L1 Action Potential Flashcards
Basic functions of neuron
to integrate and relay info from other neurons in a neural circuit
about 86 billion in one body
Basic structure of neuron
Body
Axon
Dendrites
Myelin sheaths
Axon terminal
Interneurons
located in spinal cord
local circuit neurons, relatively short axons
connect brain regions
Projection neurons
extend to distant targets, both afferent (sensory/towards NS) and efferent (motor/away NS)
Glial cells
-supportive functions for neurons, not transmitting electrical signals
-maintains ionic environment
-modulates the rate myelin sheath
-controls the uptake and metabolism of neurotransmitters
-providing scaffold for neural development
-recovery from neural injury
-connects. brain and immune system
-facilitates flow of interstitial fluid in sleep
Types of glial cells
astrocytes
oligodendrocytes
microglial
Astrocytes
only in central NS
starlike appearance
maintain chemical environment, forms blood-brain barrier, secrete substances that form new synaptic connections
Oligodendrocytes
lay down myelin for CNS
stem cells can generate new ones after injury
Schwann Cells
lay down myelin for PNS
stem cells can generate new ones after injury
Microglial cells
-derived primarily from hematopoietic precursor cells
-similar to macrophages
-remove cellular debris, secrete signaling molecules that modulate inflammation
Glial stem cells
not a lot known about the importance of glial cells
retain the capacity to generate new precursor cells
2 types include astrocytes (ventricles) and oligodendrocytes (white matter)
Afferent neurons
sensory, entering CNS
Efferent neurons
motor, exiting CNS
Reflex circuit (knee-jerk)
- Hammer tap, stretches sensory receptors in extensor muscles
- Sensory neuron synapses on motor neuron and spinal interneurons
- Interneuron synapse inhibits motor neuron to flexor muscles
- Motor neuron synapses on extensor muscle fibers, contraction
- Flexor muscle relaxes b/c of interneuron
- Leg extends
Extracellular recording
electrode is placed near the nerve cell of interest to detect activity
used for detecting temporal patterns of action potential activity
Intracellular recording
electrode is placed inside the cell of interest to detect activity
can detect the smaller graded changes in electrical potential that trigger action potentials
Action potential
electrical signal that transiently reverses the negative resting potential and makes the transmembrane potential positive
all or nothing changes
self-regenerating wave of electrical activity
comes from ion fluxes
Resting membrane potential
neurons at rest generate negative potential
-60mV
more potassium inside the cell, more sodium/calcium/chloride outside the cell
Why are electrical potentials generated across the membranes of neurons?
- there are differences in concentrations of specific ions across nerve cell membranes
- membranes are selectively permeable to some of these ions
Active transporters
-actively move selected ions against concentration gradient
-create ion concentration gradient
steps: ion binds, ion transported across membrane
Ion channels
allow ions to diffuse down concentration gradient
are selectively permeable to certain ions
Types of potentials
receptor potentials
synaptic potential
action potential
Receptor potential
sensory neurons
due to the activation of sensory neurons by external stimuli (light, sound, heat).
neuron responds to touch with a receptor
potential that changes the resting potential for a fraction of a second
Synaptic potential
brief changes in resting potential
allow transmission of information from one neuron to another and produce very brief change in resting potential. These serve as means of exchanging info in CNS and PNS
Synaptic transmission
action potential is passed from one neuron to another at synaptic contacts
More permeability to potassium
resting potential of the neuron will be lesser than -60mV, about -86mV
More permeability to sodium
the resting potential will be greater than -60 mV (+64 mV)
Hyperpolarization
goes past resting potential
Depolarization
becoming more positive
Repolarization
becoming more negative
Steps of action potential
- Begin at resting potential (-60mV)
- Stimulus pushes the membrane potential to threshold potential (-50mV)
- Na+ channels open, rapidly depolarizing the membrane potential (+40mV)
- Potassium channel opens, repolarizing the membrane
- Delay in close, causes hyperpolarization (-70mV).
- Potassium channels close
Passive conduction (graded potentials)
the electrical signal “leaks” across the membrane, causing a change in membrane potential down the axon
causes a slight change farther down the axon, eventually dies out the farther it moves away from the initial stimulus/beginning of axon
action potential needs both passive and active conduction to spread
Refractory period
makes sure depolarization doesn’t flow backwards along the axon
How does action potential maintain its amplitude?
same idea as positive feedback loop
activating voltage dependent on Na+. membrane potential depolarization leads to more Na+ conductance, more Na+ entry, further depolarization
What factors increase AP conduction velocity?
Increasing diameter of axon = decreases friction = increases flow
insulting the axon with myelin = decreases leakage out of axon
Saltatory conduction
process of action potential propagation during which current flows across the neuronal membrane only at nodes of raniver
action potentials are jumping from one node to the next, allowing for non-continuous depolarization, in myelinated axons
Multiple sclerosis
varied clinical presentation caused by demyelination and inflammation of axonal pathways in the CNS
Electrical synapses
minority in the human system
typically instant, can be bidirectional
breathing neurons are an example
current flow occurs at gap junctions, which contain connexon channels which allow for passive electrical flow
Steps of chemical synapse
- Neurotransmitter is synthesized and stored in vesicles
- AP occurs
- AP causes CA channels to open, CA flows in
- CA causes vesicles to fuse with presynaptic membrane, NT is released into synaptic cleft
- Transmitter binds to receptor molecule which causes either inhibitory or excitatory response in post synaptic cell
Ligan gated ion channels
Neurotransmitter binds, channel opens, ions flow across membrane.
Allows for multiple different types of ions to flow across the membrane
G-protein-coupled receptors
Neurotransmitter binds, g-protein is activated, g protein subunits or messengers modulate ion channels, ion channel opens, ions flow across membrane
modulate ion channels
Excitatory postsynaptic potentials
an EPP leads to depolarization in the postsynaptic cell via a reversal potential that is more positive than the resting membrane potential
glutamate is an example
increases the likelihood of an action potential occurring in the postsynaptic neuron
Inhibitory postsynaptic potentials
an EPP that leads to hyperpolarization in the postsynaptic cell via a reversal potential that is more negative than the resting membrane potential
decrease the likelihood of an AP occurring in the postsynaptic neuron
example of GABA
Temporal summation
across multiple presynaptic spikes
occur close enough in time to combine and trigger an AP at axon hillock
kid saying mom over and over again
Spatial summation
across multiple presynaptic terminals
applied at the same time, in different areas, cumulative effect on membrane potential
multiple kids saying mom around the house at the same time
Synaptic plasticity
strength of synaptic connections between neurons is dynamic
can produce short-term or long-term changes with different underlying mechanisms
Short term synaptic plasticity
either facilitation or depression
affects the amount of neurotransmitter being released from presynaptic terminals in response to an action potential
Synaptic facilitation
rapid increase in synaptic strength that occurs when two ore more APs fire at the presynaptic terminal within a few miliseconds of each other
allows for calcium buildup
Synaptic depression
causes neurotransmitter release to decline during sustained synaptic activity
decrease of vesicles available to release NT
decrease strength of synapse
Habituation plasticity
process that causes the animal to become less responsive to repeated occurrences of a stimulus
ex: smells slowly decrease over time
shorter effects
Sensitization plasticity
process that allows an animal to generalize an aversive response elicited by a noxious stimulus to a variety of other non-noxious stimuli
dogs w/shock collar; pairing a shock w/fence
longer effects
What causes gill withdrawal?
- Touching the siphon –> activates sensory neurons
- form excitatory synapses that release glutamate onto respective interneurons, and motor neurons
- motor neuron release ACh, exciting the gill muscle
pain is conveyed by the modulatory interneuron
Repeated stimulation of the siphon results in habituation. Which synaptic change occurs during habituation?
the synapse between the sensory and motor neurons is depressed
What structure can be found exclusively at an electrical synapse?
connexon
What occurs during habituation at a cellular level?
transmission at the glutamatergic synapse (between sensory and motor) is depressed
there is a decrease in the number of vesicles available for release, causing a decreased transmission from presynaptic to postsynaptic
What occurs during sensitization at a cellular level? (short term)
recruits additional neurons
What occurs during sensitization at a cellular level? (long term)
changed gene expression
1. interneurons will release serotonin, which binds to the G-protein and stimulates production of cAMP.
2. cAMP binds to protein kinase A, which blocks K+ from leaving the cell
3. Prolonged AP causes more CA+ channels to be opened, which causes more release of neurotransmitters, more motor neuron activity
Long-term potentiation
long-lasting increase in synaptic strength
high frequency stimulus
if you want to cause a chain reaction, you have to at least provide a weak stimulation to the following synapse
changes occur if stimulation is less than 100ms apart
Long-term depression
long-lasting decrease in synaptic strength
incorrect sequencing of events can lead to LTD
no changes occur/LTD occurs if the stimulation or firing is greater than 100ms apart from each other
Trisynaptic pathway
1.Neurons in entorhinal cortex
2.travels to synapse on granule cell layer of dentate gyrus
3. Granule cells give rise to mossy fibers, which synapse on CA 3 cells
4. CA3 cells lead to fibers that leave the hippocampal formation adn schaffer fibers
5. CA1/schaffer fibers leave hippocampus and project to subiculum
6. cells from the subiculum proect back to the entorhinal cortex, completes the loop
Why is the trisynaptic pathway important?
gives evidence for LTD and LTP
LTP has been shown to occur throughout the circuit
NMDA receptors
having a molecule of magnesium blocking the channel
need HIGH frequency to dispel the Mg2+
allows both Ca and Na into the cell, which creates LTP along the post-synaptic neuron
ultimately not needed, but more receptors = greater stimulus = LTP
AMPA receptor
just need NT to bind to allow Na into the postsynaptic
only allows sodium into the postsynaptic neuron
LTP and AMPA
LTP causes more AMPA receptors
more AMPA receptors increases sensitivity to glutamate, which means its easier to produce an AP
LTP and NMDA
LTP does NOT cause more NMDA receptors
NMDA is important for LTP inductions and not LTP expression
LTD and AMPA
when post synaptic neurons aren’t being stimulated, the cell begins to internalize/destroy the AMPA receptors it does not need
