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:
Sodium channels open.
Na⁺ enters the neuron.
The inside becomes less negative.
If the neuron reaches approximately −60 mV (threshold), many more sodium channels open.
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:
Potassium channels open.
K⁺ leaves the neuron.
Sodium-potassium pumps restore original ion concentrations.
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
Action potential reaches the axon terminal.
Vesicles release neurotransmitters into the synaptic cleft.
Neurotransmitters bind to receptors on the postsynaptic neuron.
Ion channels open.
New action potential may be triggered.
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 |