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25 terms

C&T: Membrane Physiology - Synaptic Transmission

Cards cover material taught at the University of Michigan Medical School, 2013-14. Learning Objectives 1. Describe the mechanism by which depolarization of the presynaptic terminal causes release of neurotransmitter. 2. Define EPSPs and IPSPs and explain how they are generated. 3. Describe the difference between ionotropic and metabotropic neurotransmitter action. 4. Define temporal and spatial summation in the postsynaptic cell, and explain the mechanism of synaptic integration. 5. Explain how…
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Ca2+
Depolarization of the presynaptic terminal opens voltage-gated ion channels that permit the influx of this ion.

After binding with calmodulin, the ion-calmodulin complex causes vesicles (1-2) filled with neurotransmitter to migrate towards the presynaptic membrane. After vesicles fuse with the membrane, they release their neurotransmitter contents (1 quantum = several hundred) into the presynaptic terminal.
Depolarization
In the post-synaptic cell, neurotransmitter binds to receptors on gated-ion channels.

If the neurotransmitter opens non-selective cation channels, increases g(nscc) - both Na and K move across - but more Na, the opening will lead to this kind of change in membrane potential.
Hyperpolarization
In the post-synaptic cell, neurotransmitter binds to receptors on gated-ion channels.

If the neurotransmitter opens votage-gated K channels, increases g(K), the opening will lead to this kind of change in membrane potential.
Depolarization or hyperpolarization (depending on value of E(Cl) relative to resting potential)
In the post-synaptic cell, neurotransmitter binds to receptors on gated-ion channels.

If the neurotransmitter opens votage-gated Cl channels, increases g(Cl), the opening will lead to this kind of change in membrane potential.
Excitatory PostSynaptic Potential (EPSP)
Depolarizing change in membrane potential tends to move V toward threshold for action potential; thus, it is known by this name.


*It actually pushes current toward the Trigger Zone.
Inhibitory PostSynaptic Potential (IPSP)
Hyperpolarizing change in membrane potential tends to move V away from the threshold for action potential; thus, it is known by this name.

*It actually attracts current away from the Trigger Zone.
IPSP (hyperpolarization)
If the neurotransmitter opens chloride channels, the effect depends on whether E(Cl) in the postsynaptic cell is more negative or more positive than resting potential.

If E(Cl) is more negative then resting potential, this potential will result from receiving a presynaptic action potential.
EPSP (depolarization)
If the neurotransmitter opens chloride channels, the effect depends on whether E(Cl) in the postsynaptic cell is more negative or more positive than resting potential.

If E(Cl) is more positive then resting potential, this potential will result from receiving a presynaptic action potential.
Ionotropic
This is a binding site for neurotransmitter that is located on the channel itself - DIRECT action.

*faster action, but lasts shorter
Metabotropic
This membrane protein binds neurotransmitter, and then the receptor activates an intracellular G-protein, which either effects the gated-ion channel itself or uses secondary messengers to activate the channel - INDIRECT action.

*slower action, but lasts longer
voltage-gated Na channel
Neurotransmitters can also close channels. Hyperpolarization would result from closing this voltage-gated ion channel.

*opposite of opening effect
Termination of transmitter action
- Diffusion away into extracellular fluid
- Reuptake by active transport into presynaptic cell for re-use
- destruction by enzymes in the synaptic cleft or on post synaptic membrane (ex. acetylcholinesterase)
Neurotransmitters
These molecules are classified in this group.
Temporal Summation
Refers to ONE presynaptic cell firing multiple action potentials. These build up in time post-synaptically. They add up and push V towards the AP threshold.
Spatial summation
Refers to MULTIPLE presynaptic terminals firing at the same time. These add up to a total potential that pushes toward the AP threshold.
Integration
Refers to the totality of signals moving at the trigger zone. There may be excitatory signal and an inhibitory signal, or multiple of each. The excitatories push current toward the TZ, while inhibitatories pull current away from the TZ. The balance of all inputs dictates cellular response.
Determinants synaptic activity
- distance from trigger zone
- geometry of cell (length constant depends on cell geometry)
Diversity of postsynaptic receptors (common ligand)
This is how the same neurotransmitter can induce an excitatory or inhibitory response. Some will activate an AP, some will inhibit it.
Presynaptic inhibition
Neuron C prevents the influx of calcium needed for vesicle fusion and neurotransmitter release (A -> B).
AP frequency
This is a function of graded potential at the trigger zone.
Afferent neurons
These types of neurons can have sensory membrane can be on the endings of the neuron or on a separate receptor neuron.
Neuromuscular junction
This synaptic transmission is always EXCITATORY and NON-INTEGRATIVE.

Many more vesicles full of Acetylcholine (ACh) are released.

ACh receptors are on non-selective cation channels in the postsynaptic membrane at the motor end-plate.

Since once AP invades all terminals simultaneously, there is a LARGE (>20mV) end-plate potention (EPP) in the postsynaptic cell - ALWAYS REACHES AP in the postsynaptic cell

*Major differences with two neuron synapse are capitalized
Electrical synapse
This synaptic transmission exists through gap junctions, allowing a quick signal to be passed from one cell to another.

Advantage: much faster - allowing multiple cells to work together.

Disadvantage: no integration of signals (major regulator feature). However, regulation of these junctions can come from upstream horomones or neurotransmitters.
Synaptic transmission
This process is generalized in the picture.
Insulin pathway
Increase glucose -> increase ATP -> close K channels (depolarization) -> open calcium channels (vesicle fusion) -> insulin release