Neurotransmission Flashcards
Excitable cells communicate via
Chemical neurotransmission
Synapses
Specialised structures where neurones contact each other
At synapses
Electrical signal is converted into a chemical message and then back to an electrical message
Action potential dependent neurotransmitter release
- Action potential invades the presynaptic terminal
- Membrane depolarisation occurs
- Voltage gated calcium channels open allowing calcium into the presynaptic terminal
- Increase in calcium promotes vesicle fusion to the presynaptic terminal
- Vesicles release transmitters into the synaptic cleft
Synthesis and storage of neurotransmitters
precursors molecules and/or synthesis enzymes located in the presynaptic terminal -> enzymes travel along the axons slowly -> and are used to synthesise neurotransmitters and package them into vesicles
Vesicles allow
Trains of action potentials
Exocytosis
Release of neurotransmitter into the presynaptic terminal
Endocytosis
The replenishing of vesicles
Docking
Vesicles binding the the presynaptic membrane -> before an action potential invades the terminal
Ca2+ sensing
Calcium ion entry triggers fusion of the vesicle
Endocytosis mechanisms
New vesicle membrane ‘pinched off’ generating a new vesicle
Loading
New vesicle is filled with neurotransmitter
Exocytosis/endocytosis cycle
Docking -> Ca^2+ sensing -> endocytosis -> Loading
Allows exocytosis to occur at any given rate
Metabolic receptors
Slow response
Requires ATP to activate a second messenger - like a signalling cascade
Ionotropic receptors
Fast response
Ion channels open when neurotransmitter binds allowing ions to move into postsynaptic membrane
Excitatory neurotransmitters
Increase the excitability of the postsynaptic neuron
Inhibitory neurotransmitters
Decrease the excitability of the post synaptic neuron
Excitatory postsynaptic potential - EPSP
Resting potential -> action potential invades presynaptic terminal triggering release of neurotransmitter binds to post-synaptic receptors opening ion channels -> ions move into cell depolarising it -> after release event membrane potential returns to resting
Inhibitory postsynaptic potential - IPSP
Inhibitory molecules like GABA
Ligand binds causing conformational change opening a channel pore allowing inhibitory ions through -> Cl- therefore moves into the cell -> causes hyperpolarisation -> requires Strom her stimulus to trigger an action potential so therefore inhibitory
Spatial summation
Summation not EPSPs generated at different synapses