Assessment Statements
State that some neurotransmitters excite postsynaptic transmission and others
inhibit postsynaptic transmission.
Explain how decision-making in the CNS can result from the interaction between the
activities excitatory and inhibitory presynapatic neurons at synapses.
Explain how psychoactive drugs affect the brain and personality by either increasing
or decreasing postsynaptic transmission.
List three examples of excitatory and three examples of inhibitory psychoactive
• Excitatory: nicotine, cocaine, amphetamines
• Inhibitory: benzodiazepines, alcohol, tetrahydrocannabinol (THC)
Explain the effects of cocaine and THC in terms of their action at synapses in the
Discuss the causes of addiction, including genetic predisposition, social factors and
dopamine secretion.
Be sure you have a solid understanding of action potentials and synapses as you work
through this subtopic.
Command terms:
Assessment statements from: Online IB Biology Subject Guide
Communication via Synapses
Synapses are a fundamental part of neural
pathways as they regulate decision-making
in terms of exciting or inhibiting the postsynaptic neurons.
• Action potentials (AP) reach terminal
bud of the pre-synaptic neuron.
• Neurotransmitters (NT), chemical
messengers, diffuse across the synapse
to bind with receptors on the postsynaptic membrane.
Work through this tutorial:
Neurotransmitters are:
• Excitatory, which means they excite the
post-synaptic neuron (contributing to
depolarisation and propagation of the
• Inhibitory, hyperpolarising the postsynaptic neuron and preventing AP.
Neurotransmitters can be excitatory or inhibitory
Neurotransmitters (NT) are proteins
• diffuse across the synaptic cleft
• bind with a receptor on the post-synaptic neuron.
Whether or not the post-synaptic neuron propagates the
action potential depends on:
• Which NT diffuses across
• Which receptors they bind to
• Which ions flow in/out of the post-synaptic neuron
• Whether or not depolarisation reaches threshold
Excitatory NTs cause depolarisation
• e.g. ACh, dopamine
NT binds, Na+ channels open, Na+ rushes in
Membrane potential depolarises, AP propagated
Inhibitory NTs cause hyperpolarisation
• e.g. GABA, dopamine (on different pathways)
NT binds to receptor
K+ channels open, K+ rushes out
OR Cl- channels open, Cl- rushes in
Membrane potential become more negative
Action potential is prevented from propagating
This is a useful example of an inhibitory neurotransmitter.
Decision-making in the Central Nervous System (CNS)
The axons of many pre-synaptic neurons feed
into the dendrites of one post-synaptic
neurons via synapses.
The ‘decision’ whether or not to propagate
the action potential along the axon of the
post-synaptic neuron takes place
in a region of the cell body
called the axon hillock.
This is achieved through summation
of the incoming impulses. If the total
axon hillock
impulse reaches threshold,
the post-synaptic neuron depolarises and
the action potential is propagated.
If the sum does not reach threshold,
the AP is not propagated.
There are two main methods of summation:
temporal and spatial.
Diagram adapted from:
Decision-making in the Central Nervous System (CNS)
Test out temporal and spatial summation:
Temporal summation
• Action potentials arrive in rapid
• Depolarisation in the axon hillock is
• If it reaches threshold before
repolarisation, the AP is propagated.
Spatial summation
• Action potentials arrive simultaneously
from multiple sources
• Some neurotransmitters are excitatory
(increasing depolarisation)
• Other NTs are inhibitory
• Summation in the axon hillock is
• If it reaches threshold the AP is
Diagram adapted from:
How do psychoactive drugs affect the brain?
Before thinking about how drugs affect the
synapses, be sure you understand how they
work and are reset.
• Some NTs have a normal excitatory function
• Other NTs have a normal inhibitory function
In general, psychoactive drugs can:
1. Increase or decrease the release of NTs (e.g.
THC – cannabis)
2. Breakdown re-uptake proteins which are
responsible for returned used components
of NTs to the pre-synaptic neuron (ready to
use again)
3. Block re-uptake proteins (e.g.cocaine)
4. Mimic or block NTs, binding to the receptors
on post-synaptic membranes
5. Inhibit production of new NTs
Work through the excellent animations and explanations from
Excitatory drugs increase
post-synaptic transmission
• Nicotine, amphetamines, cocaine
What is the effect of cocaine?
• Dopamine acts as excitatory NT
• Dopamine is re-uptaken by pumps on the presynaptic membrane.
With Cocaine:
• Cocaine blocks re-uptake pumps
• Dopamine remains in synaptic cleft
• More dopamine continues to be released
• Summative increase in post-synaptic transmission
Effects on mood:
• Dopamine is involved in reward pathways,
enhancing feelings of pleasure
• Longer-lasting feelings as dopamine is not reuptaken
Effects on behaviour:
• feelings of euphoria
• increased energy and alertness
• highly addictive
• association with depression as body reduces
production of own dopamine over time
Inhibitory drugs decrease
post-synaptic transmission
• Alcohol, benzodiazapines, THC
What is the effect of tetrahydrocannibol (THC)?
• Dopamine release is moderated (inhibited) by GABA
With THC:
• THC mimics cannabinoids and inhibits GABA release
by binding to cannabinoid receptors
• GABA cannot inhibit dopamine release
• More dopamine is released
Effects on mood:
• Dopamine is involved in reward pathways,
enhancing feelings of pleasure
• Not as extreme release of dopamine as with cocaine,
but still higher than normal
Effects on behaviour:
• intoxication
• hunger
• memory impairment
• potential dependency
A scale of harm for drugs
Which dots represent:
• tobacco?
• alcohol?
• heroin?
• cocaine?
• THC/ cannabis?
• ecstasy?
Drag the red dot to point you
think represents alcohol.
How can drugs cause physical
How can drug use lead to
addiction (dependency)?
What factors contribute to
development of addiction?
ActivePrompt link: or
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