Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
|
Ia afferents and the myotactic relfex:
• The neuotransmitter released by Ia afferents • The receptor to which the NT binds • The post-synaptic cells (2) the NT incites and the activity it causes • Describe the reciprocal innervation of Ia afferents and how the NT modulates activity of the anatagonistic muscle |
Ia afferents and the myotactic relfex:
• Glutamate • AMPAR, an ionotropic receptor • Motor neuron- depolarization/activation ---> APs and EPSPs Interneuron - depolarization/activation • The activation of interneurons causes them to release Glycine which generated an IPSP on the antagonistic muscle. This insures the antagonistic muscle does not contract at the same time the agonist muscle does during the reflex |
|
|
Ia afferents and the myotactic relfex:
• The neuotransmitter released by Ia afferents • The receptor to which the NT binds • The post-synaptic cells (2) the NT incites and the activity it causes • Describe the reciprocal innervation of Ia afferents and how the NT modulates activity of the anatagonistic muscle |
Ia afferents and the myotactic relfex:
• Glutamate • AMPAR, an ionotropic receptor • Motor neuron- depolarization/activation ---> APs and EPSPs Interneuron - depolarization/activation ---> APs and EPSPs • The activation of interneurons causes them to release Glycine which generated an IPSP on the antagonistic muscle. This insures the antagonistic muscle does not contract at the same time the agonist muscle does during the reflex |
|
|
The motor unit:
• Its components (4) • how the motor unit of fine motor control vs postural motor control differ |
The motor unit:
• a motor neuron cell body, its myelinated axon, the NMJ and the skeletal fiber it iNN • the motor unit of fine motor control has its soma iNN very few (~10) muscle fibers while postural motor control iNN a relatively larger amount of fibers (~2000) |
|
|
Def of motor nucleus
|
A cluster of motor neuron cell bodies distributed over a few segments of the spinal cord
|
|
|
Notable Features of Neuromuscular Transmission:
1) Every muscle fiber has ..... , with the muscle fiber receiving input from ...... 2) The NMJ is the site where ...... is released by ........ and binds to........ 3) Every impulse in a motor neuron evokes ........ and a ......... in every muscle fiber 4) There are no ......... |
Notable Features of Neuromuscular Transmission:
1) has only one excitatory synapse, receiving input from just one motor neuron 2) where ACh is released by Ca2+ dependent exocytosis and binds to ionotropic receptors in the end plate 3) evokes an impulse in every muscle fiber of a motor unit, a twitch contraction in every muscle fiber 4) There are no inhibitory synapses in muscle fibers |
|
|
How the contraction of a muscle fiber is inhibited
|
Since there are no inhibitory synapses in muscle fibers,
then the motor neuron that iNN the muscle must be synaptically inhibited ex. interneuron on a motor neuron |
|
|
The location where a motor neuron is not myelinated
|
Near the muscle fiber, the point at which its axon branches into presynaptic terminals
|
|
|
The Life Cycle of Ach:
• The type of neuron that synthesizes and releases it • The location of Ach synthesis • The enzyme that synthesizes it • The enzyme that degrades it • Where the degrading enzyme is made and released • The product of ACh breakdown and what happens to it |
The Life Cycle of Ach:
• Cholinergic • Cytoplasm of the nerve terminal • ChAT • AChE • Is made in the terminal of the cholinergic cell and released into the cleft • ACh ---> Choline + Acetyl; Choline is recycled through uptake into the synaptic terminal by a Na+/Choline transporter |
|
|
Microanatomy of the NMJ (Part I):
• Define the active zone • Types of channels near the active zone and their fxn • The location of the nACh receptors • The location of ACh-esterase and its significance • |
Microanatomy of the NMJ:
• The site of transmitter release from synaptic vesicles • v-gated Ca2+ channels; facilitate the emptying of NTs from the vesicles and into the cleft • Tips of the jxnal fold at the end plate • It is tethered to the basal lamina and the end plate membrane; this allows for fast degradation of ACh |
|
|
Types of channels contributing to the NMJ (6) (Part 2)
|
• V-gated Na+ channels in the nodes of Ranvier along the axon of the motor neuron
• V-gated Na+ & K+ channels at the nerve terminal • V-gated Ca2+ channels in the synaptic membrane to promote exocytosis of neurotransmitters • ACh-Gated channels to allow depolarization of the motor end plate • V-gated Na+ channels in the jxnal fold of the end plate to depolarize the muscle • V-gated Na+ & K+ channels in the muscle membrane to propagate the AP |
|
|
nACh receptors is this kind of a channel
|
cation (ionotropic) channel
|
|
|
Structure of the nACh Receptor:
• Number of subunits and how the fetal and human forms differ • Difference in Fxn btwn adult and child nAChR • The number of agonists that must bind to open the channel • Briefly describe how desensitization works with the nAChR |
Structure of the nACh Receptor:
• Five - fetal: 2α-β-γ-δ - adutt: 2α-β-ε-δ • The fetal form is open longer but has smaller cation currents, the adult form has a shorter open time but allows large cation currents and allows for more frequent opening • Two agonists must bind to open • it occurs when agonist molecules bind longer to the channel than usual. The prolonged binding induces the receptor to under go a conformational change that close the channel, even with the agonist bound |
|
|
The EPP:
• How it's formed • How it spreads • The EPP declines in amplitude with distance. What is the major factor behind this? • T/F - an EPP does not cause an AP and so does not evoke an impulse at the muscle end plate |
The EPP:
• The depolarization of the nerve terminal leads to the release of ACh into the NMJ. ACh binds to nAChR, leading to the opening of channels at the end plate and an influx of cations, thus generating an EPP • It spreads with decrement in both directions along the end plate • The length constant of the muscle fiber • F; It does not cause an AP, but it does evoke an impulse at the muscle end plate. The EPP does lead to a release of Ca2+ from the SR and a contraction cycle |
|
|
Neurotoxins:
• can block impulse conduction leading to this condition (2 names) • 5 sites of action of neurotoxins |
Neurotoxins:
• muscle or flaccid paralysis • 5 sites if action - along the axon - at the nerve terminals - at the synaptic cleft - the motor end plate - on the muscle fiber |
|
|
Two neurotoxins that that block impulse conduction along the axon
|
TTX and Saxitoxin
|
|
|
Three toxins that interfere with the nerve terminal
|
Botulinum toxin, α-Latrotoxin, ω-Conotoxin
|
|
|
Six toxins that interfere with the NMJ and their mode of action
|
Physostigmine, Neostigmine
Malathion, Parathion Sarin Tabun They reduce activity of AChE. Only Physo- and Neo- stigmine are reversible |
|
|
Botulinum Toxin:
• Source • Mode of action • Cellular Result |
Botulinum Toxin:
• Anaerobic bacteria • At the nerve terminal, it interferes w/ docking of the synaptic vesicles, irreversibly inhibiting exocytosis • Flaccid paralysis, due to failure of ACh release b/c of vesicular exocytosis being inhibited |
|
|
α-Latrotoxin:
• Source • Mode of action • Cellular Result |
α-Latrotoxin:
• Spider venom from a black widow • Causes a large influx of Ca2+, leading to massive release of ACh and its eventual depletion from the nerve terminal • Flaccid paralysis, due to irreversible failure of ACh release after the initial surge of ACh from the Ca2+ influx |
|
|
ω-Conotoxin:
• Source • Mode of action • Cellular Result |
ω-Conotoxin:
• Snail toxin • irreversibly binds to v-gated Ca2+ channels at the nerve terminal • Flaccid paralysis due to the inability of vesicles to fuse with the nerve terminal ending and release ACh |
|
|
Agonists of ACh:
• Name 3 • Briefly describe how their use could lead to desensitization |
Agonists of ACh:
• Carbachol, Nicotine and Succinylcholine • Though these agonists resemble ACh and bind to the nAChR, they are not recognized by AChR and thus cause prolonged binding, possibly leading to desensitization |
|
|
Antagonists of ACh:
• 2 reversible competitor • 1 irreversible competitor • The condition they cause |
Antagonists of ACh:
• Curare and Pancuronium • α-Bungarotoxin • Flaccid paralysis |
|
|
Hexamethonium:
• Type of inhibitor • Its mode of action • What it can treat |
Hexamethonium:
• Competitive ACh antagonist • binds to nAChR in the sympathetic ganglia • High BP |
|
|
Lamber-Eaton Syndrome:
• Type of disease • Cause • Result • Two tx and how they work |
Lamber-Eaton Disease:
• Auto-immune • ABs are directed against v-gated Ca2+ channels in the motor nerve terminals • Impaired entry of Ca2+ ---> less ACh release ---> EPPs can't reach threshold • 1) 4-aminopyridine - blocks K+ channels and re-polarization, leading to longer impulse duration at the nerve terminal. This enhance Ca2+ entry into the nerve terminal, giving more time to vesicle fusion and release of ACh 2) Neostigmine and related compunds - inhibits AChE in the cleft, allowing more time for ACh to bond at the end plate |
|
|
Myasthenia Gravis:
• Cause • Is ACh synthesis or release affected? • Tx |
Myasthenia gravis:
• Autoimmune disease where Abs target nAChR at the end plate • Neostigmine and related compounds; usually given in conjunction is atropine, an antagonist of ACh on the cardiovascular system |
|
|
Muscle Relaxation During Anesthesia and Surgery:
• Two classifications, their mode of action and how they differ • an Example of each |
Depolarizing Agents-
• are short-acting agonists of ACh and are not broken down by AChE. They lead to relative long opening of cation channels at the end plate, leading to inactivation of v-gated Na+ channels in the muscle cll membrane ---> muscle fibers can't be excited ex. Succinylchloline Non-depolarizing agents - • Reversible antagonists bind to nAChR and are longer acting in comparison to depolarizing agents ex. Pancuronium |
|
|
Botulism Neurotoxin A would be clinically used for this condition
|
Muscle hyperactivity/spasms since it reduces output of ACh
|
|
|
Tetanus toxin:
• infects these neurons • Can lead to these conditions (2) |
Tetanus toxin:
• infects inhibitory motor neurons neurons and prevents this • Hyperreflexia due to disturbance of the reflex arc or Abolition of reciprocal innervation leading to both agonist and antagonistic muscles being simultaneously stimulated ---> spasms |
|
|
Strychnine poisoning:
• Mode of action • Clinical manifestations |
Strychnine poisoning:
• Blocks Gly receptors in the VNS • Muscle spasms, convulsions and inteference w/ breathing |
