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26 Cards in this Set
- Front
- Back
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Describe the structure of the chemical synapse. |
Chemical transmission is unidirectional with a presynaptic cell, a cleft, and a postsynaptic cell.
A terminal bouton resides at the end of the presynaptic neuron, this contains copious synaptic vesicles harboring neurotransmitter molecules. |
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Describe the structure of the electrical synapse. |
The electrical synapse involves a pair of connexons forming a gap junction (continuous pore) between two cells that is permeable to ions & small molecules. This is a bidirectional flow dependent upon concentration & electrical gradient. This flow is the conduction of the passive electrotonic current aspect of the action potential propagation. |
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Describe the structure of a gap junction. |
Six connexins together form a connexon channel in a cell membrane. A pair of connexons make a continuous pore or gap junction between adjacent membranes. |
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Describe the gap junctions involvement in the conduction of the passive electrotonic current. |
This enables the adjacent cell to become depolarized as the action potential moves close to the gap junction in the initial cell. |
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Explain how chemical transmission is achieved. |
Neurotransmitter molecules are synthesized & packed in vesicles. . . . An AP arrives at the presynaptic terminal. . . . Voltage gated Calcium ion channels open. . . . A rise in calcium ions triggers fusion of synaptic vesicles with the presynaptic membrane. . . . Transmitter molecules diffuse across the synaptic cleft & bind to specific receptors on the postsynaptic cell. . . . Bound receptors activate the postsynaptic cell. . . . Neurotransmitter is being cleaved, is taken up by the presynaptic cell or diffuse away. . . . |
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Describe an ionotropic receptor. |
These involve ion channels that are gated by neurotransmitters binding to the receptor. . . .
This is a fast response of ~1 ms. . . .
Examples include Nicotinic receptors found through the ANS & in skeletal muscle. |
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Describe metabotropic receptors. |
These are G-protein coupled receptors that trigger a second messenger system in order to produce their effect. . . .
This is a slower response of ~minutes. . . . Examples include Muscarinic receptors found in the atria of the heart & are coupled with Heterotrimeric G-proteins. |
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Remember that Post-Synaptic Responses that occur in a neuron as a consequence of the ligand-gating of ionotropic channels are typically produced as a result of what? |
Sodium Ion influx |
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Where do you find Ionotropic receptors? |
Nicotinic receptors in the ANS & Skeletal muscle. |
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Where do you find Metabotropic receptors? |
Muscarinic receptors in the atria of the heart connected to a GPCR. |
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Explain how Excitatory and inhibitory postsynaptic responses can be produced. |
Excitatory responses cause depolarization of the postsynaptic membrane & usually involve sodium or calcium ions through the ionotropic receptor/channels into the postsynaptic cell.
Inhibitory responses keep the membrane negative or hyperpolarized & usually involve the increasing of Potassium efflux or by allowing chlorine ions influx. |
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Describe how synaptic transmission can be modified by drugs. |
Presynaptic terminal - inhibiting the release or fusion of the vesicle contents into the synaptic cleft. . . . Postsynaptic receptor - inhibiting a receptor blocks neurotransmission. . . . Degrading enzymes or the Reuptake process - blocking degradation or reuptake will enhance neurotransmission through higher concentrations. . . . |
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Describe SSRIs |
Selective Seratonin Reuptake Inhibitor.
Stops the reabsorption of seratonin which causes an increased concentration and thus an increase in neurotransmission on the postsynaptic membrane. |
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Define the terms Motor End plate, Motor Unit, Motor Axon, & Muscle fiber. |
Motor end plate is the terminal ends of the axons that form a terminal arborization or a branching to innervate 10-500 muscle fibers. 1 end-plate region per muscle fiber. . . . Motor unit - Motor neuron Axon + Muscle Fiber. . . . Motor Axon - axon of the motor neuron. Muscle fiber - portion of the muscle surrounded by the endomysium. |
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Describe the structure of the neuromuscular junction & how it relates to function. |
Presynaptic | Synaptic Cleft | Postsynaptic
The cleft is ~30-50 nm wide
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Name the neurotransmitter & receptor type that mediate neuromuscular transmission |
Acetylcholine & Acetylcholine receptors |
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Explain what is meant by an 'end plate potential', how it is generated, & how it is important for initiating an action potential in the muscle fiber. |
Chemically induced change in the electrical potential of the motor end plate (the portion of the muscle-cell membrane that lies opposite the terminal of a nerve fiber at the NMJ. . . . .
Nerve impulse > release of neurotransmitter ACh from terminal > binds to receptor on end plate > open channel > influx of Na+ into the muscle cell > depolarizes the membrane > enzyme degrades ACh > channels close > membrane return to resting state. |
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Explain how neuromuscular transmission can be affected and/or inhibited by various agents including toxins, drugs, & antibodies. |
1. Neurotransmitter release by presynaptic terminal
2. Alter reuptake or Degradation 3. Response by postsynaptic cell 4. Image of blocking agents |
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Describe the Acetylcholinesterase inhibitor useful in treating Myasthenia Gravis |
Physostigmine |
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Describe the aspect of neurotransmission inhibited by the Botulinum toxin. |
ACh release due to inability of the vesicle docking at the presynaptic membrane. |
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Describe Myasthenia Gravis, the location of neurotransmitter interference, and the s/sx. |
Myasthenia Gravis - primary autoimmune disorder, that attacks the neuromuscular transmission. Location of assault: auto-antibodies against the nicotinic ACh receptors & muscle-specific TK receptors. These are on the postsynaptic side AKA Muscle. . . . S/SX:dysarthria, muscle weakness, reduced exercise tolerance, SOB, ptosis, more evident at the end of the workday. EXCEPT: muscle strength test is normal.
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Describe Lambert-Eaton Syndrome, the location of neurotransmitter interference, and the s/sx. |
Lambert-Eaton Syndrome is an autoimmune disorder characterized by muscle weakness in the limbs. Location: Antibodies attack the presynaptic voltage-gated calcium channels. S/SX: Very similar to MG yet with autonomic dysfunction, dry mouth, muscle weakness, & hx of small cell lung CA. These usually improve during the day. |
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Describe Botulism, the location of neurotransmitter interference, and the s/sx. |
Botulinum toxin, enough said.
Location: the toxin irreversibly inhibits the vesicle docking at the presynaptic membrane.
S/SX: nausea, vomiting, diarrhea, dry mouth, muscle weakness (low score muscle strength test) |
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Predict the effect of inhibition of Acetylcholinesterase on neuromuscular transmission |
Inhibit the enzyme that breaks down ACh will induce greater neuromuscular transmission. |
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Name a drug used to treat Myasthenia Gravis that inhibits Acetylcholinesterase |
Physostrigmine
Pyridostigmine bromide or Mestinon |
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Explain the purpose of a synapse and the need for synaptic transmission |
Purpose: transmission of information from cell to cell via synapses through either chemical or electrical means. |
