Neurons, Resting Potentials, Action Potentials, and Synapses
Learning Outcomes
Contrast the relative concentrations of important ions inside and outside cells.
Explain how the resting potential is established.
Describe how voltage-gated channels function in action potentials.
Neuronal Function and Membrane Potential
Neuronal signaling relies on creating an electric potential across the plasma membrane.
Electric charge in cells is carried by ions, with manipulation of concentrations across membranes being crucial for signaling.
Resting Membrane Potential
An electrical difference exists across the plasma membrane, termed the resting potential.
Typical resting membrane potential for vertebrate neurons averages around -70 ext{ mV} (from -40 ext{ mV} to -90 ext{ mV}).
This negative value indicates that the inside of the cell is negatively charged relative to the outside.
Factors Contributing to Membrane Potential
Sodium-Potassium Pump (Na+/K+ Pump)
Pumps 3 sodium ions (Na+) out for every 2 potassium ions (K+) brought in.
Establishes higher K+ concentration inside and higher Na+ outside, crucial for the membrane potential.
Membrane Permeability
More K+ leak channels than Na+ channels, making the membrane more permeable to K+.
K+ diffuses out of the cell, contributing to negativity inside the cell.
Impermability to Negative Ions
Membrane is impermeable to negatively charged molecules (e.g., proteins, nucleic acids), which build up inside and maintain negative charge.
Resting Potential and Equilibrium Potential
The resting potential results from a balance of electrical forces attracting K+ in and diffusion pushing K+ out.
Nernst Equation for K+: EK = 58 ext{ mV} imes ext{log} igg( rac{[K^+]{out}}{[K^+]_{in}}igg)
For K+, calculated equilibrium is -90 ext{ mV}.
Measured resting potential of -70 ext{ mV} reflects minor Na+ leakage affecting the potential.
Action Potentials and Membrane Changes
Neurons exhibit graded potentials (small, local changes) and action potentials (larger, rapid changes).
Action Potentials: Triggered by reaching a threshold of approx. -55 ext{ mV}.
Mechanism of Action Potentials
Depolarization Phase
Triggered by opening voltage-gated Na+ channels leading to Na+ influx.
Membrane potential rapidly shifts towards +35 to +40 mV (peak of action potential).
Repolarization Phase
Following peak, Na+ channels close, and K+ channels open allowing K+ to exit, restoring negative charge inside.
Hyperpolarization Phase
K+ channels remain open longer, causing potential to dip below resting level, resulting in hyperpolarization.
Propagation of Action Potentials
Each segment of the axon generates a new action potential, leading to propagation of the signal along the axon.
Refractory Periods:
Absolute Refractory Period: Na+ channels inactivated; no new action potential can occur.
Relative Refractory Period: Larger stimulus needed to generate action potentials due to partial repolarization.
Velocity of Impulse Conduction
Velocity increases with larger axon diameters and myelination.
Saltatory Conduction: Action potentials jump between nodes of Ranvier, speeding up impulse transmission.
Synaptic Transmission
Neurons communicate via synapses:
Presynaptic Cell: sends signal,
Postsynaptic Cell: receives signal.
Types of Synapses:
Electrical Synapses: Direct signaling via gap junctions for rapid communication.
Chemical Synapses: Release neurotransmitters to transmit signals across the synaptic cleft.
Mechanism of Chemical Synapses
Action potentials at the presynaptic terminal cause Ca²+ influx, triggering neurotransmitter release via exocytosis.
Neurotransmitters bind to receptors on the postsynaptic membrane, generating graded potentials.
Types of Neurotransmitters
Acetylcholine: Major neurotransmitter at neuromuscular junctions influencing muscle contraction.
Amino Acids:
Glutamate: Major excitatory neurotransmitter in CNS.
GABA and Glycine: Inhibitory neurotransmitters.
Biogenic Amines:
Include dopamine, norepinephrine, serotonin. These neurotransmitters are involved in mood, movement control, and responses to stress.
Neuropeptides: Functions as classical neurotransmitters or neuromodulators affecting neuronal communication.
Neurotransmitter Action and Drug Effects
Prolonged stimulation can reduce receptor sensitivity (habituation).
Drugs like cocaine inhibit dopamine reuptake, causing prolonged neurotransmitter presence in synapses, engaging rewards pathways.
Nicotine binds to acetylcholine receptors, leading to modulation of those receptors and potentially altering sensitivity in chronic use.
Summary of Neuron Integration
Neural communication involves both excitatory (EPSPs) and inhibitory (IPSPs) synapses that integrate signals and determine neuronal responses.
Summation Types:
Spatial Summation: Many different synapses contribute to reach threshold.
Temporal Summation: Rapidly repeated signals from one synapse leading to an action potential.
In summary, neuronal function and communication rely heavily on electrochemical gradients, the generation and propagation of action potentials, and complex interactions of neurotransmitters in synapses.
Membrane Potential Alteration in Response to a Stimulus
Membrane potential can change in response to various stimuli due to ion movement across the cell membrane.
Graded Potentials and Action Potentials
Graded Potentials:
Localized changes in membrane potential that vary in magnitude and do not propagate along the membrane.
Action Potentials:
Large, rapid changes in membrane potential that occur once a threshold is reached (around -55 mV).
Phases of Action Potential:
Depolarization Phase:
Triggered by the opening of voltage-gated Na+ channels, leading to Na+ influx and a rapid rise in membrane potential towards +35 to +40 mV.
Repolarization Phase:
Na+ channels close, and voltage-gated K+ channels open, allowing K+ to exit and restore a negative internal environment.
Hyperpolarization Phase:
K+ channels may remain open longer than necessary, causing the potential to dip below resting levels, resulting in hyperpolarization.
Propagation of Action Potentials
Propagation:
Action potentials propagate along axons through the sequential opening of Na+ and K+ channels.
Saltatory Conduction:
In myelinated axons, action potentials jump between nodes of Ranvier, increasing speed (impulse conduction is faster).
Unidirectionality:
Action potentials can only move in one direction due to the refractory periods (absolute and relative), preventing backflow.
Signal Integrity:
Action potentials maintain their strength as they propagate along axons because of the regeneration at each segment of the membrane.
Electrical vs. Chemical Synapses
Electrical Synapses:
Utilize gap junctions for direct cytoplasmic connections allowing rapid ion influx, enabling fast communication between neurons.
Chemical Synapses:
Use neurotransmitter release to transmit signals across the synaptic cleft, which bind to receptors on the postsynaptic membrane.
Excitatory and Inhibitory Postsynaptic Potentials
Excitatory Postsynaptic Potentials (EPSPs):
Result from Na+ influx, moving the membrane potential closer to threshold, increasing the likelihood of action potential generation.
Inhibitory Postsynaptic Potentials (IPSPs):
Result from Cl- influx or K+ efflux, moving the membrane potential further from threshold, decreasing the likelihood of action potential generation.
Summation:
Spatial Summation:
EPSPs from multiple synapses combine to reach threshold.
Temporal Summation:
Rapidly repeated EPSPs from a single synapse accumulate, potentially reaching threshold.
Neurotransmitter Action: Acetylcholine Example
Acetylcholine:
Major neurotransmitter in neuromuscular junctions; it is released from presynaptic terminals upon action potential arrival.
Binds to acetylcholine receptors on postsynaptic cells, leading to ion channel opening, resulting in an EPSP and potential action potential generation.