9.2 Synaptic transmission and neurotransmitter release

Synaptic transmission is the cornerstone of neural communication. Neurons release neurotransmitters into synapses, which bind to receptors on target cells, triggering electrical or chemical changes. This process is crucial for information processing in the nervous system.

Neurotransmitter release is a complex, calcium-dependent process. When an action potential reaches a synapse, calcium influx triggers vesicle fusion with the cell membrane, releasing neurotransmitters. This mechanism allows for precise control of neural signaling and forms the basis for synaptic plasticity.

Chemical synapse structure and function

Synaptic components and their roles

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• Chemical synapses are specialized junctions between neurons that transmit information via neurotransmitters
• The presynaptic terminal contains synaptic vesicles filled with neurotransmitters, mitochondria, and other organelles necessary for energy production and vesicle recycling
• The postsynaptic membrane contains neurotransmitter receptors, which can be ionotropic (directly opening ion channels) or metabotropic (activating second messenger cascades)
• The synaptic cleft is a narrow space between the pre- and postsynaptic membranes that allows for rapid diffusion of neurotransmitters (typically 20-40 nm wide)

Neurotransmitter release and binding

• The presynaptic neuron releases neurotransmitters into the synaptic cleft through exocytosis of synaptic vesicles
• Released neurotransmitters bind to receptors on the postsynaptic neuron, causing changes in its membrane potential
• Ionotropic receptors directly open ion channels, leading to rapid changes in postsynaptic membrane potential (e.g., AMPA and NMDA receptors for glutamate)
• Metabotropic receptors activate second messenger cascades, resulting in slower and longer-lasting changes in postsynaptic neuron excitability (e.g., mGluR receptors for glutamate)

Neurotransmitter release and calcium

Calcium-dependent exocytosis

• Neurotransmitter release occurs when an action potential reaches the presynaptic terminal, causing voltage-gated calcium channels to open
• The influx of calcium ions triggers the fusion of synaptic vesicles with the presynaptic membrane, releasing neurotransmitters into the synaptic cleft
• Calcium binds to specific proteins, such as synaptotagmin, which are involved in the docking and fusion of synaptic vesicles with the presynaptic membrane
• The amount of neurotransmitter released is proportional to the concentration of calcium ions in the presynaptic terminal (typically requiring ~100 μM calcium for release)

Neurotransmitter clearance and signal termination

• After release, neurotransmitters are quickly removed from the synaptic cleft by reuptake into the presynaptic neuron or degradation by enzymes to terminate the signal
• Reuptake is mediated by specific neurotransmitter transporters (e.g., SERT for serotonin, DAT for dopamine) that use ion gradients to drive neurotransmitter uptake
• Enzymatic degradation of neurotransmitters occurs in the synaptic cleft or surrounding glial cells (e.g., acetylcholinesterase breaks down acetylcholine)

Excitatory vs Inhibitory transmission

Excitatory synaptic transmission

• Excitatory synaptic transmission occurs when neurotransmitters cause the postsynaptic membrane to depolarize, increasing the likelihood of an action potential in the postsynaptic neuron
• Excitatory neurotransmitters, such as glutamate, typically bind to ionotropic receptors that allow the influx of positively charged ions (e.g., sodium or calcium), leading to depolarization
• Examples of excitatory ionotropic receptors include AMPA and NMDA receptors for glutamate, and nicotinic acetylcholine receptors

Inhibitory synaptic transmission

• Inhibitory synaptic transmission occurs when neurotransmitters cause the postsynaptic membrane to hyperpolarize, decreasing the likelihood of an action potential in the postsynaptic neuron
• Inhibitory neurotransmitters, such as GABA and glycine, typically bind to ionotropic receptors that allow the influx of negatively charged ions (e.g., chloride), leading to hyperpolarization
• Examples of inhibitory ionotropic receptors include GABAA receptors for GABA and glycine receptors
• Some neurotransmitters, such as acetylcholine and serotonin, can have both excitatory and inhibitory effects depending on the receptor subtypes they activate (e.g., nicotinic vs. muscarinic acetylcholine receptors)

Synaptic strength and plasticity

Short-term synaptic plasticity

• Short-term synaptic plasticity includes facilitation (increased neurotransmitter release with repeated stimulation) and depression (decreased neurotransmitter release with repeated stimulation)
• Facilitation occurs when residual calcium in the presynaptic terminal enhances subsequent neurotransmitter release (e.g., paired-pulse facilitation)
• Depression occurs when the readily releasable pool of synaptic vesicles is depleted faster than it can be replenished (e.g., synaptic fatigue)

Long-term synaptic plasticity

• Long-term synaptic plasticity includes long-term potentiation (LTP) and long-term depression (LTD), which involve persistent changes in synaptic strength
• LTP is induced by high-frequency stimulation and is associated with an increase in the number of AMPA receptors at the postsynaptic membrane, enhancing synaptic transmission
• LTD is induced by low-frequency stimulation and is associated with a decrease in the number of AMPA receptors at the postsynaptic membrane, reducing synaptic transmission
• LTP and LTD are thought to be cellular mechanisms underlying learning and memory formation in the brain (e.g., hippocampal LTP in spatial memory)

Neuromodulation of synaptic plasticity

• Neuromodulators, such as dopamine and norepinephrine, can modulate synaptic plasticity by altering the properties of neurotransmitter receptors or the excitability of neurons
• Dopamine has been shown to modulate LTP and LTD in various brain regions, such as the striatum and prefrontal cortex, influencing reward-based learning and decision-making
• Norepinephrine can enhance LTP in the hippocampus and amygdala, contributing to the formation of emotional memories and stress responses