EDEXCEL Biological Psychology Essay Plans
Neurons, Neurotransmitters and the CNS
AO1: Synaptic Transmission: process by which neurones communicates at synapse:
1) Electrical impulse reaches axon terminal.
2) Triggers release of neurotransmitters from synaptic vesicles.
3) Neurotransmitters cross the synaptic gap and bind to receptor sites on the post-synaptic
neuron.
4) This generates a new electrical impulse.
5) Reuptake or enzyme breakdown stops the signal.
The Effect of Recreational Drugs on the CNS
AO1: Cocaine: stimulant drug that increases the activity of the central nervous system (CNS). It
acts as a dopamine agonist, blocking the reuptake of dopamine in the mesocorticolimbic
pathway, especially in the nucleus accumbens, which increases dopamine levels and leads to
feelings of euphoria.
Heroin: a depressant and an agonist of endorphins and dopamine. It converts into morphine in
the brain, binding to opioid receptors, leading to pain relief and feelings of well-being. It slows
down CNS activity and is highly addictive.
Long-term effects of drug use include damage to dopamine systems, tolerance, withdrawal
symptoms, and long-lasting changes in brain structure and function (e.g., reduced prefrontal
cortex activity → poor self-control).
Agonist drugs mimic neurotransmitters and enhance their effects (e.g., heroin), whereas
antagonist drugs block receptor sites, reducing neurotransmitter action (e.g., naloxone, which
blocks opioid receptors).
Mesocorticolimbic pathway: involved in the reward system and is activated by pleasurable
stimuli, including drugs. Repeated use over-activates this system, reinforcing drug-seeking
behavior and contributing to addiction.
AO3:Strength: empirical evidence: Studies using mice with lesions to the mesolimbic pathway
show that cocaine's rewarding effects are reduced, supporting the role of this pathway in
addiction. This gives biological validity to dopamine’s role in reinforcement and reward.
However, weakness: animal studies lacks full generalisability: uman brains are more complex
than animal brains, especially in terms of cognition, decision-making, and social factors. This
limits external validity, as drug effects in humans may involve more psychological and
environmental influences.
Application:Research has led to practical treatments, such as naloxone, which is an opioid
antagonist used to treat heroin overdose by blocking opioid receptors, preventing heroin from
producing effects.
Contemporary study: Li et al (2013)
AO1: AIM: To investigate whether heroin addicts show different brain activation in response to
drug-related cues compared to non-addicts, using fMRI scanning
, SAMPLE: 14 male heroin addicts (average abstinence = 89 months, except nicotine) and 14
males with no substance misuse history (control group), matched for age, education, and
handedness (right handed).
PROCEDURE: Participants were shown a picture of 24 drug and non-drug related pictures for 2s
in random order, with intervals between 4-12s. Brain activity was monitored using fMRI to
observe activation in specific areas like the posterior cingulate cortex (linked to craving).
FINDINGS: Ps addicted to heroin= cravings for it, specifically shown in posterior cingulate cortex
and reward system areas which are the areas associated with reward, memory, and
self-reflection, suggesting cue-induced craving. Positive correlation on degree of connectivity
between brain regions and length of time of heroin use.
CONCLUSION: Long-term heroin use causes long-lasting changes in brain structure and
function, particularly in areas linked to craving and addiction. Exposure to drug-related cues can
reactivate these brain areas, increasing the risk of relapse.
AO3:Strength: is well-matched samples of heroin addicts and non-addicts, controlling for
variables like age, education, and handedness = reduces participant differences as a
confounding variable and ensures any differences in brain activation (e.g., in the posterior
cingulate cortex) are more likely due to drug use, improving construct validity.
However, weakness: is ethical issues: heroin addicts are a vulnerable group, raising concerns
about informed consent and potential psychological harm (e.g., from drug-related cues causing
cravings) BUT received approval from two independent ethics committees, suggesting steps
were taken to protect participants and follow ethical guidelines.
Used a small sample size (14 per group), all male and Chinese, which reduces population
validity. Results may not generalise to women, other ethnic groups, or broader populations,
limiting the applicability of the findings to diverse real-world settings.
Application: Findings highlight how long-term drug misuse alters brain functioning, particularly in
cue reactivity and reward processing. This has practical value in designing targeted treatments,
understanding relapse triggers, and communicating the serious cognitive impact of addiction in
health interventions.
Brain Structure and Brain Function
AO1: The human brain is divided into two hemispheres (left and right).
FRONTAL LOBE: 40% cortex, controls high level cognitive functions such as planning, decision
making. Also controls voluntary movements.
PARIETAL LOBE: Contains the somatosensory cortex.Processes sensory information (touch,
temperature, pain).
TEMPORAL LOBE: contains auditory cortex, deals with sound, location, volume and pitch,
understanding language.
OCCIPITAL LOBE: contains visual cortex, controls vision by processing by left visual cortex
before right to see the right side (and vice versa to see left)
BROCA’S AREA: responsible for speech production, damaged= slow and non-fluent language
(Broca’s aphasia). In left frontal lobe.
WERNICKE’S AREA: responsible for language comprehension. Damage= fluent but
nonsensical, with poor understanding of language.
Neurons, Neurotransmitters and the CNS
AO1: Synaptic Transmission: process by which neurones communicates at synapse:
1) Electrical impulse reaches axon terminal.
2) Triggers release of neurotransmitters from synaptic vesicles.
3) Neurotransmitters cross the synaptic gap and bind to receptor sites on the post-synaptic
neuron.
4) This generates a new electrical impulse.
5) Reuptake or enzyme breakdown stops the signal.
The Effect of Recreational Drugs on the CNS
AO1: Cocaine: stimulant drug that increases the activity of the central nervous system (CNS). It
acts as a dopamine agonist, blocking the reuptake of dopamine in the mesocorticolimbic
pathway, especially in the nucleus accumbens, which increases dopamine levels and leads to
feelings of euphoria.
Heroin: a depressant and an agonist of endorphins and dopamine. It converts into morphine in
the brain, binding to opioid receptors, leading to pain relief and feelings of well-being. It slows
down CNS activity and is highly addictive.
Long-term effects of drug use include damage to dopamine systems, tolerance, withdrawal
symptoms, and long-lasting changes in brain structure and function (e.g., reduced prefrontal
cortex activity → poor self-control).
Agonist drugs mimic neurotransmitters and enhance their effects (e.g., heroin), whereas
antagonist drugs block receptor sites, reducing neurotransmitter action (e.g., naloxone, which
blocks opioid receptors).
Mesocorticolimbic pathway: involved in the reward system and is activated by pleasurable
stimuli, including drugs. Repeated use over-activates this system, reinforcing drug-seeking
behavior and contributing to addiction.
AO3:Strength: empirical evidence: Studies using mice with lesions to the mesolimbic pathway
show that cocaine's rewarding effects are reduced, supporting the role of this pathway in
addiction. This gives biological validity to dopamine’s role in reinforcement and reward.
However, weakness: animal studies lacks full generalisability: uman brains are more complex
than animal brains, especially in terms of cognition, decision-making, and social factors. This
limits external validity, as drug effects in humans may involve more psychological and
environmental influences.
Application:Research has led to practical treatments, such as naloxone, which is an opioid
antagonist used to treat heroin overdose by blocking opioid receptors, preventing heroin from
producing effects.
Contemporary study: Li et al (2013)
AO1: AIM: To investigate whether heroin addicts show different brain activation in response to
drug-related cues compared to non-addicts, using fMRI scanning
, SAMPLE: 14 male heroin addicts (average abstinence = 89 months, except nicotine) and 14
males with no substance misuse history (control group), matched for age, education, and
handedness (right handed).
PROCEDURE: Participants were shown a picture of 24 drug and non-drug related pictures for 2s
in random order, with intervals between 4-12s. Brain activity was monitored using fMRI to
observe activation in specific areas like the posterior cingulate cortex (linked to craving).
FINDINGS: Ps addicted to heroin= cravings for it, specifically shown in posterior cingulate cortex
and reward system areas which are the areas associated with reward, memory, and
self-reflection, suggesting cue-induced craving. Positive correlation on degree of connectivity
between brain regions and length of time of heroin use.
CONCLUSION: Long-term heroin use causes long-lasting changes in brain structure and
function, particularly in areas linked to craving and addiction. Exposure to drug-related cues can
reactivate these brain areas, increasing the risk of relapse.
AO3:Strength: is well-matched samples of heroin addicts and non-addicts, controlling for
variables like age, education, and handedness = reduces participant differences as a
confounding variable and ensures any differences in brain activation (e.g., in the posterior
cingulate cortex) are more likely due to drug use, improving construct validity.
However, weakness: is ethical issues: heroin addicts are a vulnerable group, raising concerns
about informed consent and potential psychological harm (e.g., from drug-related cues causing
cravings) BUT received approval from two independent ethics committees, suggesting steps
were taken to protect participants and follow ethical guidelines.
Used a small sample size (14 per group), all male and Chinese, which reduces population
validity. Results may not generalise to women, other ethnic groups, or broader populations,
limiting the applicability of the findings to diverse real-world settings.
Application: Findings highlight how long-term drug misuse alters brain functioning, particularly in
cue reactivity and reward processing. This has practical value in designing targeted treatments,
understanding relapse triggers, and communicating the serious cognitive impact of addiction in
health interventions.
Brain Structure and Brain Function
AO1: The human brain is divided into two hemispheres (left and right).
FRONTAL LOBE: 40% cortex, controls high level cognitive functions such as planning, decision
making. Also controls voluntary movements.
PARIETAL LOBE: Contains the somatosensory cortex.Processes sensory information (touch,
temperature, pain).
TEMPORAL LOBE: contains auditory cortex, deals with sound, location, volume and pitch,
understanding language.
OCCIPITAL LOBE: contains visual cortex, controls vision by processing by left visual cortex
before right to see the right side (and vice versa to see left)
BROCA’S AREA: responsible for speech production, damaged= slow and non-fluent language
(Broca’s aphasia). In left frontal lobe.
WERNICKE’S AREA: responsible for language comprehension. Damage= fluent but
nonsensical, with poor understanding of language.
