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Action potential
Neuron fires caused by changes in flow of charged molecules (ions) across the neuron’s cell membrane.
Rapid change in the membrane potential of the neuron’s caused by this movement of ions.
At rest membrane potential of neurons is polarized at -70mV
As positive Na+ ions flow into cell the membrane potential depolarizes, moving closer to 0mV.
If membrane potential reaches -50mV an action potential will be triggered.
After action potential is finished there is a refractory period where the membrane potential is hyper polarized meaning that it is even further from the threshold of activation and the neuron will be less likely to trigger another action potential until the membrane potential has returned to the resting potential of -70mV
** an action potential won’t start until enough ions enter the cell to depolarise it from -70mV to -50mV
Structure and features of neurons
Soma (cell body)
Dendrites
Synapse on dendrite
Axon (inside myelin sheath)
Myelin sheath
Terminal buttons
Propagation of action potentials
Ions are only able to flow into cell and out across the neuron membrane in the gaps between the myelin, causing the actions potential to move faster
Section summary of structure and action of neurons
Structure and features of neurons:
Cell body
Dendrites
Axon
Resting membrane potential
Action potential
voltage dependent ion channels (Na+, K+)
all or none law and rate law
Structure of synapse
100 billion neurons > 1,000,000 billion synapses > 10^1,000,000 possible circuits
Synapses enable communication between neurons
Key structural details:
terminal button
Synaptic cleft
Pre and pst synaptic membrane
Synaptic vesicles
Chemical signalling in the brain
Neurotransmitters
Neurotransmitters
Chemicals that are synthesised within the brain/neurons and are often called “chemical messengers”.
The action potential stops at the end of an axon so the presynaptic neuron can only influence the post-synaptic neuron through the release of neurotransmitters across the synapse.
Neurotransmitter release
When synaptic vesicle merges with the presynaptic membrane the contents are released into the synaptic cleft.
Sometimes referred to as “kiss and run”
Neurotransmitter reuptake
The synapse has the capacity to recycle and reuse neurotransmitter molecules after they have been released.
This is a process of reabsorption into the synapse termed endocytosis
Neural excitation (EPSP)
Excitatory postsynaptic potentials (EPSPs) depolarise the postsynaptic cell membrane
EPSPs increase the likelihood that an action potential will be triggered in the postsynaptic neuron
Glutamate is the primary excitatory neurotransmitter
Depolarise
Happens when the inside of the neuron becomes less negative (more positive) compared to the outside.
Occurs because sodium (Na+) channels open, and Na+ ions rush into the neuron.
Normally, resting membrane potential is about -70mV.
During depolarisation, can rise to +30mV
Repolarisation
After depolarisation, the neuron needs to return to its resting state.
Potassium (K+) channels open, and K+ ions leave the neuron
This causes the inside of the neuron to become more negative again
This process brings the membrane potential back towards -70mV.
“Resetting”
Neural Inhibition (IPSP)
Inhibitory postsynaptic potentials (IPSPs) hyperpolarise the postsynaptic cell membrane
IPSPs decrease the likelihood that an action potential will be triggered
Gamma aminobutyric acid (GABA) is the primary inhibitory neurotransmitter
The combined effect of EPSPs and IPSPs is called neural integration
Neural Integration
Each neuron receives inputs from many other neurons
At any time, a single neuron can simultaneously receive excitatory and inhibitory inputs impacting the flow of ions into the neuron
The neuron will only fire if the sum of the excitatory inputs is sufficiently greater than the inhibitor inputs to cause the membrane potential to pass the threshold of activation
Because each neuron intergrates the signals from the incoming neurons in this way, the combined effect of EPSPs and IPSPs is called neural integration.
Neuromodulators
Dopamine; Noradrenaline; Histamine; Serotonin
Action of neurotransmitters at receptors
Neurotransmitters don’t typically enter the post-synaptic neuron directly, bind to binding site of receptor sensitive to that neurotransmitter: opens an ion channel is one example of the effect caused by the neurotransmitter binding to the receptor
Receptors very selective: lock and key model (Each receptor can generally only be activated by one neurotransmitter (or a drug that is designed to mimic that neurotransmitter)
Action of drugs at receptors
Drugs work by mimicking the chemical structure of the natural compound (perfectly or partially)
Mimicking natural neurotransmitters or neuromodulators
Can act as AGONISTS activating the receptors like natural compound
Or can act as ANTAGONISTS blocking the receptors and preventing the natural compound from activating it
Neural signalling and behaviour - impact of drugs
Drugs impact psychological processes ONLY because they mimic/trigger the same biological responses triggered by naturally occurring substances (neurotransmitters, neuromodulators, hormones, etc)
Psychological events directly impact the biological process (observing a traumatic accident, remembering a poem at school etc) requires neurons to fire and chemical messages to be sent across neurons
Section summary of communication between neurons
Synapses
structure
Process of neurotransmitter release
Effects on postsynaptic neurons
receptor binding and ion channels
EPSPs and IPSPs
Effect of drugs on synapses
agonists vs antagonists
Neural function and behaviour