Neurons conduct electrical impulses known as action potentials.
Action potential is an electrochemical charge moving along an axon due to the movement of unequally distributed ions across the axonal plasma membrane.
At rest, the plasma membrane is polarized, meaning there is a charge difference across the membrane.
The resting membrane potential, when the neuron is not conducting an impulse, is approximately -70 mV in neurons.
The negative charge indicates that the inside of the axon's cell membrane is 70 mV less than the outside.
All living cells exhibit a membrane potential that varies based on cellular activities.
Various passive and active mechanisms maintain the net negative charge inside the cell.
Mechanisms Maintaining Resting Membrane Potential
The resting membrane potential is maintained by:
Passive Chemical Gradients:
Utilize leak channels that are always open, allowing ions to move down their concentration gradients.
The membrane has differential permeability to various ions, mainly sodium (Na+) and potassium (K+).
There is a higher permeability to potassium, hence more K+ ions move out through leak channels, causing the cell's interior to be more negative.
Although Na+ ions move into the cell due to a high extracellular concentration, their entrance is limited because of lower permeability compared to K+ ions.
Sodium-Potassium Pumps (Na+/K+ ATPase):
These are active transport mechanisms utilizing ATP to carry ions against their gradients.
For every 3 Na+ ions pumped out, 2 K+ ions are pumped in.
Constant operation is essential, as Na+ and K+ will naturally diffuse back to their original locations.
Changes in Membrane Potential
Changes in resting membrane potential arise from external stimuli affecting ionic movement across the cell membrane.
Main ions responsible are sodium and potassium. Channels can be:
Passive (Leak Channels): Always open.
Active (Gated Channels): Open in response to specific stimuli. Types include:
Ligand-gated Channels: Open in response to a specific ligand (e.g., neurotransmitters).
Voltage-gated Channels: Open when they detect a voltage change; characteristic of excitable membranes.
Mechanically gated Ion Channels: Open due to physical changes in the membrane, typically found on the dendrites of sensory neurons.
Action Potentials: Electrical Propagation
Neurons communicate through electrochemical signaling, where a neuron releases neurotransmitters to affect another neuron or effector.
Upon stimulation, the membrane potential experiences a rapid change, and the inside of the neuron briefly becomes positively charged, known as an action potential.
The transition from resting membrane potential to action potential requires reaching a threshold level at the axon hillock:
Graded Potentials: Local changes in membrane potential that accumulate from stimuli to decide if an action potential will occur.
Threshold level must be reached for action potential initiation.
Phases of Action Potential
Resting Potential: Voltage-gated sodium and potassium channels are closed, maintaining a -70 mV resting potential.
Depolarization: Voltage-gated sodium channels open if the threshold (~-60 mV) is reached; Na+ rushes into the axon, raising the membrane potential to around +30 mV.
Repolarization: Sodium channels close and potassium channels open, allowing K+ to exit the axon, restoring a negative interior.
Hyperpolarization: K+ channels are slow to close, causing a brief dip below -70 mV before returning to resting potential.
Propagation of Action Potentials
Action potentials travel like waves along the axon.
They are self-propagating due to the opening of ion channels prompted by adjacent membrane potential changes.
Continuous Propagation: Occurs in unmyelinated axons where segments are depolarized in sequence.
Saltatory Conduction: In myelinated axons, action potentials jump between nodes of Ranvier, significantly increasing the conduction speed.
Summation of Graded Potentials
Graded potentials lead to small changes in membrane potential, potentially summing to reach threshold at the axon hillock:
Spatial Summation: Multiple graded potentials from different locations combine.
Temporal Summation: Multiple potentials from the same location in rapid succession combine.
Chemical Transmission of an Action Potential
Transmission between neurons occurs in one direction across a synapse, comprising
The synaptic cleft (gap) filled with fluid between a presynaptic axon terminal and a postsynaptic neuron.
Upon reaching the axon terminal, action potentials open voltage-gated calcium channels, triggering neurotransmitter release into the synapse.
Types of postsynaptic potentials include:
Excitatory Postsynaptic Potential (EPSP): Depolarizes the neuron, moving it towards threshold, often due to Na+ or Ca2+ influx.
Inhibitory Postsynaptic Potential (IPSP): Hyperpolarizes the neuron, moving it away from threshold, often due to Cl− influx.
Removal of Neurotransmitters
After neurotransmitter release, they swiftly act and are removed by:
Enzymatic Breakdown: Enzymes in the synapse (e.g., acetylcholinesterase) inactivate neurotransmitters.
Reuptake: Presynaptic neurons reabsorb neurotransmitters, either repackaging or breaking them down.
Types of Neurotransmitters
There are over 100 identified neurotransmitters; classified by chemical structure and function (excitatory/inhibitory). Examples include:
Norepinephrine and Epinephrine: Released by adrenal glands, generally excitatory.
Dopamine: Modulates emotional responses; can be excitatory or inhibitory.
Acetylcholine: Functions in neuromuscular junctions; facilitates muscle action.
Serotonin: Regulates emotions and attention in the CNS.
GABA (gamma-aminobutyric acid): The primary inhibitory neurotransmitter that induces hyperpolarization.
Glutamate: The primary excitatory neurotransmitter, causing depolarization.
Mechanisms of Action for Neurotransmitters and Neuromodulators
Direct Effects: When neurotransmitters bind directly to ionotropic receptors, changing ion flow across the membrane (e.g., ACh, glutamate).
Indirect Effects via G Proteins: When neurotransmitters bind to metabotropic receptors, activating G proteins that modulate cellular functions and ion channels.
Indirect Effects via Intracellular Enzymes: Certain gaseous neurotransmitters like nitric oxide diffuse and affect intracellular processes.
Presynaptic Inhibition and Facilitation
Inhibitory or excitatory effects can influence rate of neurotransmitter release at various synapses:
Presynaptic Inhibition: Reduces neurotransmitter release, making action potentials less likely in postsynaptic neurons.
Presynaptic Facilitation: Increases neurotransmitter release, enhancing likelihood of action potentials.