Cocaine prevents the uptake of epinephrine, leading to increased levels in the synaptic cleft.
Muscarinic and nicotinic receptors.
No, because the transmitter can dissociate from the postsynaptic receptor after a while.
The influx of calcium ions through voltage-gated calcium channels triggers the release of neurotransmitters.
Glycine is a small-molecule neurotransmitter that opens inhibitory postsynaptic potentials (IPSP), similar to GABA.
The cell body is considered the metabolic control center, acting as a manufacturing and recycling plant for the neuron.
It leads to depolarization and suprathreshold depolarization.
Voltage-gated sodium channels open, resulting in an action potential.
Through various mechanisms that can include reuptake, degradation, or diffusion.
Kinesin motor protein.
The membrane potential reaches the threshold earlier, resulting in a shorter time period between action potentials and a larger action potential frequency.
Synaptic vesicles are responsible for the release of neurotransmitters during synaptic transmission.
Sensory receptors are specialized nerve endings that detect different stimuli and provide electrical signals sent into the CNS.
The mechanosensitive ion channel is closed under resting conditions.
Small maintained summed EPSP results in low action potential frequency.
A-alpha neurons are the fastest.
It results in a small depolarization due to the opening of few mechano-sensitive channels, leading to a smaller current.
They have a receptor potential and their cell body is located in the dorsal root ganglion or trigeminal ganglion.
Purinergic receptors.
Electrotonic depolarization occurs when the large sodium current in a region causes depolarization in the next region of the membrane, activating sodium channels there.
It blocks voltage-gated sodium channels, preventing action potential generation and pain sensation.
It produces a small receptor potential that decays, and no action potential is generated.
The two categories of electrical signals are electrotonic potentials and action potentials.
The membrane potential depolarizes again to the threshold of voltage-gated sodium channels, allowing another action potential.
Large maintained EPSP leads to high action potential frequency.
An idealized neuron has four basic regions: cell body (soma), dendrites, axon, and axon terminals.
AMPA receptors are permeable to 'one-charge' cations, primarily allowing sodium influx into the cell.
Depolarization occurs, leading to the opening of N/P type calcium channels.
Metabotropic receptors cause small hyperpolarization (IPSP) for milliseconds, stabilizing the membrane potential at negative values.
G-protein coupled receptors activate heterotrimeric G-proteins, which induce signaling changes in the postsynaptic cell, affecting the activity of ion channels and potentially causing depolarization or hyperpolarization.
Axonal transport, specifically anterograde transport.
GABA (gamma amino-butyric acid)
It breaks down Acetylcholine in the synaptic cleft.
Open mechanosensitive channels.
Action potential propagates as a regenerating response, developing at one region of the cell and inducing action potential at another location, spreading without decrement.
The activation of action potential is triggered by voltage-gated sodium channels, leading to a large influx of sodium ions.
Calcium enters the axon terminal, triggering exocytosis and the release of neurotransmitters.
An IPSP is caused by the opening of ligand-gated chloride channels and sometimes potassium channels, leading to small hyperpolarization.
Mitochondria pump out calcium, operate the Na+/K+ pump, and fill synaptic vesicles with neurotransmitters, all requiring ATP.
Axoplasm has high resistance, leading to a major percentage of current leaving and less current entering the cytoplasm of the axon.
Spatial summation occurs when action potentials at fibers A and B lead to a larger depolarizing effect than stimulation of one alone.
Excitatory fibers release glutamate, which binds to AMPA receptors.
Action potentials propagate electrical signals rapidly along nerve fibers to the CNS for processing.
They allow synchronization of depolarization between connected neurons.
The output of the CNS includes effectors such as muscles, vessels, and glands, leading to effects like muscle contraction and glandular secretion.
Dendrites receive incoming signals from other neurons.
A large depolarization causes voltage-gated K+ channels to open while voltage-gated sodium channels inactivate.
There can be many successive action potentials generated one after another.
Current flows through the lumen of gap junctions, allowing for instant flow between cells.
There are axodendritic synapses, where the axon terminal connects to the dendrite of another neuron, and axosomatic synapses, where the axon terminal forms a synapse with the cell body of another neuron.
NMDA receptors are permeable to sodium and calcium, requiring glutamate binding and depolarization to open, expelling a magnesium plug.
The gap between the presynaptic and postsynaptic membranes, approximately 20-50 nm wide.
They contain peptide transmitters, are not in a docked position, and are released upon repeated stimulation by action potentials.
GABA A and GABA C receptors
Transmitter diffusion away, uptake by presynaptic terminal, and enzymatic breakdown.
The types of glutamate receptors are ionotropic receptors (like AMPA and NMDA) and metabotropic receptors (G-protein coupled receptors).
The amplitude of the signal decreases with distance, leading to a decay in space.
A large mechanical stimulus results in a large depolarization, while a small stimulus results in a small depolarization.
Synapsin I.
A calcium signal (Ca2+).
1) Electrical 2) Chemical
Stimulating fiber C results in a small hyperpolarization, leading to an inhibitory postsynaptic potential (IPSP).
It activates the opening of K+ channels, leading to a rapid outflow of K+ and resulting in hyperpolarization (IPSP).
They facilitate the association of the vesicle to the active cytoskeleton.
C fibers are the slowest and unmyelinated.
The influx of sodium through ligand-gated channels causes a small depolarization of the postsynaptic cell, resulting in an excitatory postsynaptic potential (EPSP).
When chloride channels open, chloride ions move into the postsynaptic cell, making it more negative and resulting in hyperpolarization, which is an inhibitory postsynaptic potential (IPSP).
The binding of the neurotransmitter should evoke an effect on the postsynaptic neuron, resulting in either an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP).
Action potential is an all or none response, meaning it either develops fully or not at all.
The amplitude of an action potential is several times 10mV, typically reaching +20 or +30mV.
The electrochemical gradient of H+ allows for the accumulation of high concentrations of neurotransmitter in the vesicle, facilitating rapid release when the vesicle fuses with the plasma membrane.
1. It should be present in the presynaptic nerve terminal and synthesized by the presynaptic neuron. 2. Presynaptic depolarization should lead to its release. 3. There should be a specific receptor on the postsynaptic cell. 4. Binding should evoke an effect on the postsynaptic neuron, such as EPSP or IPSP.
The channel opens, leading to action potential generation.
Neurotransmitters bind to postsynaptic receptors, which are often ligand-gated, leading to excitatory or inhibitory postsynaptic potentials.
It results in two EPSPs, with the new one riding on the back of the first, leading to a higher amplitude.
Electrotonic potentials are graded, have low amplitude (about 1/10 mV), are localized, decay in space, and decay in time if no current is present.
Dynein motor protein.
~1-5 ms (milliseconds)
Connexin subunits form connexons, creating hemichannels.
It spreads with decrement.
Around the first myelin sheath.
Inhibitory fibers release GABA and bind to GABA-A receptors.
It leads to the opening of AMPA receptors and a small depolarization, resulting in an excitatory postsynaptic potential (EPSP).
It causes electrotonic depolarization that reaches the threshold of voltage-gated sodium channels, resulting in action potential.
A weak suprathreshold stimulus results in low frequency action potential firing.
Gap junctions between neighboring neurons that interconnect cytoplasm, allowing bidirectional transmission with no delays.
There are axodendritic, axosomatic, and axoaxonic synapses.
The presence of neurotransmitters that are released from the axon terminal to evoke effects on the postsynaptic membrane.
Typically no, except in some special cases known as retrograde signaling.
The V-type proton pump uses ATP to pump protons into the lumen of the vesicle, acidifying it and creating a high concentration of H+, which drives the uptake of neurotransmitters as a secondary active transport process.
In the spinal cord and other areas.
In the dorsal root ganglion or trigeminal ganglion.
Catecholamines act on noradrenergic receptors.
Thick fibers have a larger velocity of propagation than thin fibers because the current in thin fibers rapidly leaves the axon through the plasma membrane, spreading less.
Axon terminals form synapses where outgoing signals pass to the dendrite or another neuron.
50-400 mm/day.
100 - 120 m/s
They are filled into vesicles in the axon terminal.
Neurotransmitter-proton exchanger protein.
The vesicle membrane may become part of the plasma membrane, but in the Kiss&Run mechanism, the vesicle opens to release neurotransmitter and then closes again to move back into the axon terminal.
They contain neurotransmitter molecules and are involved in neurotransmitter release.
The cell body contains the nucleus, endoplasmic reticulum (ER), Golgi apparatus, and is responsible for synthesizing most proteins of the neuron.
The peripheral axon of primary sensory neurons runs to the skin and is mechano-sensitive.
Typically, a neuron has one axon.
The postsynaptic potential needs to reach the threshold, which is -60 mV.
An EPSP is a small depolarization lasting milliseconds, typically caused by the opening of ligand-gated non-selective cation channels, often involving glutamate.
The GABA-A channel opens, allowing chloride to flow into the postsynaptic cell, resulting in hyperpolarization and an inhibitory postsynaptic potential (IPSP).
Voltage-gated sodium channels in thick fibers allow for a larger range, resulting in a higher velocity of propagation compared to thin fibers.
An axospinous synapse is where the axon terminal attaches to the dendritic spines, which are small compartments on the dendrites.
A & B fibers, which are excitatory and attach to dendrites.
There is a decay in time of the receptor potential.
Because the receptor potential decays in space and may not reach the CNS, it needs to evoke an action potential to transmit the signal.
The mechanosensitive ion channel opens, allowing mostly sodium to flow into the nerve ending, causing a small depolarization.
Inactive sodium channels can return to a closed state.
Retrograde transport.
GABA B is a 7 TM receptor coupled to Gi protein.
In smooth muscle and heart muscle tissues.
The flow is unidirectional from presynaptic to postsynaptic, typically from the axon terminal to the dendrite or cell body of the next neuron.
It hyperpolarizes the membrane potential below the threshold line.
The frequency of action potentials depends on the amplitude of electrotonic depolarization.
The summed postsynaptic potential must reach depolarization at the threshold.
Because the region of origin has inactive voltage-gated sodium channels and activated voltage-gated potassium channels.
Thick fibers have much less electrical resistance in their interior, allowing a higher percentage of current to enter the axis of the axon and a smaller percentage to leave.
In thick fibers, the electrotonic potential decays less in space due to a larger space constant.
Neurotransmitter and proteins involved in exocytosis.
The myelin sheath acts as an electrical insulator, preventing current from leaving the axon in the regions covered by myelin, forcing it to travel inside the axon.
The C fiber forms an axo-somatic synapse and is inhibitory.
SALTATORY CONDUCTION
Stimulus intensity is encoded in action potential frequency, where a weak stimulus evokes low frequency and a strong stimulus evokes high frequency.
The action potential produced at one end will always reach the other end without loss, errors, or distortion.
The vesicles fuse to the plasma membrane, releasing neurotransmitter molecules.
A strong stimulus leads to high frequency action potential firing, with the neuron capable of producing up to 500 action potentials per second.
The result is an IPSP and EPSP that can cancel each other out, depending on their summed effects.
The voltage-gated potassium channels gradually close since there is no further depolarization to trigger them, closing after some time.
It spreads rapidly and reaches the threshold at the next node without activating voltage-gated sodium channels in between.
No further depolarization occurs, and the membrane potential will return to resting level after the activation of voltage-gated K+ channels.
Myelinated axons conduct faster due to saltatory conduction.
Unidirectional (anterograde, orthodromic)
The thickness of the fiber and whether the axon is myelinated or unmyelinated.
The neuron decides whether to fire an action potential based on the incoming action potentials propagating along the fiber.
Myelination of the axon is a major determinant of the velocity of propagation, resulting in very rapid propagation of action potentials.
A large space constant indicates that the electrotonic potential decays slower.
Voltage-gated potassium channels open during depolarization, leading to a hyperpolarizing effect as K+ ions move outward, affecting the membrane potential.
At the axon hillock, which is the initial segment of the axon.
They are activators of GABA A, acting as tranquilizers that induce sleepiness and relaxation.
V-type proton pump.
