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35 Cards in this Set
- Front
- Back
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Otto Loewi |
Vagusstoff - Acetylcholine discovery (slows heart rate, causes excitation of skeletal muscles)
Discovered first NT |
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Henry Dale |
Described different types of cells that produce NT (cholinergic - ACh, etc.)
NT criteria
1) Synth and stored in PrS neuron 2) Released from AxTerm upon excitation 3) Mimics other NTs |
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Electrical synapses |
Communicate via gap junctions |
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Chemical synapses |
Most synaptic transmission
- NT crosses SynCleft binding to PoS neuron, leading to direct or indirect change in MemP |
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What is the process by which an AP arriving at the AxTerm causes the release of NT at a synapse? |
PrS AP depolarizes the SynTerm, leading to release of NT via exocytosis, then the NT binds to receptors on PoS which alters ionic permeability of PoS, leading to changes in MP. |
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What is the time between a PrS AP arriving at AxTerm, and detection of PoS AP |
0.5 msec |
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Fusion takes |
60 microseconds |
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Define the proteins involved in vesicle fusion |
SNARE Protein system
Synaptobrevin Syntaxin SNAP-25 Synaptotagmin |
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Define the role of synaptogagmin |
Calcium binding protein (2 sites) that triggers vesicle fusion once calcium has entered the voltage sensitive calcium channel.
i.e. a calcium sensor |
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Where does the energy from vesicle fusion come from? |
ATP |
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What is the name of the ATPase that hydrolyzes ATP to allow vesicle fusion to occur? |
NSF (n-ethylmaleimide sensitive factor) |
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How is the vesicle membrane removed from the presynaptic plasma membrane?
Energy source and relevant proteins/enzymes. |
GTP - Energy source Dynamin - GTPase involved in endocytosis. |
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What would happen if you gave a patient a dynamin-inhibitor? |
Dynamin is a GTPase involved in the reuptake of NTs.
If dynamin isn't functioning, than NTs will remain at the synaptic cleft, which allows them to continue acting on the PoS cell prolonging activity.
Dynamin-antagonist = NT-agonist |
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In what ways can NTs be removed from the synaptic cleft? |
Diffusion, enzymatic degradation, reuptake to PrS neuron. |
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How is ACh removed from SynCleft? |
Acetylcholinesterase - AChE
Breaks down AChE so that the AChR does not desensitize (which would lead to paralysis)
Can degrade 25k per second.
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Larotoxin |
From black widow spiders. Causes mass exocytosis of vesicles (including ACh), independent of Ca2+ content. |
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Sarin |
ACh inhibitor, prevents degradation of ACh (by interfering with acetylcholinesterase) causing mass muscle depolarization
(Recall that acetylcholinesterase degrades ACh after it's work is done in the cell, allowing muscles to relax, when that is inhibited, muscle depolarization happens at an alarming rate, causing death by paralysis of diaphragm muscle, ceasing breathing. asphyxia) |
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alpha bungarotoxin |
From the cobra snake, binds irreversibly to nicotinic receptor of ACh in the NMJ. Causes death by paralysis. |
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Toxin from Clostridium |
(Anaerobic bacteria) releases toxins causing botulism and tetanus
Proteases that cleave core SNARE complex proteins used for vesicle fusion (inhibits ACh from being released, thus no muscle excitation is possible). |
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Curare |
Naturally occurring poison used in poison darts - blocks AChR channels from opening, causing paralysis. |
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Organophosphates |
Like DTT, insecticide, inhibits AChE (acetylcholinesterase) causing neuromuscular paralysis by causing a buildup of ACh in the synaptic cleft causing excessive depolarization of the PoS, refractory to subsequent activation. |
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Define and describe how an EPSP can occur |
Excitatory post synaptic potential - Increases cell permeability to Na and Ca, reduces permeability to K.
Depolarizes neurons |
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IPSP |
Inhibitory post synaptic potential - Increases permeability to Cl ions.
Hyperpolarizes neurons |
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Define and describe synaptic integration |
The concept that IPSPs and EPSPs can summate to create or inhibit an AP from occurring, depending on which prevails. |
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Spatial summation |
APs arriving from multiple terminals |
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Temporal summation |
Multiple APs traveling down one axon staggered
(Rapid firing causes repeated depolarization of membrane, w/o time to go back to resting place) |
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What is the amount of time that a PSP will last at a given membrane location?
Time constant |
tau = membrane resistance * membrane capacitance
Temporal summation
The time it takes for constant applied voltage to build up to 63% of its final value. |
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What is the length constant and how can it be calculated? |
lambda = membrane resistance / resistance of cytoplasm
Spatial summation
It is the distance aling a neurite at which a constant applied voltage will decay to 37% of its original value
The greater the membrane resistance, (i.e. the fewer channels open), the longer the PSP travels for. |
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Define and describe presynaptic inhibition |
Generally: prevents NT release in one presynaptic axon terminal. i.e. selects which targets are activated.
AP is generated, but is stopped at only one of many terminals. |
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Define postsynaptic inhibition |
AP is blocked from happening at cell soma, inhibitory neuron generates IPSP which prevents AP from occurring. Blocks NT release at all targets. |
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Define shunting inhibition |
Prevention of current flow from soma to axon hillock
Garden hose analogy |
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How is GABA synthesized? |
Glucose, pyruvate, glutamate --> GABA via GAD (glutamic acid decarboxylase) |
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What is GAD and what does it do? |
glutamic acid decarboxylase
Converts glucose, pyruvate, and glutamate to GABA and needs vitamin B6 to have activity.
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What can a vitamin B6 deficiency cause? |
Reduced GABA production (GAD requires B6), so reduced inhibitory activity (seizures, etc.) |
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What is the basic structure of a GABA receptor? |
Remember the isoforms (each subunit can be encoded by any of several genes, and different subtypes) 6 alpha 3 beta 2 gamma |
