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113 Cards in this Set

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What is a synapse?
A junction that mediates information transfer from one neuron to another neuron or to an effector cell
1. Presynaptic neuron
2. Postsynaptic neuron
1. Presynaptic neuron – conducts impulses toward the synapse

2. Postsynaptic neuron – transmits impulses away from the synapse
What are the 5 types of synapses?
1. Axodendritic
2. Axosomatic
3. Axoaxonic
4. Dendrodendritic
5. Dendrosomatic
Differentiate btw the 5 types of synapses?
1. Axodendritic – synapses between the axon of one neuron and the dendrite of another

2. Axosomatic – synapses between the axon of one neuron and the soma of another

3. Axoaxonic (axon to axon)

4. Dendrodendritic (dendrite to dendrite)

5. Dendrosomatic (dendrites to soma)
Discuss Electrical synapses?
They are less common than chemical synapses and they correspond to gap junctions found in other cell types
What are the 4 roles of electrical synapses in the CNS?
1. Arousal from sleep
2. Mental attention
3. Emotions and memory
4. Ion and water homeostasis
Discuss chemical synapses?
They are specialized for the release and reception of neurotransmitters
What are the two parts of chemical synapses?
1. Axonal terminal of the presynaptic neuron, which contains synaptic vesicles

2. Receptor region on the dendrite(s) or soma of the postsynaptic neuron
What are the 6 differences between electrical and chemical synapses?
1. Electrical have a 3.5nm distance btw pre & post synaptic cell membranes and chemical has 20-40nm

2. Electrical have cytoplasmic continuity btw pre & postsynaptic cells and there is none for chemical.

3. Electrical have gap juntion channels and chemical have presynaptic vesicles & active zones and postsynaptic receptors as ultrastructural components.

4. Electrical have ion current as their agent of transmission and chemical uses chemical transmitters.

5. Electrical have no synaptic delay & chemical have for 1.5ms or longer.

6. Electrical have a bidirectional mode of transmission and chemical have a unidirectional mode of transmission.
Differentiate btw current flow at:
1. electrical synapses
2. chemical synapses.
1. At an electrical synapse, some of the current injected into a presynaptic cell escapes through resting ion channels in the cell membrane. However, some current also flows into the postsynaptic cell through gap junction channels.

2. At chemical synapses, all of the injected current escapes through ion channels in the presynaptic cell. However, the resulting depolarization of the cell activates the release of neurotransmitter molecules packaged in synaptic vesicles, which then bind to receptors on the postsynaptic cell and lead to open ion channels that initiating a change in membrane potential in the postsynaptic cell.
What is a gap-junction channel?
A gap-junction channel is a pair of hemichannels, one in each apposite cell, that structurally connects electrical synapses of two cells where they match up in the gap junction through homophilic interactions and it provides a direct means of ion flow between the cells. This bridging of the cells is facilitated by a narrowing of the normal intercellular space at the gap junction
Distinguish between a connexon and a connexin?
-Connexons are the hemichannels of a gap junction and they are made up of six identical connexins that have 4 membrane spanning regions.

-The connexins have a pore in the center of their structure that is open and when the subunits rotate about 0.9 nm at the cytoplasmic base in a clockwise direction.
What determines the synaptic delay at chemical synapses?
It is determined by the time course of Ca2+ influx in the presynaptic cell and receptor binding of the neurotransmitter.
What happens when there is an action potential in the presynaptic cell?
-The voltage-gated Ca2+ channels in the terminal open and a Ca2+ current flows into the terminal. (Note that the Ca2+ current is turned on during the descending phase of the presynaptic action potential owing to delayed opening of the Ca2+ channels.)

-The Ca2+ influx will then trigger the release of neurotransmitter. The postsynaptic response to the transmitter begins soon afterward and if the response is sufficiently large, it will trigger an action potential in the postsynaptic cell called the excitatory postsynaptic potential (EPSP)
Discuss synaptic transmission at chemical synapses?
-An action potential arriving at the presynaptic terminal of an axon causes voltage-gated Ca2+ channels at the active zone to open and there is a high influx of Ca2+ near the active zone, which causes vesicles containing neurotransmitter to fuse with the presynaptic cell membrane and release their contents into the synaptic cleft.

- The released neurotransmitter molecules then diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane. These receptors cause ion channels to open (or close), thereby changing the membrane conductance and membrane potential of the postsynaptic cell. The complex process of chemical synaptic transmission is responsible for the delay between action potentials in the pre- and postsynaptic cells compared with the virtually instantaneous transmission of signals at electrical synapses.
Discuss synaptic delay?
It is the time needed for a neurotransmitter to be released, diffuse across the synapse, and bind to postsynaptic receptors.
This time is btw 0.3-5.0 ms and it is the rate-limiting step of neural transmission
Discuss neurotransmitters?
-Neurotransmitters are imported into synaptic vesicles by the H linked antiporter system that uses a V pump.

-The synaptic vesicles with the neurotransmitters then move to the active zone and there is vesicle docking at the plasma membrance.

-Due to the high influx of Ca2+, there is exocytosis of the neurotransmitter into the synaptic cleft.

-After the neurotransmitter performs its job, there is reuptake of the neurotransmitter into the synaptic vesicle and the vesicle is coated with clathrin.

-The synaptic vesicle is then recovered via endocytosis and there is uncoating of the vesicle and the process starts back up again.
What are synaptic proteins?
They are proteins that restrain synaptic vesicles to prevent accidental mobilization, they target freed vesicles and dock them to active zones where they are primed for fusion and exocytosis, and the proteins retreive the fused membranes by endocytosis.
Discuss synaptic vesicles and synapsin?
-Synaptic vesicles outside the active zone have a reserve pool of neurotransmitters but they are restrained to cytoskeletal filaments of the terminal by SYNAPSIN.
What is synapsin?
It is a peripheral membrane protein that cross links the vesicles and the nerve terminals.
Synapsin is an endogeneous substrate for what 2 things?
1. cAMP kinase
2. Ca2+/calmodulin -
dependent kinase
What happens to synapsin when nerve terminals become depolarized?
Ca2+ enters the nerve terminals when they are depolarized and synapsin becomes phosphorylated by the Ca2+/calmodulin dependent kinase and the phosphorylation frees the synaptic vesicles from the terminals and they then move to the active zone.
What are RAB3 proteins?
-They are involved in targeting of synaptic vesicles to docking sites for release.
-They bind to GTP and hydrolyze it to GDP in order to efficiently target synaptic vesicles and they also bind to synaptic vesicles through a hydrophobic hydrocarbon group of the Rab ptotein. They are released from synaptic vesicles into the cytoplasm during exocytosis.
What is VAMP?
VAMP resembles a viral fusion peptide
It is also called synaptobrevin and it is an integral protein in the vesicle membrane (V-SNARE) that binds to target receptor proteins (T-SNARES) so that synaptic vesicles dock and undergo exocytosis.
What are the 2 T-SNARES in the brain?
1. SYNTAXIN = a nerve terminal integral membrane protein

2. SNAP-25 = a peripheral membrane protein
Compare synaptotagmin and neurexin?
1. Synaptotagmin is a V-SNARE and neurexin is a T-SNARE and they participate in vesicle docking and an increase in free Ca2+ causes synaptotagmin to cause pore fusion and release of neurotransmitter.
What is NSF protein?
It uncurls the SNARE complex and also functions in membrane fusion with synaptotagmin and this uncurling needs ATP.
What happens to clathrin coat once the neurotransmitter is released?
The clathrin coat of the vesicles is removed and the neurotransmitter is imported back into the vesicle again through endocytosis and there is cycling.
What does Tetanus toxin do?
It cleaves VAMP and inhibits synaptic transmission
Compare :
1. Botulinim toxin A
2. Botulinim toxin B
3. Botulinim toxin C
1. Botulinim toxin A: cleaves

2. Botulinim toxin B: cleaves

3. Botulinim toxin C: cleaves
What does a-Latrotoxin do
It is a spider toxin that binds to and intereferes with neurexins and cause massive vesicle depletion and high transmitter release
What are Neurexins?
Neurexins are a family of cell surface receptors which may also participate in cell-to-cell recognition or in the interaction of the axonal surface with the extracellular matrix.
What is Synaptophysin
It is an integral membrane protein in synaptic vesicles that is phosphorylated by tyrosine kinases and may regulate release.
What is the role of vesicle transporters?
They are involved in accumulation of neurotransmitter within the synaptic vesicle.
What is the role of synaptotagmin in the synaptic cleft?
synapyotagmin causes neurotransmitter to be released into the synaptic cleft via exocytosis.
What happens when a neurotransmitter is bound to a postsynaptic neuron?
It can produce a continuous postsynaptic effect, block reception of additional “messages” and it must be removed from its receptor
What are 3 ways to remove neurotransmitters?
1. Are degraded by enzymes
2. Are reabsorbed by astrocytes or the presynaptic terminals
3. Diffuse from the synaptic cleft
What is Excitatory synapse?
It mainly signals the influx of sodium ions into the postsynaptic neuron and produces a EPSP that depolarizes the neuron and it is always excitatory.
What is Inhibitory synapse?
It signals the outflow of potassium ions from the postsynaptic neuron or the influx of chloride ions into the postsynaptic neuron.
It produces an IPSP, tends to hyperpolarize the neuron and it is always inhibitory.
Are EPSPs and IPSPs graded potentials or action potentials and why is this?
They are graded potentials because there is a decremental spread of graded potentials as the distance increases.
What happens when three excitatory neurons fire?
Their graded potentials separately are all below threshold but when their graded potentials arrive at the trigger zone together, they sum to create a suprathreshold signal and generate an action potential.
What is the effect of an inhibitory potential on two excitatory potentials?
The two excitatory potentials are diminished by summation with an inhibitory potential because the summed potentials are below threshold and no action potential is generated.
Differentiate btw the two types of summation that EPSPs and IPSPs undergo ?
1. Temporal summation – presynaptic neurons transmit impulses in rapid-fire order

2. Spatial summation – postsynaptic neuron is stimulated by a large number of terminals at the same time
What happens if an excitatory presynaptic input (EX1) is stimulated a 2nd time after the 1st EPSP in the postsynaptic cell has died off?
A 2nd EPSP of the same magnitude will occur
What happens if an excitatory presynaptic input (EX1) is stimulated a 2nd time before the 1st EPSP in the postsynaptic cell has died off?
A 2nd EPSP will add onto, or sum with, the 1st EPSP, resulting in temporal summation, which may bring the postsynaptic cell to threshold.
What happens if there is simultaneous activation of two (Ex1 and Ex2) or more excitatory presynaptic inputs?
The postsynaptic cell will be brought to threshold by spatial summation of the EPSPs
What happens if there is simultaneous activation of an excitatory (Ex1) and an inhibitory (In1) presynaptic input?
There will be no change in the postsynaptic potential because the resultant EPSP and IPSP cancel each other out.
Discuss spatial summation
-Spatial summation is when a number of different inputs on the cell are excited at the same time.
Discuss graded potentials and the length constant, lambda
Graded potential decreases the further you get from the site of stimulation and the distance when that graded potential has decreased 37 % of its maximal value(lost 63 % of its initial value) is the lentgh constant, lambda. Any stimulation performed past the length constant cannot be summated.
These inputs have to be close together, less than lambda. If these inputs are far apart, more than lambda, you will not get summation. Graded stimulation decreases the further you get from the site of activation. Lambda is an intrinsic quality of the particular cell itself. (value varies according to cell type).
What must occur in order to get a summation?,
The distance between the synapses have to be less than lambda. The cell on the bottom right has a lambda of 0.1 millimeter, so the synapses have to be less than 0.1 millimeters apart for summation to occur.
What is lambda equal to ?
It is equal to the square root of the membrane resistance divided by the resistance of the tube.
Diff btw Temporal summation and spacial summation regarding action potential?
Temporal summation is an action potential by one input, and spacial summation is an action potential by two different inputs.
Regarding temporal summation, what happens when:
1. a second action potential (A2) occurs too late after the first one(A1)?

2. the second action (A2) potential occurred very soon after the first one (A1)?
1. If the second action potential (A2) occurred too late after the first one(A1) no summation occurs.

2. If the second action potential (A2) occurs very soon after the first one (A1), summation occurs.
Temporal summation is due to what? and what is Tau (T)?
It is due to electrical properties because it is a RC circuit.
Tau (T) or time constant is the lentgh of time the membrane resistance decreases to 63 % of its maximal value(the lentgh of time it takes to decrease to 37 % of its maximal value). It takes some time for the membrane resistance to increase to its maximal value. That second input has to be delivered in less than tau in order to get summation.
What is the effect of a Long (100 ms)and short(20 ms) time constant on temporal summation?
A long time constant(100 ms) will give you temporal summation, as opposed to short time constant(20 ms).
What happens in:
1. A presynaptic cell with an action potential arriving every 2 milliseconds, and the postsynaptic cell having a tau of 1 millisecond?

2. A presynaptic cell with an action potential arriving every 2 milliseconds, and the postsynaptic cell having a tau of 10 milliseconds?
1. The response will die, with no summation.

2. There will be summation.
What does an IPSP regulate?
It regulates the frequency of firing.
What will happen to D and A together if B is presynaptic to A, and will inhibit A, which will inhibit response in C?
D and A together will produce a response because there is no inhibitor involved.
Compare postsynaptic inhibition and presynaptic inhibition?
1. Postsynaptic inhibition occurs over a wide variety of barriers while presynaptic inhibition is more specific.

2. All targets are inhibited equally in a postsynaptic inhibition but in presynaptic inhibition only one target cell is affected.
Why does presynaptic inhibition occur?
Presynaptic inhibition occurs when the Ca2+ current in the terminal of a presynaptic neuron is depressed by a second presynaptic inhibitory neuron.
What are the three possible mechanisms for the presynaptic inhibition?
1. Simultaneous closure of Ca2+ channels and opening of voltage-gated K+ channels, which decreases the influx of Ca2+ and thus enhances repolarization of the cell.

2. Increased conductance to Cl-, which decreases (or short-circuits) the amplitude of the action potential in the presynaptic terminal.

3. Direct inhibition of the transmitter release process independent of Ca2+ influx
What is the effect of presynaptic inhibition on the amount of transmitter released by the first presynaptic neuron?
It reduces the amount of transmitter released by the first presynaptic neuron, so the synaptic potential recorded in the postsynaptic cell is depressed
When does presynaptic facilitation occur?
-It occurs when the K+ current in the terminal of a presynaptic neuron is depressed by a second presynaptic facilitating neuron, leading to an increase in the duration of the action potential.
-Therefore the Ca2+ current causes an increase in transmitter release and this enhances the amplitude of the synaptic potential in the postsynaptic cell
The effectiveness of presynaptic input can be altered by what 2 things?
1.presynaptic facilitation
2.presynaptic inhibition.
Compare presynaptic facilitation and presynaptic inhibition in terms of neurotransmitter release from the presynaptic axon terminal.
Each is influenced by another nearby axon.
1. In presynaptic facilitation, there is enhanced release of the neurotransmitter from the presynaptic axon terminal.

2. In presynaptic inhibition, there is reduced release of the neurotransmitter from the presynaptic axon terminal.

Each is influenced by another nearby axon.
What is the role of Neuropeptides?
- They act mainly as neuromodulators in the sense that they modulate at the synapse,bringing about long-term changes here.

- Also, they are molecules consisting of 2 to 40 amino acids that do not produce EPSPs or IPSPs.
What are the two types of synaptic receptors for chemical synapses?
1. Ionotropic receptors
2. Metabotropic receptors
What are ionotropic receptors?
-They mediate direct gating of ion channels and they are an integral part of the molecules that forms the channel it regulates.

-They are also called receptor - channel or ligand gated channel and they have 5 subunits that each have 4 membrane spanning alpha helical regions. These receptors are involved in fast responses by the neurotransmitters.
What are metabotropic receptors?
-They mediate indirect gating of ion channels and they are separate from the ion channels they regulate. The receptors have 1 subunit with 7 membrane spanning alpha helical regions and they are involved in slow responses because they use a second messenger system.
Describe the second-messenger cascade of metabotropic receptors?
The metabotropic receptors activate a GTP binding protein or G protein and the G protein stimulates adenyl cyclase, which converts ATP to cAMP. The cAMP activates the cAMP-dependent protein kinase (cAMP-kinase), which phosphorylates the channel (P), leading to a change in function.
Describe the muscarinic acetylcholine receptor in the heart muscle plasma membrane?
The receptors are linked by a trimeric G protein to K+ channels. Acetylcholine binds to the receptor and triggers activation of the G(i-alpha) subunit and its dissociation from the G(beta-gamma) subunit. The released G(beta-gamma) subunit binds to and opens the associated effector, a K+ channel, which leads to an increase in K+ permeability, hyperpolarization of the membrane, and reduction of the frequency of heart muscle contraction.

-Though not shown here, activation is terminated when the GTP bound to G(i-alpha) is hydrolyzed to GDP and G(i-alpha)-GDP recombines with G(beta-gamma).
How is the muscarinic acetylcholine receptor terminated?
It is terminated when the GTP bound to G(i-alpha) is hydrolyzed to GDP and G(i-alpha)-GDP recombines with G(beta-gamma).
Describe Nicotinic acetylholine receptors, or nAChRs?
-They are directly gated ionotropic receptors at the neuromuscular junction that form ion channels in skeletal muscles cells' plasma membranes.
- The receptor-channel complex consists of five subunits, all of which contribute to forming the pore. When two molecules of ACh bind to portions of the alpha-subunits exposed to the membrane surface, the receptor-channel changes conformation. This opens a pore in the portion of the channel embedded in the lipid bilayer, and both K+ and Na+ flow through the open channel down their electrochemical gradients but not calcium.

-Each subunit is composed of four membrane-spanning alpha-helices (labeled M1 through M4). The five subunits are arranged such that they form an aqueous channel, with the M2 segment of each subunit facing inside and forming the lining of the pore (see turquoise cylinders). Note that the gamma-subunit lies between the two alpha-subunits.
Distinguish btw GABA A and GABA B?
1. GABA A is ionotropic, and it is inhibitory by letting chlorine ions enter the cell(opens chloride channels).

2. GABA B is metallotropic, and it is inhibitory by letting potassium leave the cell(opens potassium channels, causing hyperpolarization or the G protein can inhibit the calcium channel and this will also hyperpolarize the membrane.
What are the 2 types of ionotropic glutamate receptors?
1. NMDA Glutamate Receptor
2. AMPA Glutamate Receptor
1. What is the NMDA Glutamate Receptor?
2. The dysfunction of the channel is assoc. with what disease?

3. What happens if magnesium is bound to the receptor site?
1. Activation of NMDA receptors results in the opening of an ion channel which is permeable to Ca++, Na+ and K+ ions. It will only open in the prsesence of glycine.

2. Schizophrenia

3. It inhibits the receptor and when the membrane is depolarized sufficiently, it ejects magnesium, and calcium can go in.
What is the AMPA receptor is an ionotropic receptor, and allows sodium to get into the cell.
It is an ionotropic glutamate receptor, that allows sodium and potassium to get into the cell but not calcium.
1. What must bind to the NMDA for the channel to work?

2. What enhances glutamate release?
1.Glycine and also glutamate.

2. Paracrine from postsynaptic cell.
What is the effect of Cocaine on synaptic transmission?
It blocks the reuptake of dopamine, permitting dopamine to remain in the synaptic cleft and continue to interact with its receptor site. Dopamine plays a role in pathways involved in pleasure.
What is the effect of Parkinson’s disease on synaptic transmission?
It is attributed to a gradual destruction of dopamine-secreting neurons, leading to a deficiency of dopamine in regions of the brain that control complex movements.
What is the effect of Strychnine on synaptic transmission?
It inhibits the receptor binding of glycine, which prevents postsynaptic inhibition and convulsion, muscle spasticity and death can result from unchecked excitatory pathways.
What is the effect of Tetanus toxin on synaptic transmission?
It can prevent the release of GABA from neurons that inhibit a-motor neurons. Uncontrolled muscle spasms can result from unchecked excitatory inputs.
Distinguish btw:
1. Convergence of input
2. Divergence of output
1. In convergence of input, one cell is influenced by many others.

2. In divergence of output, one cell influences many others.
What is the neuromuscular junction?
It is a synapse between a neuron and a skeletal muscle fiber.
Differentiatte btw a multipolar interneuron and the motor neuron.
The motor neuron terminates on a muscle fiber, as opposed to a multipolar interneuron.
What happens when a motor neuron reaches a skeletal muscle?
it divides into many terminal branches, each of which forms a neuromuscular junction with a single muscle cell (muscle fiber).
1. What are presynaptic boutons?

2. What does each presynaptic bouton contain?
1. They are multiple swellings that each branch of the motor neuron forms over a specialized region of the muscle fiber membrane, called the end-plate, and they are covered by a thin layer of Schwann cells. Also, they are separated from the muscle membrane by a 100 nm synaptic cleft.

2. It contains mitochondria and synaptic vesicles clustered around active zones, where the acetylcholine (ACh) neurotransmitter is released.
What is immediately under each bouton in the end-plate?
There are several junctional folds, which contain a high density of ACh receptors at their crests.
What does the presynaptic terminal and the muscle fiber secrete into the basement membrane?
The enzyme acetylcholinesterase, which inactivates the ACh released from the presynaptic terminal by breaking it down into acetate and choline.
What is the role of the basement membrane that covers the muscle fiber?
It organizes the synapse by aligning the presynaptic boutons with the postsynaptic junctional folds.
Where is an action potential propagated in a motor neuron?
It is propagated to the terminal button in order to get an end plate potential that will cause local current flow btw the depolarized end plate and adjacent membrane.
What is Curare and Tubocurarine?
-Curare is a plant toxin that blocks the binding of acetylcholine to the nicotinic acetylcholine receptor and prevents the end-plate potential from reaching the threshold for an action potential.
-Tubocurarine is the purified active agent, which blocks neuromuscular transmission by binding to the nicotinic acetylcholine receptor, preventing its activation by acetylcholine.
Why is the synaptic potential considered a graded potential?
The amplitude of the synaptic potential decays with distance from the site of initiation in the end-plate. The decay results from leakiness of the muscle fiber membrane. Since the current leaks out all along the membrane, the current flow decreases with the distance from the end-plate. Consequently, the local depolarization produced by the synaptic potential of the membrane decreases with distance.
Compare the end-plate current and the end-plate potential?
The end-plate current rises and decays more rapidly than the end-plate potential because the synaptic current must first alter the charge on the membrane capacitance of the muscle before the muscle membrane is depolarized.
What happens at the normal muscle resting potential of –90 mV?
The single-channel currents and total end-plate current are large and inward because of the large inward driving force on the current flow through the ACh-gated channels. This large inward current produces a large depolarizing end-plate potential.
What happens at more positive levels of membrane potential in the muscle?
The inward driving force on Na is less and the outward driving force on K is greater. This results in a decrease in the size of the single-channel currents and in the magnitude of the end-plate currents, thus reducing the size of the end-plate potential.
What happens at the reversal potential of the muscle?
The inward Na flux is balanced by the outward K flux, so there is no net current flow at the end-plate and no change in Vm. Further, depolarization to +30 mV inverts the direction of the end-plate current, as there is now a large outward driving force on K and a small inward driving force on Na. As a result, the outward flow of K hyperpolarizes the membrane. On either side of the reversal potential the end-plate current drives the membrane potential toward the reversal potential.
What must occur in order to trigger an action potential at the muscle?
The depolarization produced by the end-plate potential must open a sufficient number of Na channels to exceed the cell’s threshold.
Describe the ACh receptor-channel?
-It has five subunits and it takes two acetylcholine molecules to bind to the receptor site and there is a selectivity pore that has negative charges due to negatively charged amino acids on each subunit so the positive molecules can go through.
What is the effect of black widow spider venom on the neuromuscular junction?
It causes explosive release of acetylcholine
What is the effect of Clostridium botulinum toxin on the neuromuscular junction?
It is a toxin responsible botulism, a form of food poisoning and it blocks release of acetylcholine
What is the effect of Lambert-Eaton syndrome on the neuromuscular junction?
Patients have circulating self produced antibodies against the type of voltage-gated Ca2+ channels present in nerve terminals, and thus experience muscular weakness and diminished stretch reflexes.
What is the effect of curare on the neuromuscular junction?
It reversibly binds with acetylcholine receptor sites
What is the effect of Alpha-Bungarotoxin or snake venom protein on the neuromuscular junction?
It irreversibly binds with acetylcholine receptor sites
What is the effect of Myasthenia gravis on the neuromuscular junction?
Patients have self produced antibodies that inactivate acetylcholine receptor sites so there is severe weakness
What is the effect of orgaphosphates on the neuromuscular junction?
They irreversibly inhibit acetylcholinesterase and prevent inactivation of acetylcholine
What is the effect of Neostigmine on the neuromuscular junction?
Neostigmine is a short-term anti-acetylcholinesterase drug. In myasthenia gravis patients, this drug prolongs the action of ACh at the neuromuscular junction by permitting it to build up.
What is the effect of Tetrodotoxin and saxitonin?
It results in stiffness, inhibiting the skeletal muscle fibers from snails.
What is an adverse effect of BOTOX ?
is very potent. You got Nicotine affecting acetylcholine channels. These toxins either constant contraction of diaphragms or no contraction at all, preventing breathing, resulting in pulmonary problems.
What is the problem in myasthenia gravis?
There is a decrease in the junctional folds, and the number of acetylcholine receptors is decreased, but there is a simplified synaptic fold, a widened synaptic space, but a normal nerve terminal.
What happens as action potentials propagate along an axon?
They produce electric potentials that can be recorded from the surface of the nerve.
What are compound action potentials?
When a nerve bundle is stimulated, many axons produce action potentials synchronously. The resulting electric responses recorded from the surface of the nerve are called compound action potentials to distinguish them from the action potentials generated by individual axons.
What is the role of neostigmine in myastenia gravis? increases the duration of action of ACh at the neuromuscular junction and thus can compensate for the reduced ACh activity in myastenia gravis
-It increases the duration of action of ACh at the neuromuscular junction and thus can compensate for the reduced ACh activity in myastenia gravis by reversing the decrease in amplitude of evoked compound action potentials in myastenic patients.