Mechanism of Synaptic Transmission — Revision Notes

⚡ 30-Second Revision

Sequence: — AP $\rightarrow$ $Ca^{2+}$ influx $\rightarrow$ NT release $\rightarrow$ NT binds $\rightarrow$ PSP $\rightarrow$ NT inactivation.
$Ca^{2+}$: — Triggers NT release from presynaptic terminal.
Neurotransmitters (NTs): — Chemical messengers (e.g., Acetylcholine, GABA, Glutamate).
Synaptic Cleft: — Gap between neurons.
EPSP: — Excitatory Postsynaptic Potential (depolarization, e.g., $Na^+$ influx).
IPSP: — Inhibitory Postsynaptic Potential (hyperpolarization, e.g., $Cl^-$ influx or $K^+$ efflux).
NT Inactivation: — Enzymatic degradation, Reuptake, Diffusion.
Chemical Synapse: — Unidirectional, slower, modifiable.
Electrical Synapse: — Bidirectional, faster, gap junctions.

2-Minute Revision

Synaptic transmission is the process of communication between neurons. It begins when an action potential (electrical signal) reaches the presynaptic terminal. This depolarization opens voltage-gated calcium channels, causing $Ca^{2+}$ ions to rush into the terminal.

This $Ca^{2+}$ influx is the critical trigger for the release of chemical messengers called neurotransmitters, which are stored in synaptic vesicles. These vesicles fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft.

The neurotransmitters then diffuse across the cleft and bind to specific receptors on the postsynaptic membrane. This binding opens ion channels, leading to a change in the postsynaptic membrane potential.

If positive ions enter, it causes an Excitatory Postsynaptic Potential (EPSP), making the neuron more likely to fire. If negative ions enter or positive ions leave, it causes an Inhibitory Postsynaptic Potential (IPSP), making the neuron less likely to fire.

Finally, neurotransmitters are rapidly removed from the cleft by enzymatic degradation, reuptake, or diffusion to ensure precise and transient signaling.

5-Minute Revision

The mechanism of synaptic transmission is the core process of neural communication. It starts with an electrical impulse, the action potential (AP), arriving at the presynaptic terminal. This depolarization opens voltage-gated calcium channels, leading to a rapid **influx of $Ca^{2+}$ ions**.

This calcium influx is the crucial signal that triggers the exocytosis of synaptic vesicles, which contain neurotransmitters (NTs). The NTs are released into the synaptic cleft, the tiny gap between neurons.

Once in the cleft, NTs rapidly diffuse and bind to specific receptors on the postsynaptic membrane. This binding causes a conformational change in the receptor, typically opening ligand-gated ion channels.

The resulting ion movement alters the postsynaptic membrane potential, creating a postsynaptic potential (PSP). PSPs can be either Excitatory (EPSP), caused by depolarization (e.g., $Na^+$ influx) making the neuron more likely to fire an AP, or Inhibitory (IPSP), caused by hyperpolarization or stabilization (e.

g., $Cl^-$ influx or $K^+$ efflux) making the neuron less likely to fire. The summation of these PSPs at the axon hillock determines if a new AP is generated.

To ensure precise, transient signaling, NTs are quickly removed from the cleft by three main mechanisms: enzymatic degradation (e.g., acetylcholinesterase breaking down acetylcholine), reuptake into the presynaptic terminal or glial cells (e.

g., serotonin, dopamine), or diffusion away from the synapse. This entire process converts an electrical signal into a chemical one and back, allowing for complex information processing and modulation within the nervous system.

Remember the key players: AP, $Ca^{2+}$, NTs, receptors, and ion channels.

Prelims Revision Notes

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Synapse Structure: — Presynaptic terminal, synaptic cleft, postsynaptic membrane.
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Action Potential Arrival: — Electrical signal (AP) reaches presynaptic terminal, causing depolarization.
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Calcium Influx: — Depolarization opens voltage-gated $Ca^{2+}$ channels. $Ca^{2+}$ rushes into the presynaptic terminal.
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Neurotransmitter Release: — $Ca^{2+}$ influx triggers fusion of synaptic vesicles (containing NTs) with presynaptic membrane. NTs released into synaptic cleft via exocytosis.
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Diffusion: — NTs diffuse across the synaptic cleft.
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Receptor Binding: — NTs bind to specific receptors on the postsynaptic membrane.
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Postsynaptic Potential (PSP) Generation:

* EPSP (Excitatory Postsynaptic Potential): NT binding causes depolarization (e.g., $Na^+$ influx), making neuron more likely to fire AP. * IPSP (Inhibitory Postsynaptic Potential): NT binding causes hyperpolarization or stabilization (e.g., $Cl^-$ influx or $K^+$ efflux), making neuron less likely to fire AP. * PSPs are graded potentials, not all-or-none.

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Neurotransmitter Inactivation: — Rapid removal of NTs from cleft:

* Enzymatic Degradation: Enzymes break down NTs (e.g., acetylcholinesterase for ACh). * Reuptake: NTs actively transported back into presynaptic terminal or glial cells (e.g., serotonin, dopamine). * Diffusion: NTs diffuse away from cleft.

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Key Neurotransmitters:

* Acetylcholine (ACh): Excitatory at neuromuscular junction. * Glutamate: Primary excitatory NT in CNS. * GABA: Primary inhibitory NT in CNS (opens $Cl^-$ channels). * Glycine: Inhibitory NT (spinal cord). * Dopamine, Serotonin, Norepinephrine: Modulatory, can be excitatory or inhibitory depending on receptor.

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Synaptic Delay: — Time taken from AP arrival at presynaptic terminal to PSP generation.
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Chemical vs. Electrical Synapses: — Chemical are slower, unidirectional, modifiable, involve NTs. Electrical are faster, bidirectional, direct ion flow via gap junctions.

Vyyuha Quick Recall

Calm Neurons Release Bright Potentials Inside:

Calcium Influx
Neurotransmitter Release
Receptor Binding
Bright (Postsynaptic) Potentials (EPSP/IPSP)
Inactivation (of neurotransmitter)