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13.1 Neuronal Anatomy, the Resting Potential & the Action Potential
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13.1 Neuronal Anatomy, the Resting Potential & the Action Potential 13.2 Conduction Velocity, Synaptic Transmission & Postsynaptic Summation 13.3 Neurotransmitter Systems, CNS/PNS Organisation & Reflex Arcs 13.4 Hormone Classification & the Hypothalamus-Pituitary Axis 13.5 Negative Feedback Architecture, Endocrine Glands & Calcium Homeostasis 13.6 Cardiac Anatomy, Electrophysiology, the Cardiac Cycle & Cardiac Output 13.7 Vascular Hemodynamics, Starling Forces, Blood Components & Hemostasis 13.8 Respiratory Anatomy, Ventilation Mechanics & Pulmonary Surfactant 13.9 Spirometry, Dead Space, Gas Exchange & Haemoglobin Allostery 13.10 Carbon Dioxide Transport, the Chloride Shift & Acid-Base Control of Breathing
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13.1 Neuronal Anatomy, the Resting Potential & the Action Potential
Key Takeaways Explain This Topic AI
The resting membrane potential (-70 mV) is primarily maintained by passive potassium leak channels and the electrogenic Na+/K+-ATPase, which pumps 3 Na+ out of the cell for every 2 K+ pumped in using ATP hydrolysis.
An action potential is an all-or-none electrical impulse initiated at the axon hillock when local depolarization reaches threshold (-55 mV), triggering rapid opening of voltage-gated Na+ channels followed by inactivation at +35 mV and repolarization via voltage-gated K+ channels.
The absolute refractory period is enforced by the inactivation gate (h-gate) of voltage-gated Na+ channels, preventing any subsequent action potential regardless of stimulus strength, whereas the relative refractory period occurs during K+-mediated hyperpolarization (-80 mV) requiring a suprathreshold stimulus.
Last updated: September 2026
13.1 Neuronal Anatomy, the Resting Potential & the Action Potential
Note
Foundational Standard : The nervous system coordinates rapid, point-to-point biological communication through electrical impulses and chemical synapses. The MCAT demands mastery of the biophysical equilibria establishing resting and active membrane potentials, the molecular mechanics of voltage-gated channels, synaptic transmission cascades, neurotransmitter clearance, autonomic neuroanatomy, and spinal reflex circuits.
Neuronal communication integrates electrical signaling across individual cellular membranes with chemical signaling across specialized intercellular junctions. Mastering this discipline requires tracking the movement of specific ions across lipid bilayers, calculating electrochemical gradients, and understanding the pharmacological and physiological regulation of neural circuits.
Structural Anatomy of the Neuron
A neuron is an asymmetric, electrically excitable eukaryotic cell structurally partitioned into distinct functional domains:
Soma (Cell Body) : Contains the nucleus, extensive rough endoplasmic reticulum ( Nissl bodies for high-volume protein and neuropeptide synthesis), Golgi apparatus, and mitochondria. It serves as the primary metabolic and biosynthetic hub.
Dendrites : Highly branched, tapering cytoplasmic extensions covered in dendritic spines. Dendrites receive incoming synaptic inputs from presynaptic neurons and convey graded, decremental electrical signals toward the cell body.
Axon Hillock : The conical region connecting the soma to the axon proper. It contains the highest density of voltage-gated sodium ( N a V Na_V N a V ) channels in the unmyelinated neuron and functions as the trigger zone (integrator) where graded post-synaptic potentials undergo summation. If net local potential reaches threshold, an action potential is fired.
Axon : A singular, uniform cylindrical projection extending up to a meter in length. It propagates action potentials away from the soma toward target effector cells or subsequent neurons via continuous or saltatory conduction.
Myelin Sheath & Nodes of Ranvier : Myelin is a lipid-rich, multi-layered insulating sheath produced by Schwann cells in the Peripheral Nervous System (PNS; one Schwann cell wraps a single internode) and by Oligodendrocytes in the Central Nervous System (CNS; one oligodendrocyte wraps internodes on up to 50 axons). The gaps between adjacent myelin segments are the nodes of Ranvier , which harbor high concentrations of N a V Na_V N a V and K V K_V K V channels.
Axon Terminal (Synaptic Bouton) : The swollen distal terminus containing abundant mitochondria, smooth endoplasmic reticulum for calcium sequestration, and membrane-bound synaptic vesicles packed with neurotransmitters.
The Resting Membrane Potential ( V m V_m V m )
In a quiescent neuron, an electrical potential difference exists across the plasma membrane, termed the resting membrane potential ( V m V_m V m ) , typically − 70 mV -70\text{ mV} − 70 mV (inside negative relative to the extracellular fluid). This electrical polarity is established and maintained by two primary mechanisms:
1. Differential Permeability and Potassium Leak Channels
The resting neuronal membrane is approximately 25 to 30 times more permeable to potassium ( K + K^+ K + ) than to sodium ( N a + Na^+ N a + ) due to the presence of continuously open, non-gated K + K^+ K + leak channels (two-pore domain K + K^+ K + channels). Potassium, maintained at high intracellular concentration (~140 mM inside vs. ~4.5 mM outside), diffuses down its chemical concentration gradient out of the cell. As positive charges exit, the interior of the cell becomes increasingly electronegative. This accumulating negative charge creates an opposing electrical force pulling K + K^+ K + back into the cell. Equilibrium is reached when the outward chemical driving force precisely equals the inward electrical driving force, defined by the Nernst Equation for a single ion at physiological temperature ( 37 ∘ C = 310 K 37^\circ\text{C} = 310\text{ K} 3 7 ∘ C = 310 K ): E i o n = R T z F ln ( [ i o n ] o u t [ i o n ] i n ) = 61.5 z log 10 ( [ i o n ] o u t [ i o n ] i n ) E_{ion} = \frac{RT}{zF} \ln\left(\frac{[ion]_{out}}{[ion]_{in}}\right) = \frac{61.5}{z} \log_{10}\left(\frac{[ion]_{out}}{[ion]_{in}}\right) E i o n = z F RT ln ( [ i o n ] in [ i o n ] o u t ) = z 61.5 lo g 10 ( [ i o n ] in [ i o n ] o u t )
For Potassium ( K + K^+ K + ): E K = 61.5 + 1 log 10 ( 4.5 140 ) ≈ − 90 mV E_K = \frac{61.5}{+1} \log_{10}\left(\frac{4.5}{140}\right) \approx -90\text{ mV} E K = + 1 61.5 lo g 10 ( 140 4.5 ) ≈ − 90 mV
For Sodium ( N a + Na^+ N a + ): E N a = 61.5 + 1 log 10 ( 145 12 ) ≈ + 65 mV E_{Na} = \frac{61.5}{+1} \log_{10}\left(\frac{145}{12}\right) \approx +65\text{ mV} E N a = + 1 61.5 lo g 10 ( 12 145 ) ≈ + 65 mV
Because the resting membrane is predominantly permeable to K + K^+ K + , the overall resting potential ( V m = − 70 mV V_m = -70\text{ mV} V m = − 70 mV ) lies close to E K E_K E K , as modeled mathematically by the Goldman-Hodgkin-Katz (GHK) Voltage Equation : V m = R T F ln ( P K [ K + ] o u t + P N a [ N a + ] o u t + P C l [ C l − ] i n P K [ K + ] i n + P N a [ N a + ] i n + P C l [ C l − ] o u t ) V_m = \frac{RT}{F} \ln\left(\frac{P_K[K^+]_{out} + P_{Na}[Na^+]_{out} + P_{Cl}[Cl^-]_{in}}{P_K[K^+]_{in} + P_{Na}[Na^+]_{in} + P_{Cl}[Cl^-]_{out}}\right) V m = F RT ln ( P K [ K + ] in + P N a [ N a + ] in + P Cl [ C l − ] o u t P K [ K + ] o u t + P N a [ N a + ] o u t + P Cl [ C l − ] in )
2. The Electrogenic N a + / K + Na^+/K^+ N a + / K + -ATPase Pump
Continuous leak of K + K^+ K + out of the cell and minor leak of N a + Na^+ N a + into the cell would eventually dissipate these transmembrane concentration gradients. The N a + / K + Na^+/K^+ N a + / K + -ATPase (sodium-potassium pump) counteracts this rundown by utilizing the energy of primary ATP hydrolysis to transport 3 N a + 3\text{ }Na^+ 3 N a + ions out of the cell and 2 K + 2\text{ }K^+ 2 K + ions into the cell against their steep electrochemical gradients. Because it moves three positive charges out for every two positive charges moved in, the pump is electrogenic , contributing directly to approximately − 3 to − 5 mV -3\text{ to }-5\text{ mV} − 3 to − 5 mV of the resting membrane potential while permanently maintaining the chemical driving forces required for excitability.
The Action Potential: Phases, Gating Kinetics & Refractory Periods
An action potential is a rapid, transient, all-or-none allosteric electrical cycle propagated without attenuation along the axonal membrane.
Action Potential Phase Membrane Potential ( V m V_m V m ) Dominant Ion Movement State of N a V Na_V N a V Channels State of K V K_V K V Channels
Resting State − 70 mV -70\text{ mV} − 70 mV Dynamic leak of K + K^+ K + outward Closed (Activation m m m -gate shut; Inactivation h h h -gate open) Closed (Delayed rectifier gate shut)
Threshold Depolarization − 70 mV → − 55 mV -70\text{ mV} \to -55\text{ mV} − 70 mV → − 55 mV Local influx of N a + Na^+ N a + via ligand/mechanogated channels Opening initiated at threshold ( − 55 mV -55\text{ mV} − 55 mV ) Closed
Rapid Depolarization − 55 mV → + 35 mV -55\text{ mV} \to +35\text{ mV} − 55 mV → + 35 mV Massive, explosive N a + Na^+ N a + influx down electrochemical gradient Fully Open (Both m m m -gate and h h h -gate open; high g N a g_{Na} g N a ) Closed (Slowly transitioning toward open)
Peak & Inactivation + 35 mV +35\text{ mV} + 35 mV Net N a + Na^+ N a + current ceases; K + K^+ K + begins exiting Inactivated (Inactivation h h h -gate shuts; ball-and-chain plug) Opening rapidly
Repolarization + 35 mV → − 70 mV +35\text{ mV} \to -70\text{ mV} + 35 mV → − 70 mV Robust K + K^+ K + efflux down electrochemical gradient Inactivated → \to → De-inactivating/Closed Fully Open (High g K g_K g K )
Hyperpolarization − 70 mV → − 80 mV -70\text{ mV} \to -80\text{ mV} − 70 mV → − 80 mV Continued K + K^+ K + efflux toward E K E_K E K ( − 90 mV -90\text{ mV} − 90 mV ) Closed (De-inactivated: m m m -gate shut, h h h -gate reset open) Slowly Closing (Delayed rectifier deactivation)
Restoration − 80 mV → − 70 mV -80\text{ mV} \to -70\text{ mV} − 80 mV → − 70 mV Passive leak & N a + / K + Na^+/K^+ N a + / K + -ATPase maintain baseline Closed (Excitable state) Fully Closed
Molecular Mechanics of Refractory Periods
Absolute Refractory Period : Spans from the initial firing at threshold through the peak and early repolarization phase. During this window, the inactivation gates ( h h h -gates) of voltage-gated N a + Na^+ N a + channels are physically closed. Even a massively suprathreshold stimulus cannot open these channels because they must first undergo repolarization-dependent reset (de-inactivation). This ensures unidirectional forward propagation of the action potential and imposes an upper mathematical limit on neuronal firing frequency.
Relative Refractory Period : Follows the absolute refractory period during the hyperpolarization phase. At this point, the N a V Na_V N a V channel inactivation gates have reopened ( m m m -gates are closed, restoring the excitable closed state), but the delayed rectifier K V K_V K V channels remain open, driving V m V_m V m down toward − 80 mV -80\text{ mV} − 80 mV . Because the membrane is further from threshold ( − 55 mV -55\text{ mV} − 55 mV ) and membrane conductance to K + K^+ K + is elevated, an action potential can be initiated, but only by an exceptionally strong, suprathreshold stimulus .