Neuronal Electrical Activity & Neurotransmitter Release

Excitable Cells & Modes of Communication

• Neurons and muscle cells are the two primary excitable cells in the body.

  • “Excitable” = capable of depolarization↔repolarization cycles.

  • Other excitable examples: pancreatic β-cells (insulin release) and select endocrine cells.

• Neurons communicate through two integrated phases:

  • Electrical phase: propagation of voltage changes (graded potential → action potential).

  • Chemical phase: release of neurotransmitters across a synapse.

Dendrites & Ligand-Gated Sodium Channels

• Dendritic structure

  • Highly branched to maximize surface area of the soma.

• Ion channels present

  • Predominantly ligand-gated Na⁺ channels.

  • Gate opens only when an external ligand binds (purple in diagram).

  • Ligand never enters; it merely triggers gate opening.

• Possible ligands

  • Classical neurotransmitters, hormones, or non-molecular stimuli (e.g., heat, odorants).

• Effect: Na⁺ influx → local depolarization that initiates the graded potential.

Graded Potentials in the Cell Body

• Definition: Variable-strength voltage changes that decrease with distance.

• Key numerical landmark: threshold at the axon hillock -55\ \text{mV}.

• Behavior

  • Amplitude depends on initial stimulus strength.

  • Distance-dependent decay due to internal resistance and ion leakage.

• Important contrast:

  • Graded potential: analog, diminishes, summative.

  • Action potential (AP): digital, all-or-nothing, non-decremental.

Attenuation Factors (Why Graded Potentials Fade)

• Cytoplasmic resistance

  • Viscous/gel-like cytoplasm impedes ion flow, lowering voltage with distance.

• K⁺ leakage channels

  • Always open; K⁺ exits, making interior more negative.

  • Competes directly with Na⁺ inflow; the stimulus must overcome continual K⁺ efflux.

Threshold at the Axon Hillock

• Voltage must still be \ge -55\ \text{mV} upon arrival to trigger an AP.

• Examples

  • If initial depolarization near dendrites is only -55\ \text{mV}, attenuation will drop it below threshold → no AP.

  • A stronger stimulus (≈ +20\ \text{mV} near dendrites) may decay to -55\ \text{mV} by the hillock → AP fires.

Action Potential Propagation (Axon)

• Initiation:

  • Threshold reached → first voltage-gated Na⁺ channel opens.

• Domino analogy

  • Opening of the first channel guarantees the sequential opening of all others along the axon.

• Characteristics

  • All-or-nothing: Either the complete sequence fires or none.

  • No decrement: Signal maintains amplitude to the terminal.

Calcium-Mediated Neurotransmitter Release (Axon Terminal)

• Arrival of AP → opens voltage-gated Ca²⁺ channels.

• Ca²⁺ influx triggers Ca²⁺-dependent exocytosis of synaptic vesicles.

  • Vesicles fuse with membrane → neurotransmitter released into synaptic cleft.

• Nearly identical mechanism to pancreatic β-cell insulin secretion.

Analogies & Cross-System Connections

• Pebble-in-pond: Graded potential = ripples that weaken outward (Silverthorn textbook analogy).

• Domino row: Action potential = cascade where tipping the first ensures the last will fall.

• Cross-reference videos/lectures on:

  • Ion gradients & selective permeability.

  • Pancreatic β-cells for exocytosis mechanics.

Key Numerical Values & Mini-Formulae

• Resting membrane potential (typical): \approx -70\ \text{mV} (implicit).

• Threshold at axon hillock: -55\ \text{mV}.

• Example robust depolarization: +20\ \text{mV} at dendrites to secure -55\ \text{mV} at hillock.

• Competing fluxes:

  • Na⁺ influx (through ligand-gated or voltage-gated channels).

  • K⁺ efflux (through leakage channels).