Synaptic Transmission Flashcards
Dendrites
receive information from synapses or stimulus and “passively” propagate
postsynaptic potentials
Axon hillock
site of action potential activation in
response to integration (summing) of passive postsynaptic potentials that
depolarize the cell above a threshold
Axon
conducts signals in the form of action potentials
Synapse
transmits signals to down stream partners that allows rapid cell-to-cell communication
Synaptic modulation
allows for both robust function as
well as higher levels of complexity including learning and memory
Electrical Synapse
Current flows from the presynaptic neuron into postsynaptic neuron via the electrical connection of the gap junction; current passing through one neuron during depolarization will be passed onto the adjacent neuron
- FAST (responsible for reflexes where transmission must be <ms)
Gap junction
a hemi-channel made of 6 connexins that can close in response to modulatory
factors like:
- low pH
- elevated Ca2+
- voltage- gated
- chemical neurotransmitters
allow for simple electrical connection between pre and post-synaptic neurons
Escape Reflexes
FAST synaptic transmission <1ms
Graded response
dependent on number of gap junctions and size/morphology of neurons
Limitations of electrical synapses
- transmission signal dependent on morphology/size of communicating
cells - no amplification of signal possible
- limited modulation of signal strength
- can not flip the sign of the response so post-synaptic neurons follows presynaptic neuron (cannot have an inhibitory response in postsynaptic neuron upon excitatory stimulus in presynaptic neuron)
Chemical synapse
Signal transmitted across synaptic cleft (~20-40 nm) by diffusion of a neurotransmitter
Benefits of chemical synapses
- SLOWER than electrical synapse (a few ms) but still FAST
- HIGHLY directed (to a single receptor cell i.e one postsynaptic neuron)
- AMPLIFICATION of signal possible (one vesicle contains 1000s of NT and can open 1000s of postsynaptic channels) which can be modulated
- can be excitatory OR inhibitory (depending on what receptors are present and what channels are open/closed)
Active zone
site on the presynaptic neuron where NT-containing vesicles are released
SNARE Complex
organization of proteins that when extracellular calcium enters the cell, causes fusion of NT-containing vesicles and release of NTs
What occurs after an action potential?
voltage-gated calcium channels open and NT release can be done; calcium MUST be around in order to release NT
What causes voltage-gated calcium channels to open?
Depolarization of the presynaptic neuron
Process of NT release
SNARE proteins form SNARE complex–> pull vesicle close to membrane and pull membranes of pre and postsynaptic neurons together -> calcium influx changes conformation of SNARE complex –> fusion and exocytosis of vesicle and NT release
Botulinum Toxins
proteases that
inhibit neurotransmitter release by
cleaving the SNARE protein; muscle unable to contract for lack of neurotransmitter, and relaxes; result is temporary muscle rigidity
Neurological Disorders with ineffective synaptic transmission
- Parkinson’s disease
- writer’s cramp
- neck muscle spasm
In which way is calcium critically implicated in synaptic transmission?
A. Calcium is the prime activator of
G-proteins.
B. Influx through voltage-gated Ca
channels couples electrical
excitation to the activation of
the SNARE proteins that initiate
exocytosis.
C. Ca-coupled transporters clear
the released neurotransmitter
from the synaptic cleft.
D. The opening of post-synaptic
channels requires that the level
of intracellular calcium be
elevated.
B. Influx through voltage-gated Ca
channels couples electrical
excitation to the activation of
the SNARE proteins that initiate
exocytosis.
Quantal Release
post-synaptic electrical recording
without stimulation; random fluctuations in membrane potential can cause fusion of individual NT-containing vesicles sitting at the membrane
Mini End-Plate Potential (MEPP)
post-synaptic response to spontaneous release of one vesicle with NO stimulation
End-Plate Potential (EPP)
the summation of many MEPPs (many vesicles) in response to an action potential
Quantal content
of MEPPS per EPP (tells indicates the quantal content of ONE vesicle or one MEPP)
1 quantum of NT
has 1000s of NT per vesicle
Synaptic plasticity
Vesicle release can be modulated to control synapse strength
Fates of NT released into synaptic cleft
- diffusion
- reuptake
- degradation
MEPP’S (Miniature end Plate
Potentials):
A. Are recorded in the axon
innervating the muscle.
B. Can be recorded when the
axon is cut off from the
muscle.
C. Result from the release of
100’s of vesicles from the
presynaptic terminal.
D. Are recorded from the
muscle (postsynaptic cell).
D. Are recorded from the muscle (postsynaptic cell).
Ionotropic receptors
the channel ITSELF in the membrane is the receptor, and binds NT to open up the channel
- FAST response
Metabotropic receptors
relies on a signaling cascade that eventually opens the channel; can bind NT, activate other proteins and result in opening of many channels to get more or less AMPLIFICATION depending on needs
- SLOWER, but longer lasting effects
- can MODULATE/MAINTAIN effects (i.e attention, learning/memory…)
- typically G-protein coupled signaling pathway
Excitatory postsynaptic potential
(EPSP)
Depolarization above threshold that will
trigger an action potential
Ex:
- voltage-gated Na+ channels
Inhibitory postsynaptic potential (IPSP)
hyperpolarizing the cell making it more difficult to reach threshold and trigger an action potential:
Ex:
- voltage-gated K+ channels
- opening Cl- channels (Cl- only moves around when coupled with depolarization bc ECl- is close to RMP)
Major inhibitory neurotransmitter(s)
GABA, Glycine
GABA a receptors
ionotropic receptor that opens a Cl- channel
GABA b receptors
indirectly (metabotropic) activates K+ channels through a second messenger. K+ efflux hyperpolarizes the cell
Glycine receptors
ionotropic receptors that opens a Cl- channel
Post-synaptic responses:
A. Are amplified by
ionotropic receptors.
B. Are of fixed amplitude
(similar to action
potentials).
C. Sum up to make an
Action Potential.
D. Can be modulated to
change the response
size
D. Can be modulated to
change the response
size
Neuromuscular Junction (NMJ) muscle innervation
- innervated by ONE motor neuron
- One action potential in motor nerve causes activation of the muscle
- no summation
- strong synapses
- EPP as large as 70 mV (larger than an AP) to ensure “one-to-one” transmission with a safety factor of
1.5-4
2 modes of Synaptic integration
convergence and divergence
Convergence
many synapses from many presynaptic cells can affect a SINGLE postsynaptic neuron
- allows information from many cells to influence one cell’s activity
Divergence
a single presynaptic neuron can branch out to affect MULTIPLE postsynaptic neurons
- allows one cell to affect multiple pathways
Postsynaptic temporal summation
stimulation of MULTIPLE action potentials at ONE synapse that arrive at the synapse at DIFFERENT times can add onto one another to generate an AP in the next neuron
- slower recovery of the postsynaptic response allows for another AP to be fired
Postsynaptic spatial summation
addition of MULTIPLE inputs from different LOCATIONS on the neuron
Can inhibitory inputs summate?
YES
Synaptic Integration:
A. Is not needed to fire the
post-synaptic interneuron
(i.e. one synapse is enough).
B. Does not work because the
post-synaptic response is of
a fixed amplitude and can
not be summed.
C. Effectively weights the
influence of each synapse
based on where it is on the
dendritic tree.
D. Weights all synapses equally
because they all have the
same post-synaptic
response.
C. Effectively weights the
influence of each synapse
based on where it is on the
dendritic tree
- closer to cell body = stronger response
Application of Botulinum Toxin
at the neuromuscular junction will:
A. Reduce the release of
acetylcholine from the
presynaptic terminal in
response to an AP.
B. Enhance muscle
contraction in response to
an AP.
C. Inhibit Ca Influx through
voltage-gated Ca channels.
D. Reduce the size of the
MEPP if one was to occur
A. Reduce the release of
acetylcholine from the
presynaptic terminal in
response to an AP.
Many inhibitory synapses operate by inducing an increase in
chloride conductance in the post-synaptic membrane. The
outcome is that:
A. The cell is strongly
hyperpolarized by the resulting
Cl- influx, which is driven by its
greater extracellular
concentration.
B. The cell hyperpolarizes because
of the compensatory activation
of the electrogenic Na+/K+
ATPase
C. The threshold voltage at which
Na+ channels open is now raised.
D. Vm tends to remain near the
resting level, which is close to ECl,
thus opposing other excitatory
influences.
D. Vm tends to remain near the
resting level, which is close to ECl,
thus opposing other excitatory
influences.
