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30 Cards in this Set
- Front
- Back
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What is the definition of a synapse?
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specialized places where the information contained in the electrical activity of a nerve is transferred to another cell
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What are the 4 key elements to a synapse?
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Pre-synaptic element - sending
postsynaptic element - receiving synaptic cleft - space b/w pre and post synaptic delay - time b/w arrive of AP and potential changes in Post |
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What are the two types of synapses? Which is common in Mammals?
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Electrical and Chemical - Chemical is most common
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describe an electrical synapse
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communication via direct passage of current
small cleft (20A) pre and post connected by gap junctions no synaptic delay pre and post elements equal size uncommon in mammals CNS or PNS |
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describe a chemical synapse
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communication via chemical nuerotransmitter (NT)
NT contained in vesicles in pre large cleft (hundreds A) no electrical connection synaptic delay pre- much smaller than post- post contains NT receptors transmission usually unidirectional |
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what is a nueromuscular junction
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the synapse between a motor nueron and a skeletal muscle fiber, also called myonueral junction or motor end plate
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describe the structure of the NMJ
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1. presynaptic ending contains vesicles with Acetylcholine (ACh) contained in active zones that are regulated by voltage-gated Ca channels
2. 500A synaptic cleft 3. postsynapse - muscle membrane has junctional folds which have ACh receptors on the peaks, the peaks are lined up with the active zones. Contains Acetylcholinesterase (AChE) |
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describe the sequence of events during nueromuscular transmission (7)
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1. AP invades pre
2. depolarization opens voltage-gated Ca channels 3. Ca 2+ influx 4. influx causes synaptic vesicles to fuse with plasma membrane and release ACh 5. ACh diffuses across cleft and combines with receptors 6. ACh + receptors causes opening of monovalent cation channels resulting in depolarization called the End Plate Potential (EPP) 7. Muscle membrane surrounding the end plate becomes depolarized, opening the Na+ channels (voltage gated) and an AP is produced which propagates in both directions |
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what is the main function of the end plate potential?
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to stimulate the AP
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What is the equilibrium potential aka reverse potential?
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The membrane potential at which there is no net current due to the action of the transmitter.
It is called the reverse potential b/c if the membrane potential exceeds this level the transmitter induced potential reverses polarity. |
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How is the reverse potential determined?
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determined by the permeability change it produces.
If it increases P of only one ion, the RP will be at the equil potential of that ion. If it increases the permeability of more than one ion its reverse potential will be at somewhere b/w the EqP of the ions involved. |
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What occurs at the NMJ in the absence of nerve stimulation?
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small spontaneous depolarizations referred to as miniature end-plate potentials (MEPPs)
the smallest amount of transmitter that can be released produces a MEPP EPPs are made up of multiples of this quantal MEPP amount |
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What is the size of the EPP dependent upon? how does it fluctuate?
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The extracellular concentration of Ca2+
as Ca2 is reduced EPP becomes smaller. When the EPP can no longer be decreased by reducing Ca the nerve either produces a MEPP or nothing at all. Size of EPP under low extracellular Ca is always some integral multiple of the MEPP |
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What are some properties of NT release at the NMJ
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Each quantum ( 1 vesicles) of NT contains thousands of molecules
Normally an AP releases hundreds of quanta The amount of NT released is in far excess of that required to produce an AP in the muscle |
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Where is ACh stored, what is it made from and how is it's actions stopped?
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synthesized from dietary choline and acetyl CoA. Stored in vesicles until released. it's actions are stopped in the NMJ by AChE.
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What happens to choline after the release of ACh? How do you stop this?
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Choline is taken back up by the presynaptic ending, this uptake is blocked by hemicholinium.
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How do you prolong the action of ACh
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Anticholinesterases.
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What is Myasthenia Gravis? How is it treated?
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An autoimmune disorder in which antibodies are produced against nicotinic ACh receptors.
Nerve terminals are normal but ACh receptors at NMJ are sparse and the junctional folds are shallow. 2 major forms of disease 1- weakness in extra ocular muscles 2 - weakness of all skeletal muscles as the day progesses Treat using cholinesterase inhibitors. |
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What is Lambert-Eaton syndrome? What other health issues is it often associated with?
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A presynaptic defect in which not enough NT are released. Patients have antibodies against the voltage-gated Ca2+ channels in nerve terminals.
Reduction in Ca2+ influx causes reduction in NT release. More than 50% of patients with LES develop small cell lung carcinoma. LES can arrive up to 3 years before lung cancer is diagnosed!!!! |
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How does LES affect MEPPs and EPPs?
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MEPPS are functional and not altered but the EPP amplitude is depressed.
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What toxins and drugs affect the presynaptic AP by blocking Na channels? what is the resulting effect?
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TTX and STX. These Na channel blockers prevent the AP from reaching the presynaptic terminal and inhibit ACh release.
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What toxins and drugs affect the presynaptic AP by blocking K channels? effect?
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TEA (tetraethylammonium) and dendrotoxin (black mamba)
K channel blockers slow repolarization and enhance ACh release by allowing greater influx of Ca2+ since the voltage gates remain open longer. |
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What drugs/toxins affect the presynaptic AP by blocking Ca channels? what is the resulting effect?
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w-conotoxin (snail venom) and some small divalent cations e.g. Co2+
inhibit Ca influx and thereby inhibit ACh release |
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Describe two bacterial toxins that can inhibit NT release.
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Botulinum toxin - inhibits NT release from cholinergenic endings (both somatic and autonomic) by entering nerve ending and cleaves proteins related to vesicle fusion and exocytosis (no more vesicles!)
Tetanus toxin (lockjaw) - toxin enters peripheral nerves and travels to spinal cord where it ends up in inhibitory nuerons, inhibiting glycine release by cleaving proteins related to vesicles fusion. Glycine normally inhibits muscle contraction by inhibiting alpha-motonuerons. Therefore this toxin causes EXCESSIVE ACTIVITY |
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what are the effects of Agonist carbamylcholine or succinylcholine on nicotinic ACh receptors?
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can produce flaccid paralysis.
both activate the ACh receptor and both are resistant to AChE hydrolysis resulting in prolonged opening of the ACh channels and a prolonged depolarization of the muscle. initially there is excitation and tremors followed by relaxation due to the inactivation of voltage-gated Na channels in the muscle membrane because of the prolonged depolarization. Eventually the ACh receptors desensitize, further inhibiting synaptic transmission. |
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What is another drug/toxin that can produce flaccid paralysis? How is this different from the agonists carbamylcholine and succinlycholine?
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d-Tubocurarine (curare) is an ANTAGONIST. Acts as a competitive inhibitor of ACh binding but does not produce depolarization.
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What is the effect of inhibition of AChE on the EPP?
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Amplifies the End PLate Potential.
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Name and describe two reversible inhibitors of AChE
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Physostigmine and neostigmine.
inhibition of AChE prolongs the duration and increases the amplitude of the EPP these agents are slowly hydrolyzed and eventually lose effectiveness |
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what compounds act as IRREVERSIBLE inhibitors of AChE
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organphosphorous compounds.
produced excessive enchancement of cholinergic transmission. produce death by flaccid paralysis of respiratory muscles due to depolarization blockade. make lethal nerve gases i.e. Sarin |
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name a naturally found organophosphorous nuerotoxin? where is it found?
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Anatoxin-a. manufactured by blue-green algae (cyanobacteria) and often responsible for the poisoning of animals who drink from contaminated ponds.
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