the postsynaptic neuron.

  4. Ion channels open.

  5. New action potential may be triggered.

  6. Neurotransmitters are removed by diffusion or enzymatic breakdown.

Key idea: Nearly all brain function depends on synaptic communication.

Major Neurotransmitters

Neurotransmitter

Main Functions

Glutamate

Main excitatory neurotransmitter

GABA

Main inhibitory neurotransmitter

Dopamine

Reward, pleasure, movement, attention

Serotonin

Mood, sleep, aggression, pain regulation

Acetylcholine (ACh)

Learning, memory, muscle activation

Endorphins & Enkephalins

Pain relief and mood elevation

VX Nerve Agent and Neurotransmission

Acetylcholine (ACh) is the neurotransmitter used by:

  • Motor neurons

  • Parasympathetic nervous system

Normally, the enzyme acetylcholinesterase (AChE) breaks down acetylcholine after it has sent its signal.

How VX Works

VX blocks acetylcholinesterase.

As a result:

  • Acetylcholine accumulates in the synapse.

  • Muscles remain continuously activated.

  • Nerves cannot "switch off."

Symptoms
  • Muscle spasms

  • Excessive salivation

  • Vomiting

  • Loss of bladder and bowel control

  • Constricted pupils

  • Paralysis

  • Inability to breathe

Cause of death: Asphyxiation due to paralysis of breathing muscles.

Antidote: Atropine

Atropine blocks acetylcholine receptors.

This reduces the effects of excess acetylcholine and can save lives if administered quickly.

Phineas Gage

Phineas Gage was a railroad foreman who survived a severe brain injury in 1848 when a tamping iron passed through his skull.

The injury damaged:

  • Orbitofrontal cortex

  • Prefrontal cortex

Before the accident he was:

  • Responsible

  • Hard-working

  • Reliable

After the accident he became:

  • Impulsive

  • Irritable

  • Socially inappropriate

  • Poor at decision-making

Friends reportedly said he was "no longer Gage."

Executive Functions

Executive functions allow us to control and override automatic behaviours.

Functions include:

  • Planning

  • Problem-solving

  • Working memory

  • Attention

  • Organisation

  • Inhibition

  • Cognitive flexibility

  • Task switching

  • Abstract thinking

Main brain region: Prefrontal cortex.

Orbitofrontal Syndrome

Results from damage to the orbitofrontal cortex.

Symptoms:

  • Social disinhibition

  • Ignoring social norms

  • Rudeness

  • Impulsivity

  • Hypersexuality

  • Risk-taking

  • Rapid mood changes

Phineas Gage's behaviour closely matched this syndrome.

Neuroplasticity

Neuroplasticity: The brain's ability to reorganise and form new neural connections after injury.

Evidence suggests Gage's behaviour improved over time because his brain gradually adapted.

Sarah Scott and Broca's Aphasia

In 2009, Sarah Scott suffered a stroke caused by a blood clot resulting from an undiagnosed congenital heart defect.

The stroke caused Broca's Aphasia.

Broca's Aphasia

Named after Paul Broca.

Broca's area:

  • Located in the left hemisphere.

  • Adjacent to motor areas controlling movement.

Function: Speech production.

Effects of damage:

  • Difficulty producing language.

  • Speech becomes slow and effortful.

  • Comprehension is often relatively preserved.

Quick Exam Summary

Concept

Key Point

PET Scan

Measures brain metabolic activity using radioactive tracers

Sensory Neurons

Carry information to the brain (afferent)

Motor Neurons

Carry commands from the brain (efferent)

Interneurons

Connect neurons within neural networks

Resting Potential

Approximately −70 mV

Action Potential

Electrical signal generated when threshold is reached

Myelin Sheath

Speeds neural transmission

Synapse

Communication point between neurons

Glutamate

Main excitatory neurotransmitter

GABA

Main inhibitory neurotransmitter

Dopamine

Reward, movement, attention

Serotonin

Mood and sleep regulation

Acetylcholine

Muscle activation, learning, memory

VX Nerve Agent

Blocks acetylcholinesterase, causing paralysis

Atropine

Antidote that blocks acetylcholine receptors

Phineas Gage

Demonstrated role of frontal lobes in personality

Executive Functions

Planning, inhibition, working memory, flexibility

Orbitofrontal Syndrome

Social disinhibition and impulsivity

Neuroplasticity

Brain's ability to reorganise after injury

Broca's Aphasia

Difficulty producing speech due to left frontal damage

Brain Tumours, Aggression and Emotion

Some brain tumours can dramatically alter personality, behaviour, and emotional regulation.

Ben Parry

Ben Parry developed severe behavioural changes due to a brain tumour. After surgical removal, his personality reportedly returned to normal almost immediately.

Case 1

A 13-year-old boy experienced:

  • Severe aggression

  • Antisocial behaviour

  • Multiple suicide attempts

  • Violent attacks on others

  • Frequent restraints

After removal of a tumour from the medial temporal lobe:

  • Seizures disappeared

  • Aggressive impulses ceased

  • Academic performance improved

  • He successfully rejoined family life

Case 2

A 5-year-old boy experienced:

  • Frequent rage episodes

  • Unprovoked screaming fits

  • Violent attacks on other children

After removal of a tumour from the inferior temporal lobe, the rage episodes stopped.

Charles Whitman: The Clock Tower Sniper

On 1 August 1966, Charles Whitman killed 14 people from the University of Texas clock tower after first murdering his wife and mother.

Prior to the attack he had:

  • Increasing rage

  • Violent impulses

  • Confusion

  • Emotional instability

An autopsy revealed a large glioblastoma affecting:

  • Thalamus

  • Hypothalamus

  • Amygdala

Researchers remain divided on how much the tumour contributed to his actions, but the case highlighted the role of these brain regions in emotion and aggression.

The Limbic System

The limbic system is a network of interconnected brain regions involved in:

  • Emotion

  • Motivation

  • Memory

  • Survival behaviours

  • Reproduction

The concept originated with Paul Broca and was later expanded by James Papez, who proposed the Papez Circuit, an early model of emotional processing.

Key functions of the limbic system:

  • Processes emotions

  • Influences autonomic nervous system activity

  • Receives strong input from smell (olfaction)

  • Helps form and retrieve memories

Fight-or-Flight Response and the Autonomic Nervous System

The Autonomic Nervous System (ANS) regulates involuntary bodily functions and adjusts the body's energy use according to circumstances.

Sympathetic Nervous System (SNS)

"Fight, Fright and Flight"

Neurotransmitter: Noradrenaline

Effects:

  • Increased heart rate

  • Increased breathing

  • Increased alertness

  • Mobilisation of energy reserves

Parasympathetic Nervous System (PNS)

"Rest and Digest"

Neurotransmitter: Acetylcholine

Effects:

  • Slower heart rate

  • Digestion

  • Relaxation

  • Energy conservation

Key Facts About the ANS

  • SNS originates primarily from the thoracic spinal cord.

  • PNS originates primarily from the brainstem and sacral spinal cord.

  • Most organs receive input from both systems.

  • The systems usually produce opposing effects.

  • Both are strongly influenced by the hypothalamus and limbic system.

Major Structures of the Limbic System

Structure

Main Function

Hippocampus

Memory formation

Hypothalamus

Hormones, autonomic regulation

Thalamus

Relays sensory and emotional information

Cingulate Gyrus

Emotion and attention

Prefrontal Cortex

Emotional regulation and decision-making

Amygdala

Fear, threat detection, aggression

Septal Area / Nucleus Accumbens

Reward and pleasure

The Brain's Reward Pathway

The Ventral Tegmental Area (VTA) sends dopamine projections to the nucleus accumbens through the mesolimbic dopamine pathway.

This pathway is responsible for:

  • Pleasure

  • Reward

  • Motivation

  • Addiction

Activation can produce:

  • Euphoria

  • Pleasure

  • Sexual arousal

  • Orgasm

Many addictive drugs increase dopamine activity in this pathway.

The Amygdala

The amygdala is strongly connected to:

  • Hippocampus (memory)

  • Hypothalamus (autonomic responses)

  • Olfactory system (smell)

Functions:

  • Detects threats

  • Evaluates emotional significance

  • Initiates fight, fright, or flight responses

  • Learns from previous experiences

Damage to the amygdala may cause:

  • Reduced fear

  • Reduced empathy

  • Emotional flattening

The amygdala is also heavily involved in:

  • Anxiety disorders

  • Phobias

  • Aggression

Alcohol and the Brain

Humans possess highly efficient enzymes that metabolise alcohol.

Ethanol is:

  • Small

  • Lipid-soluble

  • Easily enters the brain

Alcohol affects multiple neurotransmitter systems but primarily influences GABA.

GABA and Alcohol

GABA is the brain's main inhibitory neurotransmitter.

Alcohol enhances the action of GABA receptors, making neurons more likely to become hyperpolarised and less likely to fire.

Effects of Alcohol

Low Doses
  • Relaxation

  • Reduced anxiety

  • Mild sedation

Moderate Doses
  • Poor coordination

  • Slurred speech

  • Impaired eye movements

  • Reduced balance

High Doses
  • Paralysis

  • Respiratory depression

  • Loss of consciousness

  • Death

Alcohol and Behaviour

Alcohol suppresses activity in the prefrontal cortex, reducing inhibition and self-control.

This can lead to:

  • Risk-taking

  • Impulsivity

  • Poor judgement

  • Social disinhibition

Alcohol also increases dopamine release in the nucleus accumbens, producing pleasure and contributing to addiction.

Alcohol Tolerance

With repeated drinking:

GABA receptors become downregulated

  • Fewer receptors

  • Reduced receptor sensitivity

As a result:

  • More alcohol is needed to achieve the same effect

  • Tolerance develops

The brain also compensates by increasing glutamate (NMDA) receptor activity.

Alcohol Withdrawal

When alcohol is suddenly removed:

  • GABA inhibition becomes inadequate

  • Glutamate activity becomes excessive

  • Sympathetic nervous system activity increases

Symptoms include:

  • Tremors

  • Sweating

  • Rapid heart rate

  • Anxiety

  • Seizures

Severe withdrawal can produce Delirium Tremens (DTs), a potentially life-threatening condition.

Alcohol and Memory

Acute Memory Loss (Blackouts)

Alcohol suppresses NMDA glutamate receptors in the hippocampus.

This disrupts transfer of information from short-term memory into long-term memory.

Result: Memory blackouts.

Previously formed memories usually remain intact.

Long-Term Memory Damage

Repeated alcohol use causes:

  • Excitotoxic damage from excessive glutamate activity

  • Shrinkage of the hippocampus

  • Poorer memory performance

Wernicke-Korsakoff Syndrome

A severe neurological disorder caused by thiamine (Vitamin B1) deficiency, most commonly associated with chronic alcohol abuse.

Why It Occurs

Heavy drinkers often:

  • Eat poorly

  • Absorb less thiamine

Without thiamine, the brain cannot efficiently metabolise glucose.

Highly vulnerable areas include:

  • Mammillary bodies

  • Medial thalamus

  • Cerebellum

  • Brainstem

Wernicke's Encephalopathy (Acute Stage)

Symptoms:

  • Confusion

  • Disorientation

  • Ataxia (poor coordination)

  • Nystagmus (abnormal eye movements)

Important: Early treatment with high-dose thiamine can reverse many symptoms.

Korsakoff Syndrome (Chronic Stage)

If untreated, Wernicke's encephalopathy may progress to Korsakoff syndrome.

Symptoms:

  • Severe anterograde amnesia (cannot form new memories)

  • Loss of recent memories

  • Confabulation (unintentional creation of false memories)

  • Hallucinations

Damage is often permanent.

Mr A: What's Happening?

Mr A's symptoms strongly suggest Wernicke-Korsakoff Syndrome caused by chronic alcohol abuse and severe thiamine deficiency.

Evidence includes:

  • Heavy long-term alcohol consumption

  • Poor nutrition

  • Confusion and disorientation

  • Ataxia

  • Abnormal eye movements

  • Memory loss

  • Confabulation

Quick Exam Summary

Concept

Key Point

Limbic System

Emotion, motivation, memory, survival

Amygdala

Fear, threat detection, aggression

Hippocampus

Memory formation

Hypothalamus

Hormones and autonomic control

Mesolimbic Pathway

Brain reward circuit

Nucleus Accumbens

Pleasure and addiction

Sympathetic NS

Fight, fright and flight

Parasympathetic NS

Rest and digest

GABA

Main inhibitory neurotransmitter

Alcohol

Enhances GABA activity

Tolerance

Downregulation of GABA receptors

Withdrawal

Excess glutamate activity and reduced inhibition

Blackouts

Failure to transfer short-term memories into long-term memory

Wernicke's Encephalopathy

Acute thiamine deficiency syndrome

Korsakoff Syndrome

Chronic memory disorder caused by untreated thiamine deficiency

Confabulation

Unintentional creation of false memories to fill memory gaps