Source: Comprehensive Study Guide on Neurons, APs, and Synaptic Transmission
Tags: synapse, synaptic transmission, chemical synapse, electrical synapse, gap junction, neurotransmitter, NT, acetylcholine, glutamate, GABA, EPSP, IPSP, ionotropic, metabotropic, GPCR, ligand-gated, calcium, exocytosis, reuptake, summation, temporal summation, spatial summation
Synaptic transmission is how neurons pass signals to one another. Electrical synapses use gap junctions for fast, direct ion flow. Chemical synapses convert the electrical signal into a chemical one (neurotransmitter release), which then triggers a new electrical response in the receiving cell. The balance of excitatory (EPSP) and inhibitory (IPSP) inputs, combined through temporal and spatial summation, determines whether the postsynaptic neuron fires.
Synapse
The junction between two neurons (or a neuron and a target cell) where signal transmission occurs. Can be electrical or chemical.
Electrical synapse (gap junction)
A direct physical connection between two cells via connexon channels. Allows ions and small molecules to pass directly, producing very fast transmission.
Chemical synapse
A synapse where the presynaptic neuron releases neurotransmitters into the synaptic cleft, and these bind to receptors on the postsynaptic neuron. Slower than electrical synapses but allows for more complex signal modulation.
Synaptic cleft
The narrow gap (roughly 20 nm) between the presynaptic and postsynaptic membranes at a chemical synapse. Neurotransmitters diffuse across this space.
Neurotransmitter (NT)
A chemical messenger released from synaptic vesicles in the presynaptic terminal. Crosses the synaptic cleft and binds to receptors on the postsynaptic membrane to produce an effect.
Voltage-gated calcium channel (vg-CaCh)
A channel at the axon terminal that opens when the action potential arrives. Ca2+ entry triggers vesicle fusion and neurotransmitter release.
Exocytosis
The process by which synaptic vesicles fuse with the presynaptic membrane and release their neurotransmitter contents into the synaptic cleft.
Ligand-gated ion channel (ionotropic receptor)
A receptor that is also an ion channel. When a neurotransmitter binds, the channel opens (or closes), allowing ions to flow directly. Fast-acting.
G-protein coupled receptor (GPCR, metabotropic receptor)
A receptor that, when activated by a neurotransmitter, triggers a G protein inside the cell. The G protein then activates secondary messenger systems, producing slower but longer-lasting and more varied cellular effects.
Excitatory post-synaptic potential (EPSP)
A small depolarization of the postsynaptic membrane caused by excitatory neurotransmitter binding. Moves the membrane potential closer to threshold.
Inhibitory post-synaptic potential (IPSP)
A small hyperpolarization of the postsynaptic membrane caused by inhibitory neurotransmitter binding. Moves the membrane potential further from threshold.
Temporal summation
The accumulation of postsynaptic potentials from repeated, rapid firing of a single presynaptic neuron. If signals arrive quickly enough, they stack.
Spatial summation
The accumulation of postsynaptic potentials from multiple presynaptic neurons firing at roughly the same time. Inputs from different locations on the dendrite combine.
Acetylcholine (ACh)
A widely distributed neurotransmitter. Mainly excitatory. Involved in muscle contraction, attention, and memory.
Glutamate
The primary excitatory neurotransmitter in the brain. Involved in learning, memory, and synaptic plasticity.
GABA (gamma-aminobutyric acid)
The primary inhibitory neurotransmitter in the brain. Reduces neuronal excitability and plays a key role in preventing excessive firing.
Electrical synapses (gap junctions)
Use connexon channels to create a direct physical link between cells
Ions flow straight through, so transmission is very fast
Signal can travel in both directions
Less common than chemical synapses in the adult human brain, but important in cardiac muscle and certain neural circuits where speed and synchrony matter
Chemical synapses
The presynaptic neuron releases neurotransmitter; the postsynaptic neuron receives it
Slower than electrical synapses (requires vesicle release, diffusion, receptor binding)
Allow for signal amplification, modulation, and one-way transmission
The vast majority of synapses in the human nervous system are chemical
Step 1: the action potential arrives at the axon terminal
Step 2: depolarization opens voltage-gated calcium channels (vg-CaCh), and Ca2+ flows into the presynaptic terminal
Step 3: the rise in intracellular Ca2+ triggers exocytosis, vesicles fuse with the membrane and release NT into the synaptic cleft
Step 4: NTs diffuse across the cleft and bind to receptors on the postsynaptic membrane, producing either an excitatory or inhibitory effect
Ionotropic receptors (ligand-gated ion channels)
NT binds directly to the channel, opening or closing it
Produces a fast, short-lived response
Example: nicotinic acetylcholine receptors, GABA-A receptors
Metabotropic receptors (GPCRs)
NT binding activates an intracellular G protein
The G protein triggers secondary messenger cascades (e.g. cAMP, IP3)
Produces a slower, longer-lasting, and more diverse range of effects
Example: muscarinic acetylcholine receptors, metabotropic glutamate receptors
Three mechanisms stop the neurotransmitter signal:
Enzymatic degradation: enzymes in the cleft break down the NT (e.g. acetylcholinesterase breaks down ACh)
Reuptake: transport proteins on the presynaptic terminal pump NT back into the neuron for recycling (e.g. serotonin reuptake, which SSRIs block)
Diffusion: NT drifts away from the cleft and is diluted in the surrounding extracellular fluid
Acetylcholine (ACh): mainly excitatory; widespread in both the central and peripheral nervous systems. Key roles in muscle contraction (at neuromuscular junctions) and cognitive functions like attention and memory
Glutamate: the brain's main excitatory NT. Critical for synaptic plasticity, learning, and memory. Excess glutamate can be neurotoxic (excitotoxicity)
GABA: the brain's main inhibitory NT. Keeps neural activity in check. Many anxiolytics and sedatives (benzodiazepines, barbiturates) work by enhancing GABA's effects
Each excitatory input produces a small EPSP (depolarization toward threshold)
Each inhibitory input produces a small IPSP (hyperpolarization away from threshold)
A single EPSP is rarely enough to trigger an action potential on its own
The neuron integrates all incoming EPSPs and IPSPs:
Temporal summation: one presynaptic neuron fires rapidly, stacking multiple EPSPs before they decay
Spatial summation: multiple presynaptic neurons fire at roughly the same time, and their EPSPs add together at the axon hillock
If the combined net depolarization reaches threshold, an action potential fires. If not, no AP is generated
NT release sequence: AP arrives → Ca2+ enters via vg-CaCh → exocytosis → NT crosses cleft → NT binds postsynaptic receptor
Signal termination: enzymatic degradation OR reuptake OR diffusion
Postsynaptic integration: Σ(EPSPs) – Σ(IPSPs) ≥ threshold → AP fires
⚠️ Calcium is the trigger for neurotransmitter release. If asked what ion is essential at the presynaptic terminal, the answer is Ca2+, not Na+ or K+.
⚠️ Ionotropic receptors are fast but short-lived. Metabotropic receptors are slow but produce longer-lasting, more varied effects. Be ready to compare them.
⚠️ The three signal termination mechanisms (enzymatic degradation, reuptake, diffusion) are a classic list question. Know all three, with an example of each.
⚠️ Temporal vs. spatial summation: temporal is one neuron firing rapidly; spatial is many neurons firing together. Both are mechanisms for reaching threshold.
⚠️ Glutamate = main excitatory. GABA = main inhibitory. This pair is almost guaranteed to appear on an exam.
⚠️ SSRIs work by blocking serotonin reuptake (one of the three termination mechanisms). If the exam connects pharmacology to synaptic transmission, know this link.
Q: What are the differences between electrical and chemical synapses?
A: Electrical synapses use gap junctions (connexon channels) for direct, fast, bidirectional ion flow. Chemical synapses use neurotransmitter release across the synaptic cleft, are slower, unidirectional, and allow for signal modulation and amplification.
Q: Describe the process of neurotransmitter release at a chemical synapse.
A: The action potential arrives at the axon terminal and depolarizes it. This opens voltage-gated calcium channels, allowing Ca2+ to enter. The calcium influx triggers exocytosis of synaptic vesicles, releasing neurotransmitter into the cleft. The NT diffuses across and binds to postsynaptic receptors, producing an excitatory or inhibitory response.
Q: How do different neurotransmitters influence post-synaptic potentials?
A: Excitatory NTs (e.g. glutamate, ACh) produce EPSPs by depolarizing the postsynaptic membrane toward threshold. Inhibitory NTs (e.g. GABA) produce IPSPs by hyperpolarizing the membrane away from threshold. The postsynaptic neuron sums these inputs to determine whether to fire.
Q: What are the three mechanisms for terminating neurotransmitter signalling?
A: Enzymatic degradation (enzymes break down the NT in the cleft), reuptake (the presynaptic terminal pumps NT back in for recycling), and diffusion (NT drifts away from the synapse and is diluted).
Q: Explain the difference between temporal and spatial summation.
A: Temporal summation occurs when a single presynaptic neuron fires repeatedly in rapid succession, so postsynaptic potentials stack before they can decay. Spatial summation occurs when multiple presynaptic neurons fire at roughly the same time, and their individual postsynaptic potentials combine. Both mechanisms help the postsynaptic neuron reach threshold.
Q: What is the role of calcium in synaptic transmission?
A: When the action potential reaches the axon terminal, voltage-gated calcium channels open and Ca2+ enters the presynaptic neuron. This calcium influx is what triggers the fusion of synaptic vesicles with the membrane (exocytosis), releasing neurotransmitter into the cleft. Without calcium entry, NT release does not occur.
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