L7 - Ion Channels
Signal Transduction
Presenter: Ben Gelfand, PharmD, PhD Student, Joint Graduate Program in Pharmacology and Toxicology
Contact: byg8@pharmacy.rutgers.edu
The Plasma Membrane
Structure:
The plasma membrane is a lipid bilayer, acting as an electrical insulator that prevents ions from passing through.
Function of Channels and Pumps:
Channels:
Facilitate the movement of ions down their electrochemical gradient via facilitated diffusion.
Selective for specific ions.
Pumps:
Employ active transport, which is ATP-dependent, to transport ions against their electrochemical gradient.
The Electrochemical Gradient
Definition:
Ions possess both a concentration gradient and an electrical gradient.
Electrochemical Gradient:
The composite of these two gradients is referred to as the electrochemical gradient.
Movement of ions across the membrane continues until the electrical and chemical gradients balance to zero.
Pumps
Sodium-Potassium Pump (Na+/K+ Pump):
Uses active transport to move sodium (Na+) and potassium (K+) ions against their electrochemical gradient.
Function:
Helps maintain resting membrane potential.
Mechanism of Action:
Binding: Cytoplasmic Na+ binds to Na+/K+ pump.
Phosphorylation: Pump phosphorylated by ATP, transitioning to a different conformation, which causes Na+ release.
K+ Binding: Extracellular K+ binds, resulting in dephosphorylation.
Return: The pump reverts to its original conformation.
Ion Channels Properties
Mechanism:
Ion channels operate via facilitated diffusion allowing ions to move down their concentration gradient.
Characteristics:
Selectivity is based on size and charge density of the ions.
Gating Mechanisms:
The opening/closing is influenced by stimuli.
Types of gating include:
Voltage-gated: Activation depends on membrane voltage.
Ligand-gated: Activation due to ligand binding.
Mechanically gated: Activated by physical stimuli such as stretch or heat.
Physiological Basis of Gating
Ion channel proteins alternate between open and closed states randomly.
The likelihood of an ion channel being open is defined as the probability (P_O) of being in the open state.
Certain stimuli positively or negatively adjust this probability.
Ligand-gated channels typically have a P_O near 100% upon ligand engagement.
Voltage-Gated Channel Structure
Structure comprises a single subunit, with a specific segment (S4) acting as a voltage sensor, reacting to voltage changes by moving within the membrane.
This movement regulates the opening or closing of the pore domain.
Ions translocate only when the pore is open, with four subunits assembling to form the active channel.
Reference: Börjesson, S.I., Elinder, F. (2008). "Structure, Function, and Modification of the Voltage Sensor in Voltage-Gated Ion Channels." Cell Biochem Biophys, 52, 149–174.
Voltage-Gated Na+ Channels
Role:
Permit Na+ influx, contributing to depolarization.
Functionality: Promote positive feedback during depolarization, increasing the probability of Na+ channel opening as depolarization continues.
States:
Closed State initially, rapidly transitions to an inactivated state post-opening, even during membrane depolarization.
Repolarization is required before reopening can occur, crucial for neuronal and cardiac action potentials.
Voltage-Gated Na+ Channel States
Channel States Summary:
Resting: Closed; Activation Gate = Closed, Inactivation Gate = Open.
Open: Both gates are open.
Inactivated: Activation Gate = Open, Inactivation Gate = Closed.
Inactivated state achieved in nanoseconds, with necessary membrane repolarization leading to return to resting state, relating to action potential's refractory period.
Voltage-Gated K+ Channels
Function:
Maintain K+ efflux causing repolarization of the neuron.
Exception noted with KIR channels that permit K+ influx, assisting in recovery from hyperpolarization post-action potential.
Feedback Mechanism:
K+ reflux exerts negative feedback, where depolarization elevates the chances of K+ channels opening, advancing repolarization.
Types:
Fast-inactivating and slow-inactivating K+ channels both exist to contribute to action potential repolarization and termination.
Voltage-Gated K+ Channels and Cardiology
Importance:
hERG K+ channels are vital for cardiac repolarization.
Blockage extends action potential duration and QT interval, raising risks of ventricular arrhythmias.
Note: This topic is not part of exam materials.
Voltage-Gated Ca++ Channels
Functionality:
Allow Ca++ influx into cells without propagating action potentials.
Sparse voltage-gated Ca++ channels along axon; primarily located at synaptic terminals.
Conversion:
Upon activation, these channels facilitate neurotransmitter release in neurons and muscular contraction in muscle cells.
Variability:
Different types exist based on tissue distribution.
Ligand-Gated Ion Channels
Definition:
Ion channels that open or close in response to ligand binding.
Types of Ligands:
Natural ligands include neurotransmitters.
Not all neurotransmitters activate ligand-gated ion channel receptors.
Examples:
Acetylcholine
Serotonin
GABA
Glutamate
Importance:
Found at nervous system synapses and essential for rapid neuronal communication.
Acetylcholine (ACh)
Abbreviation:
Refers to acetylcholine.
Role in Body Systems:
Functioning in the neuromuscular junction, autonomic nervous system, parasympathetic nervous system, and central nervous system.
Effects:
In parasympathetic system:
Causes vasodilation, secretion increases from pancreas and salivary glands, decreased heart rate.
In neuromuscular junction: Facilitates skeletal muscle contraction, promoting rest-and-digest functions.
Acetylcholine Receptors
Receptor Types:
Nicotinic Receptors:
Ion channels; increased permeability to Na+ and K+.
M1, M3, M5 Types:
GPCRs; stimulate IP3, DAG pathways and increase intracellular Ca++.
M2, M4 Types:
GPCRs; affect cyclic AMP levels and increase permeability to K+.
Note: Only nicotinic ACh receptors function as ion channels.
Nicotinic Acetylcholine Receptors
Structure:
Composed of five subunits, including at least two alpha subunits which house the ligand binding site.
Mechanism:
Ligand binding prompts opening of the channel, allowing Na+ and K+ passage, causing depolarization of the postsynaptic cell.
Localization:
Dominantly present on presynaptic neurons in the CNS, facilitating ACh release.
Reference: Nara, S. et al., 2024, Cogn Neurodyn.
Serotonin (5-HT)
Definition:
Abbreviated as 5-HT (5-hydroxytryptamine).
Neurotransmitter Functions:
Operates within the CNS and enteric nervous system.
Involved in various brain functions, including mood, attention, sleep, appetite, and pain management.
Receptor Types:
Predominantly GPCRs with the exception of 5-HT3 receptor which functions as an ion channel.
5-HT3 receptors play a role in CNS pathways associated with vomiting.
Serotonin Receptors
List of Receptor Types:
5HT1A: GPCR; targets cyclic AMP and enhances K+ conductance.
5HT1B: GPCR; influences cyclic AMP.
5HT1D: GPCR; affects cyclic AMP and decreases K+ conductance.
5HT2A: GPCR; uses IP3 and DAG to stimulate various ionic flows.
5HT2C: GPCR; interrelated with IP3 and DAG pathways.
5HT3: Ligand-gated ion channel; modulates flow of Na+, K+, Ca++.
5-HT3 Receptor
Structure:
Composed of five subunits, similar to nicotinic AChR.
Mechanism:
Ligand binding activates the ion channel, making it permeable to Na+, K+, Ca++, contributing to postsynaptic depolarization.
Clinical Relevance:
Antagonists of 5-HT3 receptors are primarily employed to manage nausea/vomiting.
Reference: Rammes, G. et al., 2004, Mol Psychiatry.
Amino Acid Neurotransmitters
Categories:
Glutamate: Principal excitatory neurotransmitter in CNS.
GABA: Main inhibitory neurotransmitter in the brain.
Glycine: Function can be context-dependent (inhibitory or excitatory).
Amino Acid Neurotransmitter Receptors
Glutamate Receptors: Types include:
Metabotropic: GPCRs utilizing IP3, DAG, or cyclic AMP pathways.
Ionotropic:
AMPA: Ion channel facilitating Na+ and/or Ca++ influx, crucial for rapid synaptic transmission.
Kainate: Ion channel similar to nicotinic/receptor channels permitting Na+ and K+ influx.
NMDA:
Ligand-dependent requiring both glycine and glutamate for activation, permeable to Na+, Ca++, and K+.
Mg++ acts as an endogenous inhibitor, playing a critical role in synaptic plasticity and memory.
GABA Receptors: Types include:
GABAA: Ligand-gated ion channel causing Cl- influx leading to postsynaptic hyperpolarization.
GABAB: GPCR incorporating IP3, DAG pathways affecting K+ and Ca2+ flows, also leading to hyperpolarization.