Neurophysiology Part 1: Neurons, Nerves, and Action Potentials

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Key terminology: nerve vs neuron; CNS vs PNS; sensory vs motor

• Nerve vs neuron

  • Neuron = a single nerve cell (the basic signaling unit).

  • Nerve = a bundle/organ containing many neurons plus other tissue (blood vessels, connective tissue); technically an organ, not a single cell.

  • A nerve can be: purely sensory, purely motor, or mixed (contains both sensory and motor neurons).

• CNS vs PNS

  • CNS = brain and spinal cord.

  • PNS = nerves outside the brain/spinal cord; contains sensory (afferent) and motor (efferent) divisions.

• Sensory vs motor terminology in both neurons and nerves

  • Sensory = signals going toward the CNS.

  • Motor = signals leaving the CNS going to muscles, organs, glands.

• Peripheral nerve example and reflex relevance

  • Some nerves are mixed (e.g., femoral nerve involved in patellar reflex).

• Cranial nerves

  • There are 12 cranial nerves; Roman numerals I–XII are important to know; names are less critical in this course.

• Somatic vs autonomic branches

  • Somatic nervous system (SNS) = voluntary control of skeletal muscles.

  • Autonomic nervous system (ANS) = involuntary control of cardiac function, smooth muscle, glands.

  • ANS splits into sympathetic (fight or flight) and parasympathetic (rest and digest).

  • Sympathetic: mobilizes body systems for activity; wide-ranging excitatory effects except the digestive system (where it slows down).

  • Parasympathetic: promotes homeostasis and maintenance; rest/digest activities (e.g., saliva, gastric secretions).

• Practical implications of autonomic control

  • Cardiac: sympathetic increases heart rate and force; parasympathetic slows heart rate.

  • Digestive: sympathetic decreases digestion; parasympathetic enhances digestion.

  • Eye: sympathetic causes pupil dilation; parasympathetic would constrict (not stated explicitly here, but implied by rest/digest context).

• Quick reminder on cortical terminology in exam prep

  • Roman numerals for cranial nerves are essential; names are less critical for this course.

Anatomy and cellular basics: neurons, nerves, and tissue composition

• Neuron = a single nerve cell; basic signaling unit.

• Nerve = multiple neurons plus blood vessels and connective tissue; an organ.

• Neurons are the cells within nerves; a nerve contains many neurons.

• Dendrites, soma (cell body), axon (axon hillock as the impulse initiation point) are the three core parts of a neuron.

• Axon terminals = synaptic terminals where neurotransmitters are released to communicate with the next neuron or target.

• Axon hillock = origin of the action potential; the site where the impulse starts.

• Axon conduction is unidirectional: from axon hillock to axon terminals.

• Synapse = the junction where two neurons come into close proximity but do not touch; includes presynaptic and postsynaptic elements.

  • Synaptic cleft = the small gap across which neurotransmitters diffuse.

  • Two-neuron terminology: presynaptic (signal-emitting neuron) and postsynaptic (receiving neuron).

  • Synapses can be axodendritic (axon to dendrite) or axosomatic (axon to soma).

• Myelin and conduction speed

  • Myelinated vs unmyelinated axons: myelin increases conduction velocity—faster transmission of action potential from hillock to terminals.

  • Schwann cells form myelin sheaths in the PNS.

  • Oligodendrocytes form myelin in the CNS.

  • Each Schwann cell typically myelinates one axon; oligodendrocytes can myelinate multiple axons.

  • Nodes of Ranvier (gaps in the myelin sheath) are critical for rapid conduction (saltatory conduction).

• Myelin’s functional significance

  • Myelinated axons transmit action potentials dramatically faster than bare axons.

Ionic basis of nerve signaling: ion channels and gradients

• Ion channels and channel types

  • Passive (leak) channels: always open; contribute to resting membrane potential (RMP).

  • Voltage-gated channels: open/close in response to membrane potential changes; crucial for action potential generation and propagation.

  • Chemically gated (ligand-gated) channels: open in response to neurotransmitter binding; mainly located on dendrites and soma; mediate synaptic (graded) potentials.

  • Gating concepts:

  • Voltage-gated channels exhibit a gate mechanism; opening/closing depends on voltage changes across the membrane.

  • Chemically gated channels open when a neurotransmitter binds; close when the neurotransmitter dissociates.

• Regional distribution of channels

  • Chemically gated channels: primarily on dendrites and soma (areas that receive signals from other neurons).

  • Voltage-gated channels: along the axon, especially at the axon hillock and nodes of Ranvier (sites of action potential generation and propagation).

• Regional localization reasoning

  • Chemically gated channels on dendrites/soma allow reception of neurotransmitters; signal is converted to electrical potentials (graded potentials).

  • Voltage-gated channels along the axon enable action potential generation and propagation (the only channels that propagate the impulse).

• Resting membrane potential (RMP)

  • Defined value: $V_m \approx -70\,\text{mV}$

  • Maintained primarily by passive/leak channels and the Na⁺/K⁺-ATPase pump that helps restore ion distributions after activity.

• Electrochemical gradient and ion movement concepts

  • Outer environment: net positive charge due to higher Na⁺ outside; inside is net negative due to higher K⁺ inside.

  • If the membrane becomes permeable to Na⁺, Na⁺ moves into the cell (down its concentration gradient), making the inside more positive.

  • If the membrane becomes permeable to K⁺, K⁺ moves out of the cell (down its concentration gradient), making the inside more negative.

  • These ion movements establish the electrochemical gradient that drives action potentials.

  • Conceptual analogy: electrical battery in the body; the membrane potential and ion gradients power neural signaling.

• Ion channel gating states and their roles in excitability

  • Passive channels: always open; maintain baseline permeability and RMP.

  • Voltage-gated channels: open/close in response to voltage changes; essential for action potential generation and propagation.

  • Chemically gated channels: open in response to neurotransmitters; mediate graded potentials and synaptic signaling.

  • Region-specific channel distribution explains how the neuron integrates and transmits signals.

The action potential: phases, thresholds, and propagation

• Core idea: an action potential is a rapid, transient reversal of membrane potential that travels along the axon to communicate with downstream neurons or effector cells.

• Three distinct phases of the action potential (rapid event)

  • Phase 1: Depolarization (rapid increase in membrane permeability to Na⁺; membrane becomes more positive).

  • Phase 2: Repolarization (K⁺ efflux increases, Na⁺ permeability decreases; returns toward negative values).

  • Phase 3: Hyperpolarization (membrane potential becomes more negative than resting potential; gradual return to resting state).

• Key numeric benchmarks

  • Resting membrane potential: $V_m \approx -70\,\text{mV}$

  • Threshold for opening voltage-gated Na⁺ channels: $V_{th} \approx -55\,\text{mV}$

  • Peak of action potential: around $+30\,\text{mV}$ (sodium influx overshoots to positive values before inactivation and K⁺ efflux restores potential)

  • Hyperpolarization may dip to around $-84\,\text{mV}$ in some cells before resetting

• Resting state vs. stimulation

  • Rest is not a phase of the action potential; it’s the quiescent, unstimulated state.

  • A stimulus can be threshold (produces an AP) or subthreshold (no AP).

• The four-part practical breakdown of the action potential progression

  • Part 0: Rest (unstimulated, baseline $V_m \approx -70\,\text{mV}$)

  • Part 1: Rest to threshold (stimulus causes Na⁺ channels to open; inward Na⁺ current depolarizes membrane toward threshold) → reach $V_{th} \approx -55\,\text{mV}$

  • Part 2: Depolarization (phase 1) – rapid Na⁺ influx → membrane potential rises toward +30 mV; Na⁺ permeability peaks and then starts to decrease as channels inactivate; simultaneous rise in K⁺ permeability begins

  • Phase 3: Repolarization (phase 2) – Na⁺ channels inactivate and close; K⁺ channels open; membrane potential falls back toward resting value

  • Phase 4: Hyperpolarization (phase 3) – K⁺ channels remain open briefly after reaching resting potential; membrane potential becomes more negative than rest; Na⁺/K⁺ pumps restore ion gradients and return Vm to resting level

• Permeability curves and interpretation

  • Na⁺ permeability: high influx during depolarization phase; increases as action potential initiates; then decreases as Na⁺ channels inactivate.

  • K⁺ permeability: lagging increase during repolarization, allowing efflux to restore negative charge.

  • The pink curve represents the action potential; the accompanying estrogen-like curves show Na⁺ and K⁺ permeability changes.

• Mechanistic summary

  • Stimulus opens voltage-gated Na⁺ channels → Na⁺ influx → depolarization toward threshold and beyond to peak (~+30 mV).

  • As Vm approaches the peak, Na⁺ channels inactivate; voltage-gated K⁺ channels open → K⁺ efflux → repolarization.

  • Hyperpolarization occurs as K⁺ channels close slowly; Na⁺/K⁺ pump and leak channels restore resting gradients.

• Absolute vs relative refractory periods

  • Absolute refractory period: during rest-to-threshold and most of phase 2; a second AP cannot be generated regardless of stimulus strength.

  • Relative refractory period: during tail end of phase 2 and all of phase 3; a second AP can occur but requires a stronger-than-original stimulus.

  • Rationale: during absolute refractory period, voltage-gated Na⁺ channels are inactivated; during relative, some channels have reset but the membrane is still hyperpolarized, so a larger depolarization is needed.

• Propagation and conduction velocity

  • Action potentials propagate along the axon; velocity is greatly increased by myelination and saltatory conduction at nodes of Ranvier.

  • In unmyelinated fibers, conduction is slower; myelination enables rapid, efficient signaling across long distances (e.g., from spinal cord to distal muscles).

• Practical and clinical implications

  • Understanding RMP and AP is foundational for all neural signaling and many clinical applications (nerve conduction studies, pharmacology of ion channels, etc.).

• Metaphors and contextual aids used in lecture

  • “Matrix/Star Wars” battery analogy: neurons as batteries generating electrical activity.

  • “Lightsaber color coding” used to visually organize channel types and their roles in signaling.

  • Uses of everyday examples (e.g., pupil dilation as a marker of sympathetic activity) to illustrate autonomic effects on the body.

Synapses and neurotransmission: how neurons talk

• Synapse definitions

  • A synapse is the junction between two neurons where signals are transmitted without physical contact.

  • Synaptic cleft is the gap across which neurotransmitters diffuse.

• Pre- and post-synaptic neurons

  • Presynaptic neuron: the neuron that releases neurotransmitter.

  • Postsynaptic neuron: the neuron that receives neurotransmitter

• Neurotransmitter diffusion and signaling

  • Neurotransmitters are released from the presynaptic terminal into the synaptic cleft and diffuse to the postsynaptic neuron.

  • The signal transfer is ultimately diffusion-driven across the cleft (high concentration on the presynaptic side, lower concentration on the postsynaptic side).

• Regional and functional specificity of synaptic types

  • Synapse naming: axodendritic (axon to dendrite), axosomatic (axon to soma).

  • Role of chemical gates and receptor specificity in determining excitatory vs inhibitory effects in the postsynaptic neuron.

• Re-examining the diffusion concept and ion gradients in the synapse

  • Diffusion across the cleft creates a chemical signal that converts into a postsynaptic response, dependent on receptor binding and ion channel changes in the postsynaptic membrane.

• The clinical and systems-level relevance of synapses

  • Synaptic function underlies all neural communication and plasticity; understanding synapses is crucial for part 3 material.

Practical clinical and study-oriented notes

• Key relationships to memorize and understand

  • Resting membrane potential is maintained by leak channels and the Na⁺/K⁺-ATPase pump.

  • Action potentials are driven by voltage-gated Na⁺ and K⁺ channels; their gating orchestrates depolarization, repolarization, and hyperpolarization.

  • Ion movements during AP are governed by electrochemical gradients: Na⁺ influx (inward current) and K⁺ efflux (outward current).

  • The propagation of the AP relies on myelination and nodes of Ranvier for rapid signaling.

  • The absolute refractory period prevents a second AP during peak Na⁺ channel inactivation; the relative refractory period allows a second AP only with a stronger-than-normal stimulus.

• Study strategy and recommended resources

  • Revisit Part 2 concepts with a focus on four-part AP breakdown and refractory periods.

  • Watch Resting Membrane Potential, Generation of an Action Potential, and Propagation videos (chapter 11) prior to next class.

  • Use IP Animation (interactive fizz) and other visual tools for reinforcing concepts.

  • Prepare a mental map of where each channel type is located and why (dendrites/soma vs axon/nodes).

• Example and clinical cues mentioned in lecture

  • Pupil dilation as an indicator of sympathetic arousal (useful in clinical assessment).

  • Observational lab notes: reflex testing lab (femoral nerve involvement, patellar reflex) will be covered next week; you’ll likely engage in a practical lab exercise using reflex hammers.

• Final takeaways for exam readiness

  • You should be able to: distinguish nerve vs neuron, CNS vs PNS roles, autonomic divisions and their effects, identify neuronal components and their functions, describe synaptic transmission, explain the resting membrane potential and action potential phases, differentiate absolute vs relative refractory periods, and outline how ion flow creates the action potential.

• Quick reminder about exam logistics

  • Exam will be on paper and scantron; details to be reviewed next class.

  • Expect to see material up to the point where the instructor stopped in tonight’s session; a second quiz may be adjusted to reflect only covered material.

Quick reference: key equations and values (LaTeX)

• Resting membrane potential

  • $V_m \approx -70\,\text{mV}$

• Action potential threshold

  • $V_{th} \approx -55\,\text{mV}$

• Action potential peak (typical)

  • $V_m \approx +30\,\text{mV}$

• Hyperpolarization opportunistic value (example)

  • $V_{hyperpolarization} \approx -84\,\text{mV}$

• General concepts

  • Ion movements during AP: Na⁺ influx (inward, depolarization) and K⁺ efflux (outward, repolarization).

  • RMP maintenance and ion gradients rely on leak channels and the Na⁺/K⁺-ATPase pump.

  • Myelin and Nodes of Ranvier accelerate conduction velocity via saltatory conduction.

• Terminology to memorize

  • Presynaptic vs postsynaptic

  • Axodendritic vs axosomatic

  • Voltage-gated vs chemically gated vs leak channels

  • Absolute vs relative refractory periods

  • Resting membrane potential (RMP) vs action potential (AP) vs synaptic potentials (graded potentials)