Chapter 3B Flashcards
In contrast to the graded potential, an
action potential is not decremental (means: ). Instead, an action potential
keeps its strength as it spreads along the
membrane.
it does
not die out
What do we call this mode of conduction (action potential does not die out)? And what does is depend on?
This mode of conduction is called
propagation, and it depends on positive
feedback.
Why can an action potential
propagate in one direction only
it
cannot propagate back toward the cell
body because any region of membrane
that has just undergone an action
potential is temporarily in the absolute
refractory period and cannot generate
another action potential.
Graded potentials vs actions potentials:
A arise mainly in dendrites and cell body
B arise at trigger zones and propagate along axon
A graded
B action
Graded potentials vs actions potentials:
A Na+ and K+ channels
B Ligand-gated or mechanically-gated ion channels
A action
B graded
Graded potentials vs actions potentials:
A Decremental (not propagated): short distances
B propagate, long distance
A graded
B action
Graded potentials vs actions potentials:
A Amplitude depending on strength of stimulus (<1 mv - 50 mv)
B all or none (typically 100 mV)
A graded
B action
Graded potentials vs actions potentials:
duration:
A typically longer (ms - minutes)
B shorter, 0.5 - 2 msec
A graded
B action
Graded potentials vs actions potentials:
polarity:
A always consists of depolarizing phase, followed by repolarizing phase, return to resting membrane potential
B May be hyperpolarizing or depolarizing
A action
B graded
Graded potentials vs actions potentials:
A refractory period: not present, summation can occur
B present, summation cannot occur
A graded
B action
CONTINUOUS VS. SALTATORY CONDUCTION
= non- myelinated vs myelinated
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Continuous conduction:Involves step-by-step
depolarization and repolarization. Occurs in …… and ….
unmyelinated axons and muscle fibers
Saltatory conduction: Mode of action potential propagation
that occurs along X axons
X = myelinated
why is saltatory conduction more energy-efficient?
Opening a smaller number of channels only at the nodes = more energyefficient mode of conduction (less ATP)
what three factors affect the speed of propagation of an action potential?
- amount of myelination
- axon diameter (larger diameter = faster)
- temperature (slower when cooled)
…. = most common demyelinating disease of CNS
MS (immune system attacks the myelin sheath or the cells that
produce and maintain it, results in sclerosis = ‘scarring’).
Most synapses between neurons are axodendritic (A),
axosomatic (B) or axoaxonic ()
A from axon to dendrite
B from axon to cell body
C from axon to axon
(p 82)
Electrical synapses have two main advantages over chemical synapses
- faster comm
- synchronization (coordinate the activity of a group of neurons or muscle fibers.
Thus a large number of neurons or muscle fibers can produce action potentials in
unison.)
chemical synapse works with neurotransmitters, electrical does not
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chemical synapse: zet in juiste volgorde
- The depolarizing phase of the nerve impulse opens voltage-gated Ca2+ channels, Ca2+ flows inward
- Binding of neurotransmitter molecules to their receptors on ligand-gated channels
opens the channels and allows particular ions to flow across the membrane. - A nerve impulse arrives at a synaptic end bulb of a presynaptic axon.
- As ions flow through the opened channels, the voltage across the membrane changes:
postsynaptic potential. Depending on which ions the channels admit, the postsynaptic
potential may be a depolarization (excitation) or a hyperpolarization (inhibition) - The neurotransmitter molecules diffuse across the synaptic cleft and bind to
neurotransmitter receptors in the postsynaptic neuron’s plasma membrane - exocytosis of the synaptic vesicles. As vesicle membranes merge with the
plasma membrane, neurotransmitter molecules within the vesicles are released into the
synaptic cleft. - When a depolarizing postsynaptic potential reaches threshold, it triggers an action
potential in the axon of the postsynaptic neuron.
1) A nerve impulse arrives at a synaptic end bulb of a presynaptic axon.
2) The depolarizing phase of the nerve impulse opens voltage-gated Ca2+ channels, which
are present in the membrane of synaptic end bulbs. Because calcium ions are more
concentrated in the extracellular fluid, Ca2+ flows inward through the opened channels.
3) An increase in the concentration of Ca2+ inside the presynaptic neuron serves as a signal
that triggers exocytosis of the synaptic vesicles. As vesicle membranes merge with the
plasma membrane, neurotransmitter molecules within the vesicles are released into the
synaptic cleft. Each synaptic vesicle contains several thousand molecules of
neurotransmitter
4) The neurotransmitter molecules diffuse across the synaptic cleft and bind to
neurotransmitter receptors in the postsynaptic neuron’s plasma membrane.
5) Binding of neurotransmitter molecules to their receptors on ligand-gated channels
opens the channels and allows particular ions to flow across the membrane.
6) As ions flow through the opened channels, the voltage across the membrane changes:
postsynaptic potential. Depending on which ions the channels admit, the postsynaptic
potential may be a depolarization (excitation) or a hyperpolarization (inhibition).
7) When a depolarizing postsynaptic potential reaches threshold, it triggers an action
potential in the axon of the postsynaptic neuron.
A neurotransmitter causes either an excitatory postsynaptic potential (EPSP) or an
inhibitory postsynaptic potential (IPSP):
- A neurotransmitter that causes depolarization of the postsynaptic membrane is
X because it brings the membrane closer to threshold (-55mV). - A neurotransmitter that causes hyperpolarization of the postsynaptic membrane
is X
X = excitatory
X = inhibitory
chemical synapse:
Opening of X channels allows
inflow of X, which causes
depolarization.
* Opening of B channels causes
hyperpolarization (B to move
into the cell: inside of the cell
becomes more negative)
* Opening of C channels causes
hyperpolarization (C to move
out: inside of the cell becomes
more negative).
X Na+
B Cl–
C K+
many types of neurons contain and release two or more different neurotransmitters (X)
co-transmitters
Neurotransmitters can be divided into two classes based on size
Small-molecules neurotransmitters:
produce brief, local effects (at
synaptic connections).
Neuropeptides: produce slow, long-lasting
effects often encompassing a significant
area surrounding the site of release
Neurotransmitter receptors are classified as:
X (fast)
B (slow)
X ionitropic
B Metabotropic
An ionotropic receptor is a X channel: the neurotransmitter binding
site and the B are components of the same protein
Neurotransmitters bind to their receptors and act quickly (one milisecond) to
open or close ion channels.
- Small-molecules neurotransmitters often bind ionotropic receptors and produce
a V effect.
X ligand-gated
B ion channel
V quick and local
- A metabotropic receptor contains a neurotransmitter binding site but lacks A as part of its structure.
- Neurotransmitters act more slowly (hundreds of milliseconds to minutes) via secondmessenger systems to influence chemical reactions inside cells.
- Neuropeptides often bind metabotropic receptors and produce B
effects
A ion channel
B slow, long-lasting
Metabotropic receptor requires a membrane protein (= X ) to open or close the
ion channel
G protein may act directly to open or close the ion cannel (A), or indirectly by
activating another molecule, a “X,” in the cytosol (B)
X G protein
X second messenger
Neurotransmitters: Their effect on the postsynaptic neuron can be:
excitatory
inhibitory
both
Removal of the neurotransmitter from the synaptic cleft is essential for normal
synaptic function, because if a neurotransmitter could linger in the synaptic cleft , it would influence …..
the
postsynaptic neuron, muscle fiber, or gland cell
Neurotransmitter is removed in three ways:
- Diffusion
- Enzymatic degradation
- Uptake by cells
A typical neuron in the CNS receives input from 1000 to 10,000 synapses.
* Integration of these inputs involves summation of the postsynaptic potentials that
form in the postsynaptic neuron.
* Recall that summation is the process by which graded potentials add together.
* There are two types of summation: X and X
spatial summation and temporal summation
Spatial summation is summation of postsynaptic potentials in response to stimuli that
occur at different X in the membrane of a postsynaptic cell at the same time.
* Temporal summation is summation of postsynaptic potentials in response to stimuli
that occur at the X location in the membrane of the postsynaptic cell but at
different X
X locations
X same
X times
The sum of all the X and X effects at any given time determines the
effect on the postsynaptic neuron.
X excitatory
X inhibitory
Substances naturally present in the body as well as drugs and toxins can modify the
effects of neurotransmitters in several ways:
1. Neurotransmitter X: stimulated or inhibited.
2. Neurotransmitter X: enhanced or blocked.
3. The neurotransmitter X can be activated or blocked.
4. Neurotransmitter X can be stimulated or inhibited
X synthesis
X release
X receptors
X removal
An agent that binds to receptors and enhances or mimics the effect of a natural
neurotransmitter is an X.
* An agent that binds to and blocks neurotransmitter receptors is an X
X agonist
X antagonist.