Chapter 10 Flashcards

1
Q

the autonomic nervous

A

the portion of the peripheral nervous system that conveys output to (visceral organs) cardiac muscle, smooth muscle, and glands

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2
Q

autonomic motor neurons regulate visceral activities by

A

either increasing (exciting) or decreasing (inhibiting) ongoing activities in their effectors

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3
Q

the autonomic nervous system is composed of three branches

A
  1. sympathetic branches
  2. parasympathetic branch
  3. enteric branch
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4
Q

most organs receive

A

dual innervation (sympathetic and parasympathetic)

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5
Q

dual innervation

A

innervation of most of the body by both sympathetic and parasympathetic neurons

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6
Q

enteric innervates the

A

gastrointestinal tract (digestive system auto innervation)

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7
Q

autonomic motor pathway

A

comprised of two autonomic motor neurons and a visceral effector

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8
Q

parasympathetic:

A

ACh–>ACh

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9
Q

sympathetic

A

ACh–>NE

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10
Q

parasympathetic nervous system

A
  1. spinal cord: the journey beings in the CNS, where parasympathetic signals originate in the spinal cord and brain stem
  2. preganglionic neurons: these signals are carries by the parasympathetic preganglionic neurons, which travel out of the spinal cord
  3. autonomic ganglion: the preganglionic neurons release the neurotransmitter acetylcholine (ACh) at the autonomic ganglia, a kind of relay station in the pathway
  4. postganglionic neurons: at the ganglion, the signal is picked up by parasympathetic postganglionic neurons, which then extends to various target organs
  5. effectors: these postganglionic neurons release acetylcholine (ACh) again, which acts on effectors such as smooth muscles, cardiac muscles, and glands, leading to responses like slowed heart rate, stimulated digestion, and increased gland secretion
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11
Q

sympathetic nervous system

A
  1. Spinal cord: The journey begins in the central nervous system (CNS) where sympathetic signals originate in the spinal cord, specifically in the thoracolumbar region (T1 to L2).
  2. Preganglionic neurons: These signals are carried by the sympathetic preganglionic neurons, which exit the spinal cord through the ventral root.
  3. Autonomic ganglion: The preganglionic neurons travel to the sympathetic ganglia, which are located near the spinal cord. There are two types of ganglia: paravertebral ganglia (forming the sympathetic chain) and prevertebral ganglia (located closer to the target organs). Here, the preganglionic neurons release the neurotransmitter acetylcholine (ACh).
  4. Postganglionic neurons: The signal is picked up by sympathetic postganglionic neurons within the ganglia. These neurons then extend to various target organs throughout the body.
  5. Effectors: The postganglionic neurons release norepinephrine (NE) (in most cases) at the target organs, which acts on effectors such as smooth muscles, cardiac muscles, and glands. This leads to responses like increased heart rate, dilated pupils, bronchodilation, and inhibited digestion.
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12
Q

preganglionic neuron

A

the first neuron that has its cell body in the brain or spinal cord

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13
Q

autonomic ganglion

A

a cluster of cell bodies of sympathetic or parasympathetic neurons located in the peripheral nervous system

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14
Q

postganglionic neuron

A

the second autonomic motor neuron in an autonomic pathway, having its cell body and dendrites located in an autonomic ganglion and its axon extending to cardiac muscle, smooth muscle or gland

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15
Q

the parasympathetic nervous system originates in

A

the brain stem and sacral region of the spinal cord

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16
Q

the sympathetic nervous system originates in

A

the thoracic and lumbar region of the spinal cord

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17
Q

the parasympathetic nervous system is also known as

A

craniosacral division of the ANS

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18
Q

parasympathetic preganglionic axons exit the CNS through

A

four cranial nerves (III, VII, IX, and X) and several sacral spinal nerves (S2-S4)

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19
Q

the parasympathetic preganglionic axons then extend to parasympathetic postganglionic neurons in terminal ganglia, which are located

A

close to or within the wall of the visceral effector

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20
Q

from the terminal ganglia, parasympathetic postganglionic axons extend to

A

cels in the visceral organ

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21
Q

because terminal ganglia are located either close to or in the wall of the visceral effector,

A

parasympathetic preganglionic axons are long and postganglionic axons are short

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22
Q

in the sympathetic nervous system, preganglionic neurons have their cell bodies in

A

the thoracic and upper lumbar regions of the spinal cord

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23
Q

the sympathetic nervous system is also called the

A

thoracolumbar division of the ANS

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24
Q

sympathetic preganglionic axons exit the CNS through the

A

thoracic and lumbar spinal nerves

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25
Q

after leaving the CNS, most sympathetic preganglionic axons extend to sympathetic postganglionic neurons in the sympathetic trunk, a

A

chain of ganglia located on either side of the spinal cord

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26
Q

other sympathetic preganglionic axons extend to sympathetic postganglionic neurons in the collateral ganglia,

A

individual ganglia that are not associated with the sympathetic trunk

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27
Q

from the sympathetic trunk or collateral ganglia, sympathetic postganglionic axons extend to

A

the visceral effector

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28
Q

because the sympathetic trunk ganglia are located near the spinal cord,

A

most sympathetic preganglionic axons are short and most sympathetic preganglionic axons are long

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29
Q

some sympathetic preganglionic axons extend to specialized cells in the adrenal medulla (inner portion of the adrenal gland) without synapsing in either the sympathetic trunk or collateral ganglia, these cells are called

A

chromaffin cells

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30
Q

chromaffin cells

A

cells that have an affinity for chromium salts due in part to the presence of the precursors of the neurotransmitter epinephrine

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31
Q

the adrenal medulla develops from the same embryonic tissue as the

A

sympathetic ganglia

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32
Q

chromaffin cells are modified sympathetic postganglionic neurons that lack

A

dendrites and axons

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33
Q

rather than extending to another organ, however, chromaffin cells release

A

hormones into the blood

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34
Q

upon stimulation by sympathetic preganglionic neurons, the chromaffin cells of the adrenal medulla release a mixture of catecholamine hormones

A

80% epinephrine, 20% norepinephrine, and a trace amount of dopamine

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35
Q

the neuroeffector junction is where

A

ANS nerve communicates with a visceral organ, the synapse between an autonomic postganglionic neuron and a visceral effector

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36
Q

the organization of the neuroeffector junction differs from a typical neuron-to-neuron synapse in two major ways

A
  1. The axon terminals of the postganglionic neuron lack synaptic end bulbs; instead, they exhibit swollen regions called varicosities, which contain synaptic vesicles with neurotransmitter.
  2. In the effector, the receptors for the neurotransmitters are not confined to a specific receptor region; rather, they are located along the entire surface of the cell.
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37
Q

the axon terminals of the postganglionic neuron lack synaptic end bulbs, instead they exhibit swollen regions called

A

varicosities

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38
Q

signal transmission at a neuroeffector junction

A
  1. An action potential arrives at a varicosity of the autonomic postganglionic axon.
  2. The depolarizing phase of the action potential opens voltage-gated Ca2+ channels, which are present in the varicosity membrane. Because calcium ions are more concentrated in extracellular fluid, Ca2+ flows inward through the opened channels.
  3. An increase in the Ca2+ concentration inside the varicosity serves as a signal that triggers exocytosis of the synaptic vesicles, causing the release of neurotransmitter into the synapse.
  4. The neurotransmitter molecules diffuse across the synapse and bind to neurotransmitter receptors in the effector cell’s plasma membrane.
  5. Binding of neurotransmitter to its receptor activates a G protein, ultimately leading to a response that either excites or inhibits the effector cell, depending on the type of receptor and G protein pathway that are activated.
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39
Q

removal of neurotransmitter from the NEJ occurs by the same mechanisms as in neuron-to-neuron synapse:

A

(1) diffusion away from the synapse, (2) degradation by enzymes in extracellular fluid or plasma membrane of the effector cell, or (3) uptake into a nearby cell via active transport.

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40
Q

the ANS uses two types of neurotransmitters and receptors

A

cholinergic: Acetylcholine (ACh) producing
adrenergic: Norepinephrine (NE) producing

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41
Q

neurotransmitter acetylcholine

A
  • released by preganglionic neurons of both systems
  • released by postganglionic neurons of the parasympathetic nervous system
42
Q

the two types of cholinergic receptors

A

nicotinic and muscarinic

43
Q

nicotinic (receptor-cationic channels)

A
  • found on postganglionic neuron cell body
  • adrenal medulla
  • all skeletal muscles
44
Q

muscarinic (G protein receptor)

A
  • found on target tissues of the parasympathetic nervous system
  • limited in the sympathetic system to sweat glands
45
Q

adrenergic neurotransmitters

A

norepinephrine and epinephrine

46
Q

norepinephrine

A

released by postganglionic cells of the sympathetic nervous system (as a neurotransmitter) or adrenal medulla (as a hormone carried by the blood supply)

47
Q

epinephrine

A

released by chromaffin cells of the adrenal medulla

48
Q

adrenergic receptors

A

alpha and beta

49
Q

alpha

A

smooth muscle contractions = vasoconstriction

50
Q

beta

A

increased heart rate, vasodilation in muscles, kidney, adipose tissue

51
Q

alpha 1

A

all smooth muscles in blood vessels and viscera, glands, kidneys

52
Q

beta 1:

A

increased heart HR and contractile force increased kidney JGA (RAAS) which increased BP

53
Q

Alpha 2

A

pre-synaptic terminals

54
Q

Beta 2

A

all smooth muscles in blood vessels, glands, lungs, and sympathetic and other symp. target tissues

55
Q

alpha 1 and beta 1

A

stimulate (heart)

56
Q

alpha 2 and beta 2

A

inhibit (lungs)

57
Q

Beta 2 location and effect on targets

A
  • smooth muscle in walls of airways, some blood vessels, and certain visceral organs, such as the urinary bladder
  • inhibition
57
Q

Alpha 1 location and effect on targets

A
  • most sympathetic target tissues
  • excitation
58
Q

Alpha 2 location and effect on targets

A
  • digestive glands and smooth muscle in certain parts of digestive tract
  • inhibition
59
Q

Beta 1 location and effect on targets

A
  • cardiac muscle and kidneys
  • excitation
60
Q

Which neurotransmitter binds to both muscarinic and nicotinic receptors?
A. epinephrine
B. acetylcholine
C. norepinephrine (noradrenaline)
D. dopamine
E. none of the choices are correct

A

B. acetylcholine

61
Q

Beta blockers (beta-adrenergic antagonists) such as Propranolol are drugs used to treat hypertension and glaucoma. These drugs have what effect on the actions of neurons on their effector, and in which branch of the ANS?
A. decrease, parasympathetic nervous system
B. decrease, sympathetic nervous system
C. increase, parasympathetic nervous system
D. increase, sympathetic nervous system

A

B. decrease, sympathetic nervous system

62
Q

autonomic tone

A

the balance between parasympathetic and sympathetic activity

63
Q

autonomic tone is regulated by the

A

hypothalamus

64
Q

autonomic tone: body organs receive constant innervation by both branches to

A

get desired effect, one branch will turn up while the other turns down

65
Q

parasympathetic responses

A

rest and digest
SLUDD

66
Q

rest and digestion

A

conserve body energy and promote the breakdown and absorption of food

67
Q

the 5 parasympathetic responses (SLUDD)

A

Salivation
Lacrimation
Urination
Digestion
Defacation

68
Q

sympathetic responses

A

fight/flight

69
Q

fight/flight response

A
  • body functions that support vigorous physical activity and rapid production of ATP
  • “E situations” = excite, emergency, exercise, embarrassment
  • diffuse and affect many organs
  • longer lasting than parasympathetic responses
70
Q

why are sympathetic responses longer that parasympathetic responses?

A
  • motor pathways diverge to more effectors
  • NE is deactivated more slowly than ACh
  • NE from the adrenal increases the effect of NE from neurons
  • systemic via blood vessels
71
Q

autonomic reflexes of both systems

A
  • help maintain homeostasis
  • involved in cardiovascular activities, digestion, defecation, and micturition (urinaiton)
72
Q

autonomic (visceral) reflexes

A
  • Sensory receptor. The sensory receptor is the distal end of a sensory neuron; it responds to a stimulus by producing a receptor potential. The sensory receptors of an autonomic reflex are usually interoceptors, which respond to internal stimuli, such as the degree of stretch of an organ wall or the chemical composition of a body fluid.
  • Sensory neuron. If the receptor potential in the sensory receptor reaches threshold, it will generate one or more action potentials in the axon of the sensory neuron. The action potentials are conveyed along the axon into the CNS.
  • Integrating center. The integrating center is a region of gray matter within the CNS that processes the incoming sensory input. The integrating center may involve just one synapse between the sensory neuron and a motor neuron, or it may involve one or more interneurons that relay signals from the sensory neuron to the motor neuron. The integrating centers for most autonomic reflexes are located in the hypothalamus and brain stem. However, some autonomic reflexes have integrating centers in the spinal cord. The reflex is a cranial reflex if integration occurs in the gray matter of the brain; the reflex is a spinal reflex if integration occurs in the gray matter of the spinal cord.
  • Motor neurons. Action potentials triggered by the integrating center propagate out of the CNS along autonomic motor neurons to an effector. In an autonomic reflex arc, two autonomic motor neurons connect the CNS to an effector: The preganglionic neuron conducts action potentials from the CNS to an autonomic ganglion, and the postganglionic neuron conducts action potentials from an autonomic ganglion to the effector.
  • Effector. The effector of an autonomic reflex arc is smooth muscle, cardiac muscle, or a gland.
73
Q

Atropa belladonna, deadly night shade extract

A
  • used to dilate pupils
  • during Renaissance used by Venetian woman for beatification
  • prolonged use leads to blindness, increased heart rate, blurred vision
74
Q

the drug atropine blocks

A

muscarinic ACh receptors

75
Q

clinically, atropine is used to

A

dilate the pupils by blocking ACh so the pupil muscles won’t contract

76
Q

atropine takes

A

time! (muscarinic = G protein signaling)

77
Q

atropine can also

A

reduce glandular secretions, and relax smooth muscle in the GI tract

78
Q

most viscera contain

A

fibers from both autonomic divisions (these may have antagonistic or cooperative effects)

79
Q

dual innervation of the iris - parasympathetic nervous system

A
  • constriction of the pupil
  • Parasympathetic fibers travel with the oculomotor nerve (cranial nerve III) to the ciliary ganglion. Postganglionic neurons then innervate the sphincter pupillae muscle, causing it to contract and the pupil to constrict.
80
Q

dual innervation of the iris - sympathetic nervous system

A
  • dilation of the pupil
  • Sympathetic fibers originate in the spinal cord (T1-T2) and travel to the superior cervical ganglion. Postganglionic neurons then innervate the dilator pupillae muscle, causing it to contract and the pupil to dilate.
81
Q

dual innervation of the iris - SLUDD and the three decreases

A

heart rate, pupil diameter, and bronchoconstriction

82
Q

autonomic control centers

A
  • present in the brain and spinal cord
  • many control centers: cardiovascular, respiratory, other
83
Q

autonomic control centers: hypothalamus, brain stem, and spinal cord contain centers that

A

control autonomic activities

84
Q

lumbar spinal cord and sacral spinal cord

A

ejaculation center, erection center, micturition center, decafaction center

85
Q

hypothalamus, midbrain, pons, and medulla

A

pupillary reflex center, pontine respiratory center, deglutition center, medullary respiratory center, cardiovascular center, salivation center, vomiting center

86
Q

Raynaud Phenomenon

A
  • exaggerated sympathetic stimulation
  • vasoconstriction in fingers and toes
  • paleness, cyanosis, and pain in digits when cold or stressed due to excessive sympathetic stimulation of smooth muscle in the arterioles
  • most common in young women
  • treated with vasodilators and Ca++ channel blockers
87
Q

the somatic nervous system

A

regulates the activity of skeletal muscles: causes skeletal muscle contractions and voluntary (conscious controls)

88
Q

the somatic motor pathways is comprised of

A

a somatic motor neuron and skeletal muscle

89
Q

the only neurotransmitter in the somatic motor pathway

A

ACh and it is always excitatory

90
Q

the steps of the somatic motor pathways

A

ACh to skeletal muscle –> nicotinic receptors–> contraction

91
Q

the neuromusclular junction

A

the site where a somatic motor neuron make a synapse with a skeletal muscle fiber

92
Q

motor end plate

A

region of the sarcolemma of a muscle fiber (cell) that includes acetylcholine (ACh) receptors, which bind ACh released by synaptic end bulbs of somatic motor neurons

93
Q

signal transmission at the neuromuscular junction

A
  1. A nerve action potential arrives at a synaptic end bulb of a somatic motor neuron.
  2. Voltage-gated Ca2+ channels present in the membrane of the synaptic end bulb open in response to the nerve action potential. Because calcium ions are more concentrated in the extracellular fluid, Ca2+ flows inward through the opened channels.
  3. An increase in the Ca2+ concentration inside the synaptic end bulb serves as a signal that triggers exocytosis of the synaptic vesicles, liberating ACh into the synaptic cleft.
  4. ACh diffuses across the synaptic cleft and binds to nicotinic ACh receptors on the motor end plate. Recall that a nicotinic ACh receptor is a type of ionotropic receptor that contains two binding sites for ACh and a cation channel. Binding of two ACh molecules to the nicotinic ACh receptor opens the cation channel. Opening the cation channel allows passage of cations (mainly Na+ and K+) through the end plate membrane, but Na+ inflow is greater than K+ outflow.
  5. The net influx of Na+ ions into the muscle fiber through the open nicotinic ACh receptors causes the motor end plate to depolarize. This change in membrane potential is called an end plate potential (EPP). An EPP is a type of graded potential that is similar to an excitatory postsynaptic potential (EPSP), which forms at synapses between neurons (see Section 7.4). However, an EPP has a larger amplitude (size) than an EPSP because there are more neurotransmitter receptors in the motor end plate and a larger number of ion channels open in response to neurotransmitter–receptor binding. Consequently, a single EPP typically is large enough to depolarize a muscle fiber to threshold (see step 6), whereas a single EPSP normally is too small to depolarize a neuron to threshold.
  6. The EPP spreads by local current flow to an adjacent region of plasma membrane on each side of the motor end plate and depolarizes these areas to threshold.
  7. The adjacent membrane areas contain voltage-gated Na+ channels, which open in response to the threshold-level depolarization. The resultant inflow of Na+ into the muscle fiber through the open voltage-gated Na+ channels initiates a muscle action potential.
  8. Since the NMJ is usually near the midpoint of the muscle fiber, once the muscle action potential arises, it propagates throughout the muscle fiber membrane in both directions away from the NMJ toward the ends of the fiber. The action potential triggers a chain of events that ultimately leads to contraction of the muscle fiber.
  9. The effect of ACh binding to its receptor lasts only briefly because ACh is rapidly broken down by an enzyme called acetylcholinesterase (AChE), which is located on the end plate membrane. AChE breaks down ACh into acetate and choline, products that cannot individually activate the nicotinic ACh receptor.
94
Q

the events at the NMJ can be altered by chemicals including

A

botulinum toxin, curare, organophosphate pesticides, black widow spider latrotoxin

95
Q

botulinum toxin

A

blocks exocytosis of synaptic vesicles at the NMJ so ACh is not released
(relaxation of forehead muscles)

96
Q

curare

A

blocks nicotinic ACh receptors on the motor end plate (recall Atropine blocks muscarinic receptors)
(muscle paralysis)

97
Q

organophosphate pesticides

A

inhibit acetylcholiesterase

98
Q

black widow spider latrotoxin

A

massive exocytosis of synaptic vesicles thus overstimulation of skeletal muscles

99
Q

which of these is a mismatch?
A. alpha-latrotoxin :: decreased ACh vesicle release
B. curare :: muscle paralysis
C. botox :: relaxation of forehead muscles
D. insecticides :: inhibition of AChE

A

A. alpha-latrotoxin :: decreased ACh vesicle release

100
Q

botulinum toxin can travel from NMJ via

A

motor neurons retrograde transport