Synaptic Physiology I, II, and III Flashcards
Electrical synapses are mediated by _________ junctions.
gap
Gap junctions are composed of __________.
six connexins
Describe how electrical synapses work.
Depolarization of the presynaptic neuron passes through the cytoplasm – which is continuous with the postsynaptic neuron.
List four advantages of electrical synapses.
1) They are faster than chemical synapses.
2) They are bidirectional.
3) They require fewer “moving pieces” – i.e., they are simpler.
4) It is easier (than in chemical synapses) to trigger synchronous activity.
Charcot-Marie-Tooth X results from a defect in the gene coding for __________.
connexin
List four disadvantages or limitations of electrical synapses.
1) They can only be excitatory.
2) It is difficult to integrate signals.
3) Signals cannot be amplified.
4) No learning or modulation of signals can take place.
What triggers exocytosis of neurotransmitters in the presynaptic neurons of chemical synapses?
Calcium entry, which itself occurs upon depolarization of the axon terminus; calcium binds to synaptotagmin on the vesicle surface, which triggers exocytosis
Describe the cellular pathology of myasthenic syndrome.
The body makes antibodies to the presynaptic calcium channels, preventing synaptic communication.
What are the important protein interactions involved in vesicle exocytosis?
Synaptobrevin on the vesicle membrane interacts with syntaxin and SNAP25 on the presynaptic membrane.
What vesicle-membrane protein senses intracellular calcium?
Synaptotagmin
Botox is produced by which bacteria?
Clostridium botulinum
Tetanus is produced by ______________.
Clostridium tetani
Botox and tetanus toxin work by ____________.
clipping SNARE complexes, thus preventing synaptic communication
What does the acronym mEPSP stand for?
Mini Excitatory Post-Synaptic Potential
Mini release is independent of ____________.
action potentials and calcium entry
Vesicles can only be released in ___________.
discrete quanta; that is, the presynaptic neuron cannot release 1.5 vesicles
Minis are not related to __________.
signalling
Describe the principle of the “driving force” in action potentials.
The driving force is the difference between reversal potential and actual potential; this force drives ions into or out of cells.
Intracellular calcium is buffered by _________.
sodium-calcium antiporters and active transport
___________ pinches off a new vesicle from the presynaptic membrane.
Dynamin
Three chemical warfare drugs – ____________ – block acetylcholine esterase.
sarin, cyclosarin, and tabun
__________ blocks the reuptake of dopamine.
Cocaine
Endplates are _____________.
neuromuscular junctions
Nicotinic acetylcholine receptors are found at ___________ and muscarinic acetylcholine receptors are found at ____________.
neuromuscular junctions (skeletal); autonomic nervous system (smooth muscle)
What are the antagonists for nicotinic and muscarinic acetylcholine receptors?
Nicotinic: curare
Muscarinic: atropine
Because of acetylcholine esterase, about ________ of the acetylcholine is consumed on its way from the presynaptic neuron to the postsynaptic neuron.
half
How many muscle fibers does one motor neuron innervate?
At least one, but can be many
How many vesicles are released per action potential at the synaptic cleft?
30 - 100
How many molecules of neurotransmitter are in each vesicle?
5,000 - 10,000
How many molecules of acetylcholine are needed to activate one nicotinic acetylcholine receptor?
Two
One vesicle depolarizes the membrane by about _______; how much depolarization is needed to excite an action potential in the postsynaptic neuron?
1 mV; 30 mV
Curare was originally used by __________.
South American tribal people to paralyze prey
What was the first medical use of curare?
Patient immobilization during surgery
Modern medicines used to immobilize patients include the following: ____________.
rocuronium, vecuronium, pancuronium (all of which are non-depolarizing agents) and succinylcholine (which is a depolarizing agent)
__________ blocks acetylcholine esterase and prolongs signals at neuromuscular junctions; it is used to treat myasthenic syndrome and myasthenia gravis.
Neostigmine
How does fragile X affect dendritic spines?
It lengthens the dendritic spines and decreases their density.
Review the cycle of glutamate/glutamine in central action potentials.
Glutamate passes across the synaptic cleft and activates a postsynaptic depolarization. It is then taken up by glial cells and converted to glutamine by glutamine synthetase. Glutamine is pumped out of the glial cells and taken up by presynaptic dendrites. Glutamine is then converted to glutamate by glutaminase.
What ion do GABA receptors allow through?
Chloride
Other than GABA, what molecules can activate GABA receptors?
Ethanol, barbiturates, benzodiazepines, and neurosteroids
Integration occurs by _____________ summation.
temporal and spatial
List the three types of central synapses.
1) Axo-dendritic
2) Axo-somatic
3) Axo-axonic
What is synaptic facilitation?
The process in which repeated activation leads to accumulation of calcium in the presynaptic terminal; further action potentials will produce greater potentials by the release of more vesicles upon repeated depolarization.
Why does synaptic depression occur?
Because presynaptic terminals use up vesicles, thereby leading to decreased strength of future action potentials
Long-term potentiation and depression occur by the process of ______________.
calcium activating transcription factors for more receptors (in the case of potentiation) and lack of calcium leading to decreased presence of surface receptors
Looking at a graph of time/amplitude, how can you identify summation and facilitation?
Summation = the cell does not repolarize completely between peaks Facilitation = the second peak has a higher amplitude (measured from the new baseline) than the first peak
What are the three possible fates of neurotransmitters after they have bound to the postsynaptic cell?
1) Diffuse into the extracellular fluid/blood (most common in NMJ)
2) Be broken down by enzymes (such as cholinesterase)
3) Be pumped back into neurons or glial cells to be recycled
NMJ (neuromuscular junction) synapses are always __________.
excitatory
The ionotropic receptor on muscle cells allows _____________ through.
all cations (it is a non-selective cation channel)
Describe the principle of the safety factor.
Presynaptic neurons secrete more neurotransmitter than is needed to ensure that a postsynaptic action potential occurs.
Which comes first, synaptic facilitation or depression?
Facilitation
What percent of prepared vesicles are released upon one depolarization?
About 10% (which can recover in five seconds)
Patients with myasthenic syndrome will get stronger with exercise due to __________, while patients with myasthenia gravis will get weaker with exercise due to ____________.
synaptic facilitation; synaptic depression (because the acetylcholine receptors are partially blocked, more vesicles are needed to stimulate a response; thus vesicles are used up faster than unaffected people)
Individual synaptic signals are much _________ in the CNS (as compared to the NMJ in the PNS).
weaker
How do inhibitory synapses work?
They cause ion channels to open that hyperpolarize the cell membrane (often potassium channels).
The main channel opened by glutamate in the CNS is _____________.
a non-selective cation channel
The main channel opened by GABA in the CNS is ______________.
a chloride channel
Importantly, inhibitory and excitatory signals don’t neatly sum. Why?
Some ion channels may open for ions whose equilibrium potential is already at or near the resting potential. As such, those channels won’t produce a big change in potential. However, if those ion channels are more permeable than others, they can prevent other ions from changing the potential as much as they otherwise would.
Which signal is longer, ionotropic or metabotropic?
Metabotropic, because the second messengers persist in the cytoplasm longer than neurotransmitters persist in the synaptic cleft
What two events do NMDA receptors need to be activated?
Presynaptic release of glutamate (which opens the channel gate) and a postsynaptic action potential (which causes the magnesium ion lodged in the channel to leave the cell)
How do NMDA channels allow for conditioning?
Suppose a cell is receiving two signals – a strong, unconditioned stimulus (such as meat to a dog); and a weak, conditioned stimulus (Pavlov’s bell). The weak stimulus can release glutamate to an NMDA channel, but the channel won’t open because the signal is not strong enough to elicit an action potential. Coupled with the UCS, which does elicit an action potential, the NMDA channels associated with the bell open and then release more AMPA channels which can subsequently generate action potentials.
What kind of channel is the glycine receptor?
Inhibitory chloride channel
