Transmission of Nerve Impulse — Revision Notes

⚡ 30-Second Revision

RMP: — $-70\,\text{mV}$, maintained by Na\textsuperscript{+}/K\textsuperscript{+} pump (3 Na\textsuperscript{+} out, 2 K\textsuperscript{+} in) and K\textsuperscript{+} leak channels.
Action Potential Phases:

- Threshold: $-55\,\text{mV}$ (all-or-none). - Depolarization: Voltage-gated Na\textsuperscript{+} channels open, Na\textsuperscript{+} influx (inside becomes positive). - Repolarization: Voltage-gated Na\textsuperscript{+} channels inactivate, voltage-gated K\textsuperscript{+} channels open, K\textsuperscript{+} efflux (inside becomes negative). - Hyperpolarization: Slow K\textsuperscript{+} channel closure, membrane briefly more negative than RMP.

Conduction:

- Continuous: Unmyelinated, slower. - Saltatory: Myelinated, faster (jumps between Nodes of Ranvier), energy efficient.

Synaptic Transmission (Chemical):

- AP arrives at presynaptic terminal $\rightarrow$ Voltage-gated Ca\textsuperscript{2+} channels open $\rightarrow$ Ca\textsuperscript{2+} influx $\rightarrow$ Neurotransmitter release (exocytosis). - Neurotransmitter binds to postsynaptic receptors $\rightarrow$ EPSP (depolarization, e.g., Na\textsuperscript{+} influx) or IPSP (hyperpolarization, e.g., Cl\textsuperscript{-} influx or K\textsuperscript{+} efflux). - Neurotransmitter removal: Degradation, reuptake, diffusion.

Summation: — Spatial (multiple inputs) and Temporal (rapid successive inputs).

2-Minute Revision

Nerve impulse transmission is an electrochemical process. Neurons maintain a negative resting membrane potential (RMP) of about $-70\,\text{mV}$ due to the Na\textsuperscript{+}/K\textsuperscript{+} pump and differential ion permeability.

When a stimulus reaches the threshold (around $-55\,\text{mV}$), an action potential (AP) is generated, following the 'all-or-none' principle. The AP begins with rapid depolarization caused by the influx of Na\textsuperscript{+} ions through voltage-gated Na\textsuperscript{+} channels.

This is followed by repolarization, where Na\textsuperscript{+} channels inactivate and K\textsuperscript{+} ions efflux through voltage-gated K\textsuperscript{+} channels, restoring negativity. A brief hyperpolarization (undershoot) may occur.

The AP propagates along the axon, either continuously (slow) in unmyelinated fibers or via faster, energy-efficient saltatory conduction in myelinated fibers (jumping between Nodes of Ranvier). At the synapse, the electrical signal becomes chemical.

Presynaptic Ca\textsuperscript{2+} influx triggers neurotransmitter release into the synaptic cleft. These chemicals bind to postsynaptic receptors, causing either excitatory (EPSP) or inhibitory (IPSP) potentials.

These potentials are integrated through spatial and temporal summation, determining if a new AP is fired in the postsynaptic neuron. Neurotransmitters are then removed by degradation, reuptake, or diffusion.

5-Minute Revision

The transmission of a nerve impulse, or action potential, is the core of neural communication. It starts with the neuron maintaining a resting membrane potential (RMP) of approximately $-70\,\text{mV}$.

This negative charge inside the cell is primarily due to the active transport of ions by the Na\textsuperscript{+}/K\textsuperscript{+} pump (3 Na\textsuperscript{+} out, 2 K\textsuperscript{+} in) and the higher permeability of the membrane to K\textsuperscript{+} through leak channels.

When a stimulus depolarizes the membrane to a critical threshold (around $-55\,\text{mV}$), an action potential is triggered, adhering to the 'all-or-none' principle.

The action potential unfolds in distinct phases: First, depolarization occurs as voltage-gated Na\textsuperscript{+} channels rapidly open, allowing Na\textsuperscript{+} ions to rush into the cell, making the inside positive (e.

g., to $+30\,\text{mV}$). Next, repolarization begins as Na\textsuperscript{+} channels inactivate, and slower voltage-gated K\textsuperscript{+} channels open, causing K\textsuperscript{+} ions to flow out, restoring the negative membrane potential.

This is often followed by a brief hyperpolarization (undershoot), where the membrane potential becomes even more negative than the RMP due to the slow closure of K\textsuperscript{+} channels, contributing to the refractory period.

Once generated, the action potential propagates along the axon. In unmyelinated axons, this is a continuous, relatively slow process. In myelinated axons, the impulse 'jumps' from one Node of Ranvier to the next, a process called saltatory conduction, which is significantly faster and more energy-efficient because ion channels are concentrated only at the nodes.

At the end of the axon, the electrical signal is converted into a chemical signal at the synapse. When the action potential reaches the presynaptic terminal, it opens voltage-gated Ca\textsuperscript{2+} channels.

The influx of Ca\textsuperscript{2+} ions triggers the fusion of synaptic vesicles containing neurotransmitters with the presynaptic membrane, releasing these chemicals into the synaptic cleft. Neurotransmitters then diffuse across the cleft and bind to specific receptors on the postsynaptic membrane.

This binding causes ion channels on the postsynaptic neuron to open, leading to either an Excitatory Postsynaptic Potential (EPSP) (depolarization, making it more likely to fire an AP) or an Inhibitory Postsynaptic Potential (IPSP) (hyperpolarization, making it less likely to fire an AP).

These graded potentials are integrated at the axon hillock through spatial and temporal summation. If the summed potential reaches the threshold, a new action potential is generated in the postsynaptic neuron.

Neurotransmitters are then rapidly removed from the cleft by enzymatic degradation, reuptake, or diffusion to ensure precise signaling.

Prelims Revision Notes

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Resting Membrane Potential (RMP): — Maintained at approx. $-70\,\text{mV}$. Key players: Na\textsuperscript{+}/K\textsuperscript{+} pump (3 Na\textsuperscript{+} out, 2 K\textsuperscript{+} in, active transport), K\textsuperscript{+} leak channels (high permeability to K\textsuperscript{+}), and impermeable intracellular anions. Inside is negative, outside is positive.
2
Action Potential (AP): — An 'all-or-none' event. Requires a threshold stimulus (approx. $-55\,\text{mV}$) to initiate.

* Depolarization: Rapid influx of Na\textsuperscript{+} ions through voltage-gated Na\textsuperscript{+} channels. Membrane potential reverses to positive (e.g., $+30\,\text{mV}$). Na\textsuperscript{+} channels open fast.

* Repolarization: Inactivation of voltage-gated Na\textsuperscript{+} channels and opening of voltage-gated K\textsuperscript{+} channels. K\textsuperscript{+} ions efflux out of the cell, restoring negative potential.

K\textsuperscript{+} channels open slower. * Hyperpolarization (Undershoot): K\textsuperscript{+} channels close slowly, causing membrane potential to briefly become more negative than RMP. * Refractory Period: Absolute (no AP possible) during depolarization/early repolarization; Relative (stronger stimulus needed) during hyperpolarization.

1
Conduction of AP:

* Continuous Conduction: In unmyelinated axons. Slower, sequential depolarization along the entire membrane. * Saltatory Conduction: In myelinated axons. Faster and more energy-efficient. AP 'jumps' from one Node of Ranvier to the next. Myelin sheath acts as an insulator.

1
Synaptic Transmission (Chemical Synapse):

* AP arrives at presynaptic terminal $\rightarrow$ opens voltage-gated Ca\textsuperscript{2+} channels. * Ca\textsuperscript{2+} influx into presynaptic terminal $\rightarrow$ triggers fusion of synaptic vesicles with presynaptic membrane $\rightarrow$ release of neurotransmitters into synaptic cleft (exocytosis).

* Neurotransmitters diffuse across cleft $\rightarrow$ bind to specific receptors on postsynaptic membrane. * Binding causes opening of ligand-gated ion channels $\rightarrow$ change in postsynaptic membrane potential.

* EPSP (Excitatory Postsynaptic Potential): Depolarization (e.g., Na\textsuperscript{+} influx), increases likelihood of AP. * IPSP (Inhibitory Postsynaptic Potential): Hyperpolarization (e.g.

, Cl\textsuperscript{-} influx or K\textsuperscript{+} efflux), decreases likelihood of AP. * Summation: EPSPs and IPSPs are integrated at the axon hillock. Spatial (multiple inputs) and Temporal (rapid successive inputs) summation determine if threshold is reached for a new AP.

* Neurotransmitter Removal: Essential for signal termination. Mechanisms: enzymatic degradation (e.g., Acetylcholinesterase for Acetylcholine), reuptake into presynaptic terminal/glial cells (e.g., Serotonin, Dopamine), or diffusion away from cleft.

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Electrical Synapse: — Direct ion flow through gap junctions. Faster, bidirectional, less common, less modifiable.

Vyyuha Quick Recall

For the sequence of ions in action potential phases: Naughty Kids Rush Home.

Naughty: Na\textsuperscript{+} influx (Depolarization)
Kids: K\textsuperscript{+} efflux (Repolarization)
Rush: Resting potential restoration (Na\textsuperscript{+}/K\textsuperscript{+} pump)
Home: Hyperpolarization (brief undershoot)