Exam #3 Page 4 Flashcards

1
Q

Axonal Ends

A

Terminal ends of motor neurons of the somatic nervous systems. Requires influx of calcium to release the neurotransmitter, “acetylcholine” (ACh)

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2
Q

Synaptic Cleft

A

Space between the axonal end and the sarcolemma of the muscle

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3
Q

Motor End Plate

A

Segment of sarcolemma which contains ACh receptors for binding of the neurotransmitter

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4
Q

Acetylcholinesterase

A

Enzyme responsible for breakdowns of ACh to prevent continued muscle fiber contraction

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5
Q

Action Potential

A

Depolarization of the sarcolemma and propagation of the electrical event down the muscle fiber

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6
Q

Depolarization

A

Changing the polarity (charge) across the sarcolemma membrane

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7
Q

Muscle metabolism

A

ATP energy necessary for contraction. Phosphorylation releases the cross-bridge connection between the myosin heads and their binding sites on the actin filaments.

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8
Q

Aerobic Respiration

A

With Oxygen. 38 ATP produced for each “glucose” molecule

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9
Q

Anaerobic Respiration

A

Without oxygen. 2 ATP produced per glucose. Lactic acid is produced when in an anaerobic condition.

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10
Q

Muscle Fatigue

A

Physiological inability to contract due to decreased ATP, lactic acid accumulation, and/or ionic imbalances

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11
Q

Oxygen Debt

A

Insufficient oxygen supplies to maintain aerobic respiration

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12
Q

Myasthenia Gravis

A

A disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness. Involves a loss of ACh receptors because the ACh receptors are attacked by their own antibodies - “Autoimmune Disease’’

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13
Q

Rigor mortis

A

Intracellular calcium levels increase because ATP is no longer being synthesized. Results in persistent cross-bridge formation.

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14
Q

Cross-bridge detachment

A

ATP is needed. Myosin head staying bound to actin, causing a constant state of contraction. Muscles stay contacted until muscle proteins break down, causing myosin to release.

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15
Q

Muscle Dystrophy

A

Inherited, muscle-destroying diseases, where cells enlarge due to deposits of fat and connective tissue

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16
Q

Duchenne Muscular Dystrophy (DMD)

A

most common and severe type. Caused by defective gene for “Dystrophin”

17
Q

Dystrophin

A

a cytoplasmic protein that links the cytoskeleton to the extracellular matrix, stabilizing the sarcolemma. Loss of the dystrophin protein leads to damaged contractile fibers, inflammation of the cells, and loss of contractile physiology and muscle mass declines

18
Q

Regeneration of muscle cells

A

Cardiac and skeletal muscle cells become amitotic but can still lengthen and thicken. Smooth muscle cells can regenerate themselves by mitosis.