Final Content Flashcards

(69 cards)

1
Q

What are the main functions of the motor system?

A

Planning, controlling, and executing voluntary movements; controlling involuntary functions like digestion.

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2
Q

Is motor control a top-down or looped system?

A

It’s a looped system that integrates descending motor plans with sensory feedback.

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3
Q

What spinal structures allow for basic motor control without brain input?

A

Reflex arcs and central pattern generators (CPGs).

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4
Q

What brain regions plan and execute voluntary movement?

A

Motor cortex and premotor cortex.

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5
Q

What structures modulate motor cortex activity for coordination and balance?

A

Basal ganglia and cerebellum.

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6
Q

What type of neuron directly causes muscle contraction?

A

Alpha motor neurons (lower motor neurons).

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7
Q

Where are alpha motor neuron cell bodies located?

A

In the ventral horn of the spinal cord.

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8
Q

What is the topographic organization of motor neurons in the spinal cord called?

A

Somatotopic organization.

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9
Q

Why are ventral horns enlarged in cervical and lumbar spinal regions?

A

They contain more motor neurons for arm and leg movement.

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10
Q

What is the neuromuscular junction (NMJ)?

A

The synapse between an alpha motor neuron and a muscle fiber.

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11
Q

What neurotransmitter is released at the NMJ?

A

Acetylcholine (ACh).

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12
Q

What receptors does ACh bind to at the NMJ?

A

Nicotinic acetylcholine receptors (non-selective cation channels).

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13
Q

What enzyme breaks down ACh at the NMJ?

A

Acetylcholinesterase.

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14
Q

What causes muscle weakness in Myasthenia Gravis?

A

Autoimmune destruction of nicotinic ACh receptors at the NMJ.

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15
Q

What is a motor unit?

A

One alpha motor neuron and all the muscle fibers it innervates.

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16
Q

What is a motor pool?

A

All the motor units that innervate a single muscle.

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17
Q

What are the three types of motor units?

A

Slow, fast fatigue-resistant, and fast fatigable.

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18
Q

Which motor units are used for endurance activities?

A

Slow motor units.

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19
Q

What is a muscle twitch?

A

A brief contraction following a single action potential.

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20
Q

What is tetanus in muscle physiology?

A

Sustained muscle contraction due to rapid action potentials (unfused or fused).

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21
Q

What determines graded muscle force?

A

Frequency of action potentials and motor unit recruitment.

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22
Q

What order are motor units recruited in?

A

From smallest to largest based on force requirements.

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23
Q

What are the three main sources of input to alpha motor neurons?

A

Sensory neurons (proprioception), upper motor neurons (from cortex/brainstem), and spinal interneurons.

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24
Q

What is proprioception?

A

The sense of body position and movement.

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25
Through which pathway does proprioceptive information ascend to the brain?
The dorsal column-medial lemniscus tract.
26
Which ion flows into the muscle fiber when acteylcholine acts on the nicotinic receptors? Sodium Potassium Chloride
Sodium
27
Where are the cell bodies of the motor neurons located? Postjunctional folds Ventral horn Dorsal root ganglion
Ventral horn
28
What neurotransmitter is released at the neuromuscular junction? Glutamate Glycine Acetlycholine Dopamine
Acetlycholine
29
How is neurotransmitter action terminated at the neuromuscular junction? By acetycholinesterase By reuptake of acetylcholine by the presynaptic neuron
By acetycholinesterase
30
Where is the cell body of sensory afferents located? Dorsal root ganglion Postjunctional folds Ventral horn
Dorsal root ganglion
31
Why was Aplysia californica an advantageous model organism for studying learning and memory?
It has a simple nervous system (only ~20,000 neurons), large neurons (up to 1 mm in diameter), and simple, accessible anatomy, making it easier to conduct electrophysiological studies.
32
What behavior did Eric Kandel and colleagues study in Aplysia californica to investigate memory?
The gill-withdrawal reflex, a defensive motor response to touch on the siphon.
33
What neural circuit mediates the gill-withdrawal reflex in Aplysia?
Glutamatergic sensory neurons from the siphon synapse on motor neurons controlling the gill.
34
What is habituation in the context of Aplysia’s gill-withdrawal reflex?
A decrease in response strength after repeated, non-threatening stimulation of the siphon, due to reduced glutamate release from the sensory neuron.
35
During habituation, which part of the gill-withdrawal reflex circuit shows decreased activity?
The motor neuron; the sensory neuron’s activity remains the same.
36
What is sensitization in Aplysia’s gill-withdrawal reflex?
An increased gill-withdrawal response following a noxious stimulus (e.g., tail shock) paired with siphon stimulation.
37
Which neurotransmitter is key to the process of sensitization in Aplysia?
Serotonin, released by interneurons in response to tail shock.
38
What is the molecular cascade triggered by serotonin in Aplysia sensitization?
Serotonin → increased adenylyl cyclase → increased cAMP → activation of protein kinase A → increased glutamate release from the sensory neuron.
39
What long-term cellular change results from repeated sensitization in Aplysia?
Gene expression changes lead to synaptic plasticity, including growth of new axon terminals and increased synaptic connections.
40
What is synaptic plasticity?
A change in synaptic strength that can be either an increase or decrease, lasting from minutes to a lifetime.
41
What does LTP stand for and what does it mean?
Long-Term Potentiation; it’s a long-lasting increase in synaptic strength.
42
What does LTD stand for and what does it mean?
Long-Term Depression; it’s a long-lasting decrease in synaptic strength.
43
Can both excitatory and inhibitory synapses undergo LTP and LTD?
Yes, both types can experience either LTP or LTD.
44
What is the primary input to the hippocampus and what pathway does it use?
The entorhinal cortex; it uses the perforant pathway.
45
What cells do entorhinal cortex neurons synapse onto in the hippocampus?
Granule cells in the dentate gyrus.
46
What are the axons from dentate gyrus granule cells called and where do they project?
Mossy fibers; they project to CA3 pyramidal neurons.
47
What are Schaffer collaterals?
Axons from CA3 neurons projecting to CA1 neurons.
48
How is LTP experimentally induced in the Schaffer collateral?
By delivering a high-frequency (100 Hz) tetanus to CA3 neurons and measuring EPSPs in CA1 neurons.
49
What does an increased EPSP amplitude after stimulation indicate?
That LTP has occurred.
50
How long can LTP last in rodents and potentially in humans?
Upwards of a year in rodents; possibly a lifetime in humans.
51
What happens when glutamate binds to AMPA receptors?
The channel opens, allowing Na⁺ in and K⁺ out, causing depolarization.
52
Why does NMDA require both glutamate binding and depolarization to open?
Because its pore is blocked by Mg²⁺ at resting potential, which is expelled upon depolarization.
53
What causes the voltage change that unblocks NMDA receptors?
Na⁺ influx through AMPA receptors.
54
What ions enter through open NMDA receptors?
Na⁺, K⁺, and Ca²⁺.
55
What kinases are activated by calcium influx during LTP?
PKA, PKC, and CaMKII.
56
What are two effects of kinase activation on AMPA receptors?
1. Phosphorylation increases their conductance. 2. Insertion of more AMPA receptors into the membrane.
57
How is LTD induced in the Schaffer collateral?
By applying low-frequency (1 Hz) stimulation for ~15 minutes.
58
What is the result of LTD on postsynaptic EPSPs?
A long-lasting decrease in EPSP amplitude.
59
What does bidirectional plasticity mean?
Synapses can be strengthened (LTP) or weakened (LTD) depending on stimulation.
60
Habituation of the gill-withdrawal reflex in Aplysia is due to: Decreased serotonin release from sensory neurons. Decreased glutamate release from sensory neurons. Increased glutamate release from sensory neurons. Increased serotonin release from sensory neurons.
Decreased glutamate release from sensory neurons.
61
Sensitization of the gill-withdrawal reflex in Aplysia involves: Decreased sensory neuron axon growth. Decreased glutamate release. A weaker withdrawal reflex. Increased serotonin release.
Increased serotonin release.
62
Eric Kandel and his colleagues used Aplysia californica to study learning and memory because: It exhibits a wide range of complex behaviors. It has a simple nervous system with large, easily studied neurons. It has a complex nervous system similar to humans. It is readily available in all parts of the world.
It has a simple nervous system with large, easily studied neurons.
63
Long-lasting plastic changes in Aplysia, resulting from repeated sensitization protocols, involve: Activation of gene expression that results in the remodeling of the synapse. The suppression of gene expression that results in less axons. A decrease in the number of synaptic connections. A decrease in glutamate release.
Activation of gene expression that results in the remodeling of the synapse.
64
What is synaptic plasticity? The degeneration of neural pathways. The ability of neurons to generate electrical impulses. The ability of synapses to change in strength. The process of forming new neurons.
The ability of synapses to change in strength.
65
Which of the following statements about long-term potentiation (LTP) are true? 1. LTP is synonymous with long-term depression (LTD). 2. LTP occurs exclusively in inhibitory synapses. 3. LTP is a prolonged increase in synaptic strength. 4. LTP can persist for various durations, from minutes to a lifetime.
3. LTP is a prolonged increase in synaptic strength. 4. LTP can persist for various durations, from minutes to a lifetime.
66
Long-term depression (LTD) is characterized by: (select all that apply) The immediate cessation of synaptic activity. An increase in synaptic strength. The formation of new synapses. A prolonged decrease in synaptic strength.
A prolonged decrease in synaptic strength.
67
Long-term depression (LTD) at the synapses between CA3 and CA1 neurons can be induced by: A single, strong electrical pulse. Low-frequency stimulation for an extended period. Blocking AMPA receptor activity. High-frequency tetanus stimulation.
Low-frequency stimulation for an extended period.
68
Which of the following statements are true about the role of NMDA receptors in synaptic plasticity? 1. They function independently of voltage changes in the postsynaptic neuron. 2. They block synaptic transmission to prevent excessive neural activity. 3. They require both presynaptic glutamate release and postsynaptic depolarization to open. 4. They allow calcium (Ca²⁺) influx when activated, triggering intracellular signaling for synaptic changes.
3. They require both presynaptic glutamate release and postsynaptic depolarization to open. 4. They allow calcium (Ca²⁺) influx when activated, triggering intracellular signaling for synaptic changes.
69
Synaptic plasticity is essential for: Maintaining constant synaptic strength. Learning and memory formation. Preventing any changes in neural circuits. Immediate reflex actions.
Learning and memory formation.