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61 Cards in this Set

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EPSP
Excitatory Post Synaptic Potential

A localized depolarization caused when an excitatory neurotransmitter is released by a presynaptic cell and binds to its receptor on the postsynaptic cell, increasing the Na+ permeability causing a localized depolarization of the postysnatpic cell membrane.
IPSP
Inhibitory Post Synaptic Potential

IPSP result from inhibitory neurotransmitter released from an inhibitory neuron that increases Cl- permeability. Example is GABA. The negative charge offsets the EPSP so an action potential does not occur.
Synapse
A junction of a pre-synaptic and a post-synaptic cell.
What happens at a synapse?
The action potential depolarizes the membrane of the nerve terminal (terminal bouton) and activates a voltage-gated Ca2+ channel. Elevated Ca2+ in the cytosol stimulates the release of a neurotransmitter that binds to a receptor that activates a ligand-gated ion channel that can depolarize or hyperpolarize the post-synaptic cell membrane.
What are ionotropic neurotransmitters and what is an example of one?
Directly bind to and activate a "ligand-gated" ion channel.

This results in a rapid change in the voltage gradient across the post-synaptic cell membrane.

Ex: Acetylcholine (Ach) activates a channel that allows Na+ to enter the cell, depolarizing it; GABA activates a Cl- channel that hyperpolarizes the post synaptic cell membrane.
What is the structure of the NICOTINIC Ach receptor?
5 subunits that span the membrane and form a pore. Ach binding causes a conformational change that opens the channel.
What kind of signal is Ach?
Excitatory (EPSP), allows Na+ to enter cell and depolarizes it.
What kind of signal is GABA?
Inhibitory (IPSP) signal, allows Cl- to enter the cell hyperpolarizing it.
What happens to the depolarization or hyperpolarization from each synapse as it travels?
The hyperpolarization or depolarization signals decay of distance (electrotonic).
What is required to produce a sufficient level of depolarization to activate voltage gated Na+ channels in the axon hillock and initiate an action potential?
Combine activity of many synapses
Localized depolarization
Caused when an excitatory neurotransmitter is released by a presynaptic cell and binds to its receptor on the postsynaptic cell, increasing the NA+ permeability causing a localized depolarization of the postsynaptic cell membrane.
What is required to obtain the depolarization needed to stimulate voltage-gated channels in the axon hillock?
Summation of many EPSPs either at the same time, TEMPORAL SUMMATION, or over the surface of the cell, SPATIAL SUMMATION.
Time constant
refers to the time course for the decay of the electrotonic charge of EPSPs
Length Constant
referst to the decay of charge over distance from EPSPs
Threshold
The minimum level of depolarization that will activate voltage gated channels
What happens after the release of neurotransmitter?
It is degraded so stimulation of post synaptic cells only occurs when presynaptic cells are stimulated.
What breaks acetylcholine in the post synaptic membrane and what is taken up by the nerve terminal?
Acetylcholinesterase, acetate and choline
What resynthesizes Ach?
Choline acetyl transferase
What are metabotropic receptors and how long does it take their effects to be felt?
neurotransmitters that bind to a G-protein-coupled receptor. Also known as muscarinic receptors.

The G protein may directly activate an ion channel (adenylyl cyclase) - or - the G protein may activate enzymes that produce second messengers (cAMP) that activate protein kinases. Protein kinases may activate or inhibit ion channels by phosphorylation.

THUS, THE EFFECTS OF METABOTROPIC RECEPTORS TAKE LONGER TO DEVELOP AND LAST LONGER.
What are neuromodulators?
Chemicals that bind to metabotropic receptors
What are the possible outcomes of the binding of ligands to metabotropic receptors?
-Beta and Gamma subunits dissociate to open or close a channel
-The activated G protein activates adenylyl cyclase to make cyclic AMP. CAMP then phosphorylates a channel to produce a prolonged open or closed state.
Can acetylcholine act on both ionotropic (nicotinic) or metabotropic (muscarinic) receptors?
Yes
What are catecholamines derived from and what are some examples of them?
Tyrosine; Dopamine, Norepinephrine, Epinephrine
Do adrenergic, dopaminergic and sertonergic synapses use similar patterns of reuptake and breakdown?
Yes
L-Dopa ameliorates the symptoms of Parkinson's disease because...
It crosses the blood-brain barrier and is converted to dopamine by neurons that contain aromatic amino acid decaroboxylase (AAAD)
From what amino acid is serotonin synthesized?
Tryptophan
What is serotonin?
Also call 5-HT
A neurotransmitter/neuromodulator in the gut, platelets and in the brain. Low levels of serotonin are associated with depression.
What are Selective Serotonin Reuptake Inhibitors (SSRIs) used for?
Prevent reuptake by presynaptic cells and effectively increase serotonin levels at the receptor level.
What degrades serotonin and catecholamines after reuptake?
Monoamine Oxidase (MAO)
How does cocaine work?
Inhibits the reuptake of norepinephrine, dopamine, and of serotonin
How many 5-HT receptors are there and what are the major types?
There are at least 15 5-HT receptors in 7 different classes. The major types exist in 3 classes, each exerting a different effect and include: 5HT-1, 5HT-2, 5HT-3
5HT-1 Receptor
G-protein activates a K+ channel to hyperpolarize post synaptic cell
5HT-2 Receptor
G protein inactivates a K+ channel to depolarize a post synaptic cell
5HT-3 Receptor
Directly activates a Na+ channel to depolarize post synaptic cell
How do motor pathways end?
With the stimulation of skeletal muscle contraction
Skeletal muscle contraction is...
NEUROGENIC, it requires stimulation by a motor nerve.
Where are motor nerves that stimulate jaw muscles located?
Trigeminal Nerve (CN 5) - has both sensory and motor branches
How does the trigeminal nerve resemble spinal nerves?
It contains both sensory and motor fibers.
Where do sensory nerves enter the spinal cord from?
The Dorsal Nerve root of the spinal cord
Where do motor nerves leave the spinal cord from?
The ventral nerve root of the spinal cord. They are large "alpha" motor neurons
What do motor nerve endings release to stimulate muscle contraction?
Acetylcholine
What are the steps in muscle contraction?
1. Action potential propagates along motor neuron to myoneural jct where acetylcholine is released.
2. Ach binds to nicotinic receptors at myoneural jct and produces depolarization termed the "end plate potential"
3. Positive charge propagates electrotonically to activate voltage-gated Na+ channels that propagate action potentials over the muscle fiber membrane (M)
Why does the myoneural junction have increased membrane area?
Folds in the muscle fiber membrane
Stimulus Transmission
The neurotransmitter Ach (ligand) is liberated in large quantities known as quanta (equal to 10,000 to 20,000 molecules), from the nerve terminal.
How is does a muscle contract?
1. The action potential travels down the axon of the motor neuron and depolarizes the nerve terminal membrane.
2. The depolarization of the membrane activates voltage gated Ca2+ channels that allow Ca2+ into the nerve ending. This is the stimulus for neurotransmitter release into the synaptic cleft.
3. Ach binds to Ach receptors in the muscle fiber membrane. The nicotinic Ach receptor is a cation channel that allows Na+ to enter depolarizing the muscle membrane. This depolarization is termed the end plate potential (EPP)
What results from the fact that Ach receptor is poorly selective for Na+ over K+?
Na+ enters the post synaptic cell and the membrane potential becomes more positive (depolarization, red arrow), K+ leaves (black arrow) and partially offsets the depolarization so the EPP is about -15mV.
What results from the EPP being obtained?
Positive charge during the EPP displaces positive charge away from the receptors at the myoneural junction, to voltage-gated Na+ channels in the adjacent membrane called electrotonic propagation. The activation of the voltage gated Na+ channels initiates an action potential that propagates over the entire muscle fiber.
What occurs after the action potential propagated by the voltage-gated sodium channels reaches the voltage-sensing Ca2+ channels?
Activation of the voltage-sensing Ca2+ channels which then activate the Ca2+ - release channels stimulate contraction
What is the sequence of events leading to an action potential in skeletal muscle fibers?
1. Action potential in presynaptic motor axon terminals
2. Increase in Ca2+ permeability and influx of Ca2+ into the axon terminal
3. Release of acetylcholine from synaptic vesicles into synaptic cleft
4. Diffusion of acetylcholine to postjunctional membrane
5. Combination of acetylcholine with specific receptors on postjunctional membrane
6. Increase in permeability of postjunctional membrane to Na+ and K+ causes EPP
7. Depolarization of areas of muscle membrane adjacent to endplate and initiation of an action potential
How does Curare affect neuromuscular junctions?
Blocks Ach receptor and paralyzes muscle. Poison arrow frogs secrete curare in skin secretion. Used for som surgeries
How does myasthenia gravis affect neuromuscular juntions?
Autoimmune disease where antibodies are developed against one's own Ach receptors. Loss of muscle tone
How does botulism affect neuromuscular junctions?
Botulina toxin blocks Ach vesicle exocytosis (weapons of mass destruction)
T-Tubule
Transverse tubule
Invagination of the sarcolemma among the myofibrils
Facilitates the conduction of waves of depolarization
Lie in the plane of the A-I junction in mammalian skeletal muscle
What is a Triad in muscle?
2 terminal cisternate + T-tubule
How does depolarization of the muscle fiber membrane produce muscle contraction?
The action potential propagates over the muscle fiber membrane via voltage-gated Na+ channels
Where does the Ca2+ released into the A-I juction bind to and what results?
Binds to troponin to permit cross-bridge formation between myosin and actin and muscle contraction
What is another name for Ca2+ release channels and why is this so?
"Ryanodine receptors"
Ca2+ release channels bind a plant substance called ryanodine
Where do muscle action potentials propagate and what results?
Along the membrane and down T-tubules. Depolarization activates Ca2+ release channels in the sarcoplasmic reticulum which release Ca2+ to the cytosol where it binds to troponin and promotes cross-bridge formation and muscle contraction.
Muscle Relaxation
-Once Ach has bound to its receptor and depolarized the muscle, an action potential is initiated and contraction occurs.
-Ach binds reversibly to the receptor and will also bind to a nearby enzyme, acetylcholinesterase (Achase) which rapidly breaks down Ach to acetate and choline.
-When nerve stimulation stops, the Ach is broken down and the muscle repolarizes and relaxes
Anticholinesterases
-nerve gasses (weapons of mass destruction)
-Insecticides
Paralytics
Curare
Succinylcholine
Pancruronium bromide