Ion Channels and Transmembrane Potentials

Flashcards covering key vocabulary terms related to ion channels, transmembrane potentials, action potentials in neurons and muscle cells, and associated clinical conditions (channelopathies).

Ion channels

Integral membrane proteins that facilitate the passive movement of specific ions across the cell membrane.

Non-gated Ion Channels (Leak channels)

Ion channels that are open most of the time, allowing ions to move across the cell membrane without a gating mechanism, contributing to the resting membrane potential.

Gated Ion channels

Ion channels that transition between open and closed conformational states in response to specific stimuli (electrical, mechanical, or chemical).

Gating

Conformational changes that control the opening or closing of the channel pore, regulating ion flux across the membrane in a stimulus-dependent manner.

Ligand-gated ion channels (LICs, LGIC) / Ionotropic receptors

Transmembrane proteins that open to allow ions (e.g., Na+, K+, Ca2+, and/or Cl-) to pass through the membrane in response to the binding of a chemical messenger (ligand), such as a neurotransmitter.

Mechanically Gated Ion Channels

Transmembrane proteins that open or close in response to mechanical forces such as stretch, pressure, or shear stress, allowing selective ions to flow across the cell membrane.

Mechanotransduction

The process by which cells convert physical stimuli into electrical or chemical signals, mediated by mechanically gated ion channels.

Voltage-gated Ion Channels

Transmembrane proteins that open or close in response to changes in membrane potential, allowing selective ions (e.g., Na+, K+, Ca2+, or Cl-) to pass across the membrane.

Resting Membrane Potential (RMP)

The stable electrical state of a cell, primarily determined by selective membrane permeability (e.g., to K+ through leak channels), ion concentration gradients, and the activity of the Sodium-Potassium Pump (Na+/K+-ATPase).

Nernst potential

The membrane potential at which there is no net flow of a specific ion across a cell membrane, balancing the electrochemical gradient for that ion.

Role of Chloride in skeletal muscle RMP

Chloride ions (Cl-) determine and stabilize the resting membrane potential in skeletal muscle, as the RMP is close to the chloride equilibrium potential due to many Cl- leak channels.

Graded (local) Potential

A localized change in the membrane potential of a neuron that varies in strength, can be depolarizing or hyperpolarizing, and is triggered by stimuli that open or close ion channels to initiate action potentials.

Action Potential

A rapid sequence of changes in the voltage across a membrane, occurring when voltage-gated Na+ channels open in response to membrane depolarization reaching a threshold, causing Na+ to flow into the cell.

Inactivation gate (Na+ channel)

A gate on voltage-gated sodium (Na+) channels that closes shortly after depolarization, blocking the pore and preventing further Na+ influx, which is crucial for terminating the action potential and ensuring its unidirectional propagation.

Refractory period

The period during and after an action potential when the axon cannot propagate another action potential, ensuring that the impulse travels in one direction only.

Muscle Action Potential (Skeletal Muscle RMP)

Skeletal muscle fibers maintain a resting membrane potential of approximately –85 mV, more negative than neurons, primarily due to open potassium and chloride channels in the sarcolemma.

Channelopathies

A heterogeneous group of disorders resulting from the dysfunction of ion channels, caused by genetic mutations or acquired alterations, affecting essential physiological processes in various body systems.

Myotonia congenita (Myotonic goats)

A hereditary disorder of muscle relaxation in goats caused by a mutation in the CLCN1 gene, leading to defective or insufficient ClC-1 chloride channels in skeletal muscle, resulting in delayed repolarization and muscle stiffness.

Hyperkalemic Periodic Paralysis (HYPP) in Quarter Horses

A disorder caused by a mutation in the SCN4A gene, encoding a voltage-gated sodium channel (NaV1.4) in skeletal muscle, leading to channels that don't close properly, causing excess sodium influx, muscle hyperexcitability, and episodes of weakness or paralysis.