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Summary Biological Psychology A-Level - Detailed Revision Notes for an A/A*

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Detailed and comprehensive revision notes for the Biological Psychology unit of Psychology A-Level (Edexcel). Packed with ALL the content you need to pass this unit. Includes perceptive evaluations and lots of extra studies to make your essays stand out! Well-formatted and easily adaptable to add your own notes. Great for A-Level students aiming for top grades and undergrad Psychology students requiring a refresher. Written by a Psychology master's student with an A* Psychology A-Level.

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Biological Psychology
The Central Nervous System
Central processing and control point for all human behaviour
Brain: processes all incoming info from the senses + responsible for controlling
resulting behaviours
Spinal cord: connects brain to rest of body, allows messages to be passed from body
to brain (+ vice versa)
Neurone
Cells that receive and transmit messages from cell to cell using neurotransmitters to
enable behaviour, thinking and emotions to be transmitted + enable the working of
the brain
 Motor neurones – receive messages from CNS
 Sensory neurones – transmit messages about senses from sensory organs to the
brain/spinal cord
 Inter/relay neurones – take messages from neurone to neurone
Cell body:
 Contains body cell organelles: nucleus (controls cell + houses neuron’s genetic
material) + mitochondria site of aerobic respiration, energy released from break
down of glucose)
Axon:
 Extension of the cell body, passes electrical impulses towards terminals
 Axon hillock – where the electrical impulse is stimulated/triggered from the top of
the axon
 Nodes of Ranvier – breaks along the myelin sheath
 Myelin sheath – layers of fatty deposits around axon – provide insulating layers
(speed up rate of transmission)
Dendrites:
 Attached to cell body, receive messages from other neurones to trigger an action
potential within the cell
Axon Terminals:
 At very end of axon
 Terminal button (bouton) – on end of each terminal, pass nerve impulses to another
neurone/muscle/ gland
 Vesicles – tiny sacs in the terminal buttons, store neurotransmitters ready to be
released into the synapse
Glial Cells:
Surround neurones, protect them and have some other functions (e.g. involved in
giving a myelin sheath to protect the axon, removing waste products from the brain,
supplying nutrients)
Neurotransmitters
Serotonin:
 Excitatory + inhibitory
 Neurotransmitter for happiness/good mood, low levels linked to
depression/anxiety
 Regulates sleep-wake cycle with melatonin – serotonin for wakefulness, levels
affected by light/exercise
 Also contributes to body temperature and appetite

,  Selective serotonin reuptake inhibitors are prescribed for people with mental
disorders like depression
Dopamine:
 Associated with pleasure feelings, which may be wanted, so dopamine is linked
to addiction (e.g. drugs), as the person carries out actions to get those feelings
 Also linked with motor control
Glutamate:
 Excitatory, associated with learning, memory + brain development (cognitive
functioning)
 Common in brain + nervous system
 Too much is harmful and can lead to stroke or even fatalities
Manufactured Drugs
 Selective serotonin reuptake inhibitors prescribed for depression
 E.g. citalopram
 Enhance serotonin levels in brain, which improves mood
 They will begin to feel happier and join in the activities that will naturally increase
serotonin levels
 Drug blocks the reuptake of serotonin, leaving more in the synapse, so there is more
chance that enough serotonin will bind to receptor to trigger an action potential
down the next neuron
Evaluation of neurotransmitters and transmission at the
synapse:
 Jovanovic used PET scanning to look at the serotonin system in women with pre-
menstrual dysphoric disorder – found control group without PMDD did show
differences in the synaptic receptors, which shows synaptic receptors have a role in
PMDD (a condition linked to low mood/depression)
 Increasing number of brain scanning studies on humans being done – produces
generalisable brain activity = scientifically credible + reliable (multiple people can
be scanned to check results)
 Allen and Stevens found that synaptic transmission regarding hippocampal neurons
was very unreliable (less than half the neurotransmitters arriving from the
presynaptic neurone were picked up by the postsynaptic neuron)  partly due to
issues with release mechanisms in low capacity synapses = not as straightforward as
it may seem + perhaps many factors at work (may not work steadily + regularly)
 Much evidence from animal studies where lesions can be made – lack of
generalisability to humans (have consciousness + more emotional functioning)
 Animal ethics


Drugs
Chemicals that have an effect on humans
Recreational Drugs:
 Taken for pleasure, e.g. cocaine, heroin, cannabis
 Often known as psychoactive substances, because they alter brain function, which
changes our mood, perception and conscious experiences
Legal Highs:
 Mimic the effect of the drug, but are not yet illegal
Drugs on the Synapse:
 Mode of action

,  Desensitisation: when more of a substance needed to get the same feeling due to
changes at the synapse, loss of response to a drug, so more is needed to get the
same effect
 Addiction: reward system in the brain giving such good feelings that the
individual must have that reward, drug needed for normal functioning
 Reward pathway:
 Brain contains a reward pathway, which causes us to experience a
pleasant/rewarding feeling
 Encourages us to repeat the behaviour that activates the pathway
 Drugs hijack this reward system and produce pleasurable feelings without
any adaptive functioning
Cocaine:
Blocks the reuptake of dopamine (increased pleasure in reward pathway + over-
stimulation of postsynaptic neurons) into the pre-synaptic neurone, so more is left in
the synapse for the message to continue. The body stops making and replacing the
dopamine – it becomes desensitised.
Nicotine:
Works on the reward pathway (pleasure centre) in the brain to give pleasure. The
brain realises too many dopamine receptors are being stimulated, so starts shutting
them down. Nicotine receptors trigger an electrical impulse in a neurone and in the
reward pathway, which release more dopamine (cellular and behavioural addiction,
body becomes desensitised). Nicotine mimics the action of acetylcholine, so its binds
of acetylcholine receptors = double binding, which stops body producing
acetylcholine – no alertness.
Cannabis:
Cannaboid receptors block the post-synaptic receptors, meaning there is a reduction
in activity. There are many cannaboid receptors in the hippocampus – cannabis binds
to cannaboid receptors, so neurotransmitters cannot bind to the receptors, so
memories cannot be formed – cannabis affects memory.
Evaluation of the arguments about the effects of drugs on
transmission
 Lot of supporting evidence with careful controls = reliable (many studies link
recreational drugs with creating excess dopamine to give a high) + high internal
validity – e.g. Olds and Milner (1954) found a pleasure centre in the brain of rats and
Straiker et al (2012) found an effect of cannabis in the hippocampus of mice (but
limited generalisability + artificial situation that could cause stress)
 Credibility in saying that the reward pathway relates to dopamine (a
neurotransmitter giving pleasure) and recreational drugs work on the reward
pathway to give pleasure
 Credible effect of desensitisation + tolerance – external info (e.g. observing addicted
people who begun recreationally + gradually require more for same experience)
backs up studies of internal processes = reliability
 Complexity in transmission hard to capture – current tools cannot measure
transmission/see individual neurons, scanning is expensive + needs to be more
sophisticated, scanning currently focuses on transmitters easily studied, so they are
the ones conclusions will be about – there may be others we cannot study yet
 Reductionist – cannabis limits hippocampal activity + leads to more dopamine
activity and there is more than one reward pathway  having one explanation for the
mode of action is rather simplistic

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