Neurophysiology (2)
Electrical Signals in Neurons
Neurons are electrically excitable due to voltage differences across their membranes.
Communication occurs via two types of electric signals:
Action Potentials: can travel long distances.
Graded Potentials: local changes only.
A flow of ions through ion channels occurs in living cells.
Types of Ion Channels
Leakage (Nongated) Channels
Remain always open.
Nerve cells have more K+ channels than Na+ channels.
Higher membrane permeability to K+, resulting in a resting membrane potential of about -70mV.
Gated Channels
Open or close in response to stimuli, leading to neuron excitability.
Voltage-Gated Channels: open due to voltage changes.
Ligand-Gated Channels: open in response to specific chemicals (e.g., hormones, neurotransmitters).
Mechanically-Gated Channels: open with mechanical stimulation.
Gated Ion Channels
Voltage-gated K+ channels open when extracellular voltage changes.
Ligand-gated channels respond to specific chemical stimuli to alter their state (open/close).
Resting Membrane Potential
Inside of cell membrane: negative ions.
Outside: positive ions, resulting in a potential difference of -70mV.
The cell is considered "polarized" due to:
Different ion concentrations between inside (e.g., K+) and outside (e.g., Na+, Cl-).
Higher permeability for K+ than Na+ (50-100 times greater).
Na+/K+ pump helps maintain resting potential by removing Na+ that leaks in.
Action Potentials
Definition
Action potentials are rapid changes in membrane potential decreasing and eventually reversing (depolarization), followed by a return to resting state (repolarization).
Graded Potentials
Small deviations from -70mV:
Hyperpolarization: membrane becomes more negative.
Depolarization: membrane becomes more positive.
Phases of Action Potential
Depolarizing Phase
Initiated by a stimulus causing graded potential to reach threshold (-55mV).
Voltage-gated Na+ channels open, allowing Na+ to rush into the cell.
The influx of Na+ changes membrane potential up to +30mV.
Repolarizing Phase
K+ channels open, but slower than Na+, allowing K+ to exit the cell.
Membrane potential returns to -70mV, may reach -90mV (after-hyperpolarization).
Refractory Period
No new action potential can be generated.
Absolute Refractory Period: strong stimulus won’t trigger another AP.
Relative Refractory Period: A strong enough stimulus may trigger an AP as K+ channels are still open.
Propagation of Action Potential
Action potentials propagate across the membrane:
The influx of Na+ affects adjacent sections, opening more voltage-gated channels.
This creates a self-propagating wave along the membrane.
Local Anesthetics
Prevent the opening of voltage-gated Na+ channels, halting nerve impulse conduction in the area.
Continuous vs Saltatory Conduction
Continuous Conduction: occurs in unmyelinated fibers with step-by-step depolarization.
Saltatory Conduction: occurs in myelinated fibers, where depolarization happens at Nodes of Ranvier, allowing impulses to jump from node to node.
Factors Affecting Propagation Speed
Axon diameter, amount of myelination, and temperature contribute to the speed of impulse transmission.
Speed of Impulse Propagation
Larger, myelinated fibers conduct impulses faster. Fiber types include:
A fibers: largest, myelinated, fastest (130 m/sec).
B fibers: medium, myelinated (15 m/sec).
C fibers: smallest, unmyelinated, slowest (2 m/sec).
Action Potentials in Nerve and Muscle
Muscle cell membranes behave differently than neuron axons; resting potentials:
Nerve: -70mV
Skeletal/ Cardiac Muscle: closer to -90mV.
Chemical Synapses
Action potentials trigger voltage-gated Ca2+ channels to open, causing neurotransmitter release across synaptic clefts.
More neurotransmitter leads to greater change in potential in postsynaptic cells.
Excitatory and Inhibitory Potentials
EPSP (excitatory): caused by opening ligand-gated Na+ channels, makes it easier for postsynaptic cell to reach threshold.
IPSP (inhibitory): caused by opening ligand-gated Cl- or K+ channels, making postsynaptic cell less likely to reach threshold.
Removal of Neurotransmitter
Neurotransmitters are removed by:
Diffusion
Enzymatic degradation (e.g., acetylcholinesterase)
Uptake by neurons or glia cells (neurotransmitter transporters).
Summation of Postsynaptic Potentials
Spatial Summation: effects from several presynaptic neurons onto a single postsynaptic neuron.
Temporal Summation: effects from rapid successive firings of a single presynaptic neuron.
Neurotransmitter Effects & Modification
Neurotransmitter effects can be modified through synthesis regulation, release manipulation, and receptor site activation or blocking.
Agonist: enhances transmitter effects.
Antagonist: blocks neurotransmitter actions.
Neurotransmitters
Examples include:
Small Molecule Neurotransmitters:
Acetylcholine
Amino Acids (e.g., GABA, Glutamate)
Biogenic Amines (e.g., Norepinephrine, Dopamine, Serotonin)
Neuropeptides:
Substance P
Enkephalins
Endorphins
Neuropeptides: longer than small molecules, play role in pain regulation and other functions.
Neuronal Regeneration & Plasticity
Plasticity allows new dendrites to sprout and new proteins to synthesize, although regeneration is limited (better in PNS than CNS).
Multiple Sclerosis (MS)
An autoimmune disorder destroying myelin sheaths in CNS, leading to muscle weakness and sensory alterations, occurring mostly in young adulthood.
Epilepsy
Characterized by recurrent, short attacks due to abnormal brain electrical discharges, with various causes, including brain damage and infections.
Neuronal Structure & Function Overview
Dendrites: receive stimuli, activated by ion channels.
Cell Body: integrates signals and produces potentials.
Axon: propagates impulses to terminals where neurotransmitter release occurs.