Flashcards in Synapses and Synaptic Transmission (3) Deck (29):
Electrical synapses allow rapid(no delay), bi-directional transmission, but what does it require to work (other than gap junctions)
Requires matching between the size of pre- and post- synaptic cells
What three properties does chemical transmission have?
2. Synaptic delay
3. Can change the sign or amplify a signal
How does depolarization cause release of NT?
Deplolarization of presynaptic membrane opens voltage gated Ca channels; influx of Ca causes vesicle fusion with the membrane (via SNARES) = exocytosis of vesicle contents
What is a quanta?
Minimal amount of NT that can be released. Contents of one vesicle = 1 quanta
How do NT cause alterations in membrane potential on the postsynaptic cell?
Bind to ligand-gated ions channels and either open or close them
What factors allow for a high safety factor at the NMJ (meaning that every time a motoneuron releases NT, all muscle fibers innervated with have an AP and contract)?
There are many release sites for NT, high numbers of receptors, high quintal content, high probability of release for each quanta, and high density of post-synaptic receptors.
Basically : everything is in excess so response is guaranteed
What NT is predominant at the NMJ? What type of receptors does it act on?
Acetylcholine; act on Nicotinic receptors on the postsynaptic membrane
What are 4 differences in CNS synapses as compared to the NMJ?
1. Low safety factor
2. Low quantal content
3. Size of postsynaptic potentials (PSPs) is smaller
4. Many different NTs, so responses can be inhibitory, excitatory or modulatory
What is the significance of the small postsynaptic potentials created in the CNS?
Many PSPs must be summated to reach threshold in for an AP (unlike in the NMJ, where one signal from the motoneuron will cause an AP for sure in physiologic conditions anyhow)
What are the two types of chemical transmission? What structures mediate the effects of each mechanism?
1. Fast transmission ( binding to ligand-gated channels)
2. Neuromodulatory (binding to G-protein coupled receptors)
What do the G protein receptors do to modulate function?
Produce biochemical changes in the cell (2nd messenger systems) that alter function and/or excitability
What are three examples of SNARE proteins?
Which protein does botulinum toxin cleave?
Synaptobrevin; specifically targets GABA synaptic transmission
What does Botox toxin do to cause paralysis?
Prevents release of Ach at the NMJ, so no contractions can be initiated.
What is an EPSP? What typically causes these, molecularly?
Excitatory postsynaptic potential. Generally opening of channels with permeability to cations (which would depolarize the cell and increase the likelihood of an AP occurring
What two molecules are the most common mediators of fast EPSPs in the CNS?
What two things can cause inhibition, or reduce the likelihood of AP firing?
1. Anything that causes hyperpolarization of the cell
2. Shunting of excitatory current (so threshold is not attained)
What is the most common inhibitory transmitter in the CNS?
What is the most common inhibitory transmitter in the spinal cord?
How do glycine and GABA result in inhibition?
Both bind to ligand gated Cl- channels; influx of negative charge hyper polarizes the cell
Why is it essential for neurons to summate inputs?
Because one synaptic input alone is far too small to elicit an AP
What is temporal summation? What determines the time window?
Occurs if two APs are fired close enough together in time that the first PSP hasn't dissipated by the time the second occurs, allowing summation of signals. The time window in which these must occur are due to the membrane time constant (resistance and capacitance properties)
What is spatial summation?
Addition of effects on two different synapses that are close enough in location for their effects to overlap. These must occur in close enough succession, so it's really a temporo-spatial summation that ultimately integrates inputs
What do brain cells metabolize exclusively for energy?
What does most of the energy in the brain used to do?
Run membrane pumps that maintain the essential ion gradients needed for function. ATP and other high energy phosphates are critical.
Why is energy required to maintain proper ion gradients?
Even at rest there is leakage of Na into the neurons and K out of neurons
How is glutamate removed from the synaptic cleft after release?
Astrocytes have 3Na/glutamate secondary active symporter. Uses the Na gradient established by Na/K ATPase to bring glutamate out of the synapse into the astrocyte.
What do astrocytes use to make ATP (process)?
Glycolysis,so produces lactate. Substrates for this are delivered to astrocytes from the circulation.