Neuron Structure and Signal Propagation (3A) - MCAT Biological and Biochemical Foundations of Living Systems

Voltage-gated K$^+$ channels opening. Potassium efflux restores the membrane potential to resting levels following sodium channel inactivation.

Time when no new action potential can occur due to Na$^+$ inactivation. Inactivated sodium channels prevent depolarization, ensuring unidirectional propagation and a recovery period.

Time when a stronger stimulus is needed due to ongoing K$^+$ efflux. Hyperpolarization from potassium currents raises the threshold, requiring greater stimulation for another action potential.

Once threshold is reached, action potential amplitude is constant. This principle ensures that suprathreshold stimuli produce full-strength action potentials, maintaining signal reliability.

Away from soma; refractory period prevents backward propagation. Orthodromic propagation occurs as the refractory state behind the action potential blocks retrograde travel.

Action potentials appear to jump node-to-node in myelinated axons. In myelinated fibers, depolarization skips insulated segments, regenerating at nodes for faster conduction.

Metabotropic receptor. Ligand binding activates G proteins, leading to second messenger cascades that modulate cellular activity over longer timescales.

Ionotropic receptor. Direct binding of ligand opens the channel, allowing rapid ion flow for immediate postsynaptic response.

Ca$^{2+}$ influx through presynaptic voltage-gated Ca$^{2+}$ channels. Action potential arrival opens calcium channels, elevating intracellular calcium to promote exocytosis of synaptic vesicles.

Increased diameter. Larger axons have lower internal resistance, allowing faster passive current spread and thus quicker conduction.

Receive synaptic input and conduct graded potentials to the soma. Dendrites integrate incoming signals from other neurons, allowing graded potentials to propagate toward the cell body for potential summation and action potential initiation.

Site of action potential initiation via voltage-gated Na$^+$ channels. The axon hillock sums graded potentials and, upon reaching threshold, triggers action potentials through the opening of voltage-gated sodium channels.

Increase conduction velocity by increasing membrane resistance. Myelin insulates axons, reducing capacitance and increasing resistance, which enables faster saltatory conduction of action potentials.

Gaps in myelin with high densities of voltage-gated Na$^+$ channels. These unmyelinated segments concentrate sodium channels, allowing action potentials to regenerate and 'jump' during saltatory conduction.

Schwann cell. Schwann cells wrap around individual PNS axons to create myelin, supporting rapid nerve impulse conduction.

Approximately $-70\ \text{mV}$. This value reflects the balance of ion gradients and permeabilities, primarily influenced by potassium efflux at rest.

Membrane potential where net flux of that ion is $0$. It represents the voltage at which the electrical driving force equals the chemical gradient, resulting in no net ion movement.

Pumps $3\ \text{Na}^+$ out and $2\ \text{K}^+$ in per ATP. This electrogenic pump maintains sodium and potassium gradients essential for resting potential and action potential generation.

K$^+$. High potassium permeability allows its equilibrium potential to dominate the resting membrane potential via leak channels.

A graded depolarization that increases action potential probability. EPSPs result from neurotransmitter-induced cation influx, bringing the membrane closer to threshold for firing an action potential.

A graded hyperpolarization that decreases action potential probability. IPSPs arise from anion influx or cation efflux, moving the membrane potential away from threshold to inhibit neuronal firing.

Summation of inputs from one synapse arriving close in time. Repeated stimulation from a single presynaptic neuron can accumulate EPSPs or IPSPs over time to reach threshold.

Summation of inputs from multiple synapses arriving together. Simultaneous inputs from different synapses integrate at the postsynaptic neuron to determine if threshold is met.

Voltage-gated Na$^+$ channels opening. Sodium influx upon depolarization rapidly depolarizes the membrane to peak potential during the action potential.