Action Potential Propagation and Synaptic Transmission Notes

An action potential starts in one region and moves to the adjacent area where the membrane becomes positively charged, which then influences the next area to generate another spike.
The area that has already fired becomes much more negative (refractory period), making it hard to fire another action potential there immediately.
A spike is generated next to the original one in the opposite direction, and the signal keeps propagating along the axon in one direction.
This stepwise spike propagation travels from one end of the axon to the other and is known as the propagation of the action potential.
The propagation can be slowed or blocked if not insulated (non-myelinated axons propagate more slowly).

The myelin sheath insulates axons and speeds up signal transmission.
Gaps in the myelin sheath are called nodes of Ranvier.
Action potentials occur at these nodes; the electrical signal “jumps” from node to node (saltatory conduction).
Saltatory conduction makes transmission much faster than in non-myelinated axons because fewer spikes are needed to cover the same distance.

When the action potential reaches the axon terminal (presynaptic terminal), it triggers processes to communicate with the next neuron.
The axon terminal contains voltage-gated calcium channels that open in response to the depolarization caused by the action potential.
Calcium entry into the presynaptic terminal is necessary for neurotransmitter release.
In brief: the action potential travels to the presynaptic terminal, opens voltage-gated Ca^{2+} channels, and Ca^{2+} flows into the terminal.
This Ca^{2+} influx signals vesicles bearing neurotransmitters to fuse with the presynaptic membrane and release their contents into the synaptic cleft.
The channels that detect the action potential are voltage-gated calcium channels (Ca^{2+} channels).
Calcium's role is to enable vesicle fusion and neurotransmitter release.

Neurotransmitters are released from vesicles into the synaptic cleft (the gap between the presynaptic and postsynaptic terminals).
The synaptic cleft is the space between the axon terminal and the dendrite of the receiving neuron.
Neurotransmitters are chemical messengers used to communicate with the neighboring cell.
After release, neurotransmitters diffuse across the cleft to bind to receptors on the postsynaptic membrane.

Neurotransmitters bind to ligand-gated channels on the postsynaptic membrane.
These ligand-gated channels are closed until a neurotransmitter binds, acting like a key that opens a door.
Upon binding, the channels open and allow ions to flow into the postsynaptic cell.
In this context, sodium ions (Na^{+}) typically flow into the postsynaptic cell, creating a positive charge inside the cell.
If the depolarization is large enough to reach the threshold potential, a new action potential is generated downstream.
Analogy note: neurotransmitter binding is like turning a key to unlock channels; ion flow follows opening of these channels.

The influx of ions through postsynaptic ligand-gated channels can depolarize the membrane, contributing to an Excitatory Postsynaptic Potential (EPSP).
If the depolarization reaches or exceeds the threshold, an action potential is triggered: the condition can be summarized as reaching the threshold potential $V_{th}$ .
Conversely, neurotransmitter binding can also lead to hyperpolarization, as ions flow in a way that makes the inside of the neuron more negative, resulting in an Inhibitory Postsynaptic Potential (IPSP).
The transcript emphasizes that the postsynaptic response depends on the type of ion flow and receptor activation, producing either EPSP or IPSP.

An action potential depolarizes the axon towards the terminal.
Voltage-gated calcium channels in the presynaptic terminal open in response to depolarization, allowing Ca^{2+} to enter.
Calcium triggers vesicle fusion with the presynaptic membrane and release of neurotransmitters into the synaptic cleft.
Neurotransmitters diffuse across the cleft and bind to ligand-gated receptors on the postsynaptic membrane.
Receptor binding opens ion channels (ligand-gated), leading to Na^{+} influx (and sometimes other ions, depending on receptor type).
Postsynaptic membrane potential changes; depolarization can trigger an action potential if the threshold $V_{th}$ is reached (EPSP), while hyperpolarization leads to IPSP and reduces the likelihood of firing.

Review the slides and watch the posted videos to reinforce these concepts.
The described sequence (action potential at the axon terminal, Ca^{2+} influx, neurotransmitter release, receptor binding, ion flow, and potential postsynaptic firing) is repeatedly illustrated throughout the lecture.