Action Potentials & Synapses Flashcards
what causes a neutron to be polarized?
unequal distribution of ions on either side of the plasma membrane
what is the charge of neurons measured in?
millivolts
how are neutrons different than most cells?
they are electrically excitable
what is the resting membrane potential of a neuron?
-70mV
what is the signal neurons use to communicate with other neurons or other targets like muscles and glands?
a change in membrane potential (voltage)
what is it called when the membrane potential decreases?
depolarization
what is it called when the membrane potential increases?
hyperpolarization
what are neurons only capable of generating GPs involved in?
local or short distance communication (typically a few mm)
what are the characteristics of graded potentials?
typically small, slow, gradual, and either decrease or increase membrane potential
what are the characteristics of action potentials?
large, typically repetitive, with rapid alternating depolarization and hyper polarization (spikes) of membrane potential
what are neurons that generate action potentials capable of?
long range signalling
where do the longest neurons in the body receive input from and travel to?
distal lower limb (like the big toe) and travel to the brainstem, a distance of ~ 1m
what does the generation of action potentials depend on?
the generation of graded potentials. Therefore all neurons that can produce APs can also produce GPs
what does an ion pump require to move potassium from the outside to the inside?
energy, ATP
what is the function of an ion pump?
it moves potassium from the extracellular space to the inside of a neutron
what is the typical concentration of K in the extracellular space?
4mM
what is the potassium concentration inside the neuron?
120mM
what else does the ion pump do?
it also moves sodium ions from inside the neuron to the outside
what is the sodium concentration outside the neuron?
140mM
what is the sodium concentration inside the neuron?
14mM
what is the function of an ion channel?
they allow some of the potassium to move from the inside to the outside down the concentration gradient
what does potassium travelling outside the neuron via an ion channel result in?
a voltage difference between the inside and outside of the cell
what does the voltage produced depend on
the extent of the concentration difference between the inside and the outside
what is the function of a sodium ion channel?
they allow some sodium to travel inside the neuron down their concentration gradient causing the inside to become more positive
is the influence of potassium or sodium much greater?
potassium because their channels are 25X more permeable than sodium channels
how are ion channels different in graded potentials?
the permeability of sodium channels can change
how does sodium channel permeability change for GPs?
at rest the permeability is low
what happens when sodium ion channel permeability increases?
Na moves down its concentration gradient moving the membrane potential in the positive direction (depolarizing)
what makes action potentials special?
the are produces by ion channels that are voltage gated
what happens when an AP reaches threshold?
voltage gated Na channel permeability rapidly increases, greatly depolarizing the neuron
what is the falling phase of the action potential due to?
the intrinsic inactivation of voltage gated Na channels and a delayed activation of voltage gated K+ channels
what causes a refractory period on AP generation?
voltage gated Na channel inactivation
what is the absolute refractory period?
the period when no matter how strong the stimulus, another AP cannot be generated
what is the relative refractory period?
the time following Na+ channel reactivation but voltage gated K+ channels are still sufficiently active to oppose depolarization to threshold
could a strong stimulus generate another action potential during the relative refractory period?
yes
do voltage gated K+ channels inactivate?
no. In fact it takes a long time for their channels permeability to return to resting levels as membrane potential hyper polarizes
what explains the brief after hyper polarization of the action potential?
it takes a long time for voltage gated K+ channels to return their permeability to resting levels
what imposes limits on the frequency at which APs can be generated?
the refractory periods and the after hyperpolarization
why are GPs limited to local or short distance?
the electrical current flows passively down the inferior of the axon and leaks through the membrane. So, if there was along distance, the amplitude of the potential change decreases
how can you make an AP travel further?
1: have voltage gated channels along the fiber so the AP is always being boosted
2: insulate the axon with myeline to decrease the decay of signal
what is the area in between balls of myeline called?
nodes of ranvier
how spaced apart are the nodes of ranvier?
every 1-2 mm
where are voltage gated Na+ and K+ channels found on a myelinated axon?
only at the nodes
why is the speed of transmission greatly increased on a myelinated axon?
because only the voltage gated channels within the nodes need to be activated
what conduction velocities can the fastest myelinated axons reach?
velocities of 80-120 m/sec
what is saltatory conduction?
the node to node transmission that occurs in myelinated axons
what also affects conduction velocity?
axon diameter - larger axons have less longitudinal resistance and thicker myelin
how do neurons communicate with eachother or with other targets like muscles and glands?
via synapses
what are the 2 basic types of synapse?
1: electrical synapses (gap junctions)
2:chemical synapses (release NT)
what are gap junctions or electrical synapses?
transmembrane channels that join to connect the interior of one cell with the interior of another
what is the direction of gap junctions?
they are bidirectional
is there a synaptic delay with gap junctions?
no
where may you find gap junctions?
they exist between cardiac and smooth muscle and various types of neurons
what is a chemical synapse (NT release)?
Its are released at axon terminals which then cross a 20-40nm wide synaptic cleft, acting on receptors at the post synaptic membrane
what direction is neurotransmission?
unidirectional : presynaptic-> postsynaptic
what are NTs contained within?
synaptic vesicles
what do synaptic vesicles fuse with?
the presynaptic membrane then contents are released into the synaptic cleft
list the sequence of events for synaptic transmission:
1: AP arrives at axon terminal
2:Voltage gated Ca2+ channels open
3: Ca2+ enters the presynaptic neuron
4:Ca2+ signals to NT vesicles
5:vesicles move to the membrane and dock
6:NTs release via exocytosis
7:NTs bind to receptors
8:signal initiated in post synaptic cell
how are newly formed vesicles loaded with NTs?
through the action of proton (H+) pump transporters
what forms the SNARE complex?
syntaxin and SNAP-25 in the plasma membrane and synaptobrevin in the synaptic vesicle
is there partial fusion of synaptic vesicles?
no. if a vesicle fuses all NTs in the vesicle are released
what is a quantum or quanta?
the amount of NT(s) release by a single vesicle
how is synaptic transmission halted?
1: transporters on the presynaptic membrane can remove NT from the synaptic cleft and recycle it
2:at the neuromuscular junction a NT (acetylcholine) can be broken down by an enzyme (acetylcholinesterase) and the choline is then transported and used to synthesize more acetylcholine
what does the action of NTs on the postsynaptic membrane lead to?
synaptic integration
what does the NT released from synaptic vesicles produce?
graded potentials that can either transiently depolarize (EPSP) or hyper polarize (IPSP)
what is the most common excitatory NT in the CNS?
glutamate
what is glutamate synthesized from?
the amino acid glutamine
what loads vesicles with glutamate?
vesicular glutamate transporter
how is glutamate removed from the synaptic cleft?
it is transported by excitatory amino acid transporters (EAATs) into astrocytes
what do astrocytes convert glutamate into?
glutamine (via the enzyme glutamine sythetase)
how is glutamine then transported back to the presynaptic neuron where its converted into glutamate?
by the enzyme glutaminase
where does glutamate primarily act at for excitatory NT?
the post-synaptic AMPA receptors
what happens when glutamate binds to AMPA?
a channel allows Na+ to enter the post synaptic neuron, leading to depolarization
what is another type of glutamate receptor?
NMDA receptors
what are NMDA receptors permeable to?
Na+ and Ca2+
what can Ca2+ act as? and what can it affect?
an intracellular second messenger. it can affect mechanisms (including gene expression)with long term consequences (ex. long term potentiation that has been associate with learning and memory)
under resting conditions what is the NMDA receptor blocked by?
Mg2+
how does the NMDA receptor get unblocked?
to remove the Mg2+ requires that the receptor is depolarized (e.g by AMPA receptors)
what does activation of NMDA receptors require?
the presence of a co-transmitter glycine
what do EPSP produced only by AMPA receptors look like?
brief
what do EPSP produced by AMPA and NMDA receptors look like?
longer duration
what is the most common inhibitory transmitter?
GABA
what is GABA synthesized from?
by the enzyme GAD
how is GABA loaded into synaptic vesicles?
by the vesicular GABA transporter (VGAT)
what do GABAa receptors do?
increase the influx of Cl-
what do GABAb receptors do?
increase the influx of K+ through K+ channels
what type of receptors are GABAa, AMPA, and NMDA receptors?
inotropic receptors
what type of receptors are GABAb?
metabotropic receptors
what is required for an effect to occur for inotropic receptors?
requires transmitter to be bound to the receptor
how does a metabotropic receptor work?
it typically involved G-protein activation that either directly or indirectly influences ion channel permeability or other intracellular processes
what are the sites on GABAa receptors where drugs can bind and have effects?
benzodiazepineszepenes (tranquilizers)
barbiturates (anesthetic effect)
alcohol
what does the amplitude of a EPSP depend on?
the strength of the signal arriving at the synaptic terminal which affects the amount of NT (glutamate release)
how can EPSPs summate?
if they are produced quickly enough this is called temporal summation
what is spatial summation?
multiple inputs
what effect can IPSPs have on EPSPs?
they can prevent EPSPs from reaching threshold (postsynaptic inhibition)
