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Neuroscience > Neuroscience Week 2: Organization and Cellular Components of the Nervous System > Flashcards

Neuroscience Week 2: Organization and Cellular Components of the Nervous System Flashcards

1
Q

Identify

A
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2
Q

Superficial epineurium

A

The outer covering of the nerve

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3
Q

Perineurium

A
  • A mechanically strong sheath that is dense and forms a protective barrier around the nerve fascicle: a blood-nerve barrier.
  • It encases two separate nerve fascicles.
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4
Q

Endoneurium

A

A loose connective tissue.

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5
Q

Deep epineurium

A
  • Accounts for the connective tissue sandwiched between the nerve fascicles.
  • We find vasculature in this region.
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6
Q

Perineurial septa

A

Pass through the nerve fascicles and carry vasculature to the nerve fibers.

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7
Q

NERVE FIBERS

A

Nerve fiber axon.

Myelin sheath surrounds myelinated axons.

Schwann cells: each myelinates at most one axon internode.

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8
Q

Nerve Fascicles Histology

A
  • Perineurium comprises a flattened form of epithelial cells. They are joined by special junctions, which helps it withstand tremendous pressure.
  • Endoneurium comprises collagenous fibers.
  • Superficial epineurium is a supporting coat: a cylindrical, dense connective tissue sheath.
  • Deep epineurium lies between the fascicles.
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9
Q

Identify

A
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10
Q

Identify

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11
Q

Identify

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12
Q

Identify

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13
Q

Identify

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14
Q

Identify

A
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15
Q

Endoneurium

A

Invests single nerve fiber layers (inflammatory infiltrate in Guillain-Barre Syndrome)

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16
Q

Perineurium

A

(blood-nerve Permeability barrier)

Surrounds a fascicle of nerve fibers.

must be rejoined in microsurgery for limb reattachment

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17
Q

Identify

A
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18
Q

Resting membrane potential is?

A

At rest membrane potential is -60 to -80mV

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19
Q

Myelin sheath in PNS

A

Schwann Cells

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20
Q

Myelin Sheath in CNS

A

Oligodendrocytes

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21
Q

Identify

A
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22
Q

Identify

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23
Q

Identify

A
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24
Q

CNS Glial Cell types

A
  • Astrocytes
  • Microglial cells
  • Ependymal cells
  • Oligodendrocytes (“Macroglia”)
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25
Q

PNS Glial Cell Types

A
  • Satellite Cells
  • Schwann Cells
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26
Q

Astrocyte Function and Location

6 listed

A
  • CNS
  • Support and brace neurons
  • Anchor neurons to supply lines
  • Determine capillary permeability
  • Guide neuron migration and synapse formation
  • Mop up potassium and neurotransmitters
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27
Q

Macroglia cell types

2 listed

A
  • Astrocytes
  • Oligodendrocytes

Both in CNS

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28
Q

Microglial cells Function and location

A

CNS

  • Monitor neuronal health
  • Phagocytose pathogens and dead neurons
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29
Q

Ependymal Cells Function and Location

A
  • Form permeable barrier
  • Cilia circulate CSF

CNS

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30
Q

Oligodendrocytes Function and Location

A

CNS

  • Similar shape to astrocyte but few processes
  • Create myelin sheath in CNS
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31
Q

Satellite Cells Function and Location

A

Function in support like astrocytes

PNS

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32
Q

Schwann Cells Function and Location

A

Create myelin sheath in PNS

PNS

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33
Q

Nerve Type and Identify

A
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34
Q

Nerve Type and Identify

A
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35
Q

Nerve Type and Identify

A
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36
Q

Nerve Types and Identify

A
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37
Q

Dendrite Function

A

Relay impulses towards the cell body (soma)

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38
Q

axon length

A

Axons can vary in length from microns to meters

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39
Q

Protein synthesis in neurons

A

Protein synthesis is mainly carried out in the soma (including peptide neurotransmitters and enzymes for synthesis of chemical neurotransmitters

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40
Q

Anterograde axonal transport is

A

kinesin dependent and carries nutrients, enzymes, etc to the axonal terminal

Herpes Simplex/Herpes Zoster uses this mechanism for reactivation

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41
Q

Retrograde Axonal Transport is

A

Dynein-dependent and returns materials for lysis or recycling

Tetanus toxin and viruses (rabies, herpes simplex, and polio) are transported into the CNS by this mechanism

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42
Q

Macroglia Embryological Origin

A

Neuroectoderm

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43
Q

Microglia Embryological Origin

A

Mesoderm

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44
Q

Ependymal Embryological Origin

A

Neuroectoderm

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45
Q

Macroglia Glial cell types

4 listed

A

Astrocytes CNS

Oligodendrocytes CNS

Schwann Cells PNS (impaired in guillain-Barre Syndrome)

Capsular (satellite cells) PNS

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46
Q

Microglia Glia cell types & Location

A

Microglia CNS

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47
Q

Ependymal Glia cell types and Location

4 listed

A
  • Ependymocytes (Ventricles and central canal of spinal cord)
  • Tanycytes (floor of 3rd ventricle and part of hypothalamus)
  • Choroidal epithelial cells (choroid plexus (CSF production))
  • Muller Cells (Retina)
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48
Q

One Oligodendrocyte can interact with?

A

~50 axons

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49
Q

Oligodendrocyte Function

A
  • Formation and maintenance of CNS myelin (axonal insulation)
  • There are interruptions in myelin important for impulse conduction
  • One Oligodendrocyte can interact with ~50 axons
  • Produces neurotrophic factors such as NGF
    *
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50
Q

Oligodendrocytes in MS

A

Damaged in Multiple Sclerosis

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51
Q

Microglia Functions and Caveat

A
  • Immune Cells of the CNS
  • Phagocytosis of debris after injury or disease
  • May contribute to the pathophysiology of neurodegenerative disorders such as Alzheimers disease
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52
Q

Oligodendrocytes derived from

A

Neuroectoderm

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53
Q

Microglia derived from

A

Bone Marrow (mesoderm)

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54
Q

Microglia in HIV

A

Fuse as multinucleated giant cells in HIV

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55
Q

Astrocyte Function

A
  • Respond to injury (reactive gliosis)
  • Produce neurotrophic factors for neuronal survival
  • Optimize interstitial space composition for synaptic transmission
  • Remove some neurotransmitters from the synaptic cleft (glutamate and GABA)
  • Vascular end feed couple neuronal activity with blood flow and support endothelial cells forming the blood-brain barrier
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56
Q

Astrocyte histological marker for pathoglogy

A

Glial Fibrillary Acidic Protein (GFAP)

Common in astrocytic tumors

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57
Q

GFAP AKA

A

Glial Fibrillary Acidic Protein

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58
Q

Glial Fibrillary Acidic Protein

A

Histological marker for pathology in astrocytic tumors

59
Q

Astrocyte neoplasms prevalence and identifying components

A
  • Common source of tumors
  • Histological marker for pathology is Glial Fibrillary Acidic Protein
60
Q

Blood-brain Barrier Function

A
  • Provides protective separation of the circulating blood from the CNS extracellular fluid, limiting the penetration of agents including (bacteria, drugs, toxins)
  • Is a biochemical barrier for selective transport in/out of CNS
61
Q

Properties which allow for better BBB penetration

A
  • ↑ Lipid solubility
  • ↓ molecular weight
  • ↓ charge (non-polar)
62
Q

How do polar molecules transport across BBB?

A
  • Transporters can facilitate the entrance of polar molecules
  • (glucose and Amino Acids via facilitated transport that does not require energy)
  • Insulin and transferrin use active transport and require energy
63
Q

The blood-brain barrier is mediated by?

A

tight junctions between capillary endothelial cells as well as a surrounding layer of astrocyte end-feet

64
Q

Parts of the brain without a normal BBB

A

Some parts of the brain, the circumventricular organs lack a normal BBB and have fenestrated capillaries

These include regions that sample the blood such as the

  • area postrema vomiting center,
  • paraventricular nuclei including the organum vasculosum lamina terminalis (OVLT) for osmolarity regulation, and neurohypophysis for antidiuretic hormone secretion
65
Q

The BBB can open in?

A

Stroke, tumors, trauma, infections, epilepsy, MS, Neurodegenerative diseases, etc.

66
Q

Acute Neuronal injury cause examples

A

Can be hypoxia-ischemia or hypoglycemia which → necrosis or apoptosis

67
Q

Acute neuronal injury is characterized by?

A

Is characterized by intense cytoplasmic eosinophilia (due to Nissi body destruction; known as red neurons) and nuclear pyknosis (irreversible chromatin condensation)

68
Q

subacute and chronic Neuronal Injury is characterized by?

A

Neuronal death (apoptosis) and reactive gliosis (e.g. as it occurs in neurodegenerative disorders)

69
Q

Axonal Reaction description

A

Response of neuronal cell body to axonal damage

70
Q

Neuronal inclusions common causes

4 listed

A
  • Can be caused by aging → (lipofuscin)
  • metabolic disorders (storage material)
  • viral diseases (inclusion bodies)
  • neurodegenerative diseases (aggregated proteins)
71
Q

Astrocytes function in NS injury

2 listed

A
  • Repair and scar formation
  • they initially develop an enlarged vesicular nucleus and eosinophilic cytoplasm (gemistocytic astrocytes) culminating in tissue gliosis
72
Q

Gemistocytic astrocytes

A

Astrocytes in NS injury

Repair and scar formation

they initially develop an enlarged vesicular nucleus and eosinophilic cytoplasm (gemistocytic astrocytes) culminating in tissue gliosis

73
Q

When Astrocytes are directly damaged they…

A

When directly damaged they can

  • form elongated eosinophilic structures (Rosenthal fibers) as seen in gliosis and tumors
  • Copora amylacea in advanced age (lamellated polyglucosan bodies)
74
Q

Gliosis

A

Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes.

75
Q

Microglia in injury

A

Following injury they proliferate and develop elongated nuclei, form aggregates around necrotic foci (microglial nodules) and aggregate around dying neurons (neuronophagia)

76
Q

Oligodendrocyte in injury

A

cell death is characteristic of demyelinating disorders

77
Q

Ependymal Cells in injury

A

do not regenerate, scar formed by subependymal astrocytes (forming ependymal granulations)

78
Q

Schwann Cells in injury

A

a central role in peripheral nerve regeneration

79
Q

Neurapraxia common causes

A

is usually caused by a mild injury (eg, ischemia, mechanical compression, metabolic or toxic factors) that results in focal demyelination. The axon distal to the injury is intact, and there is nerve continuity across the site of injury.

80
Q

Axonotmesis common causes and description

4 listed

A
  • typically occurs as a result of crush injuries, nerve stretch injuries (eg, motor vehicle accidents, falls) or percussion injuries (eg, gunshot wounds).
  • The axon is locally, but irreversibly damaged, and the myelin sheath is similarly involved.
  • However, the surrounding stroma, including the endoneurium and perineurium, remains intact.
  • undergoes Wallerian degeneration
81
Q

Neurotmesis common causes and description

A

most often occurs in association with severe lesions, such as sharp injuries, traction injuries, percussion, or exposure to neurotoxic substances. The axon, myelin sheath, and surrounding stroma are all irreversibly damaged. The external continuity of the injured nerve is usually disrupted.

82
Q

Sequence of morphological changes after injury to a Myelinated PNS axon

A
83
Q

Sequence of Morphological changes after CNS injury

A
84
Q

Types of ion-channels

A
85
Q

Gated ion channels basic function

A
  • transduce chemical signals into electrical signals
  • allow for rapid responses
86
Q

Ions flow along?

A

Concentration gradient and electric potential (electrochemical gradient)

87
Q

Sodium and potassium channels

A
88
Q

Action potentials

A
89
Q

Refractory periods

A
  • Absolute refractory period
  • Relative refractory period
90
Q

Absolute refractory period

A
91
Q

Relatively refractory period

A

When sodium channels are reset and some potassium channels are still open the membrane potential is more negative than resting potential and more difficult to overcome to initiate another potential

92
Q

Resting state

A

all gated ion channels are closed

93
Q

Depolarization

A

Na+ channels are open

K+ channels are closed

94
Q

Repolarization

A

Na+ channles inactivated

K+ channels open

95
Q

Hyperpolarization

A
  • Na+ remain closed but are reset
  • K+ channels still open
96
Q

Properties of action potentials

A
97
Q

Nonsaltatory conduction in unmyelinated axon

A
98
Q

Saltatory conduction in myelinated axons

A
99
Q

more myelinated axon

A
100
Q

Voltage-gated Na+ channels in myelinated and unmyelinated axons

A
101
Q

Question 1

A
102
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Question 2

A
103
Q

Question 3

A
104
Q

Question 4

A
105
Q

Question 5

A
106
Q

Question 6

A
107
Q

Question 7

A
108
Q

Question 8

A
109
Q

Question 9

A
110
Q

Question 10

A
111
Q

Question 11

A
112
Q

Question 12

A
113
Q

Question 13

A
114
Q

Question 14

A
115
Q

Question 15

A
116
Q

Question 16

A
117
Q

Question 17

A
118
Q

Corpora Amylacea description

A

astrocytes form lamellated polyglucosan bodies in advanced age

119
Q

Cells that determine capillary permeability in the CNS

A

Astrocytes

120
Q

Herpes Simplex/Herpes Zoster uses this mechanism for reactivation

A

Anterograde axonal transport mediated by kinesin

121
Q

Tetanus toxin and viruses (rabies, herpes simplex, and polio) are transported into the CNS by this mechanism

A

Retrograde axonal transport and is mediated by Dynein

122
Q

What are Muller Cells and where are they?

A

an ependymal cell in the retina

123
Q

What are Tanycytes and where are they located?

A

Tanycytes are ependymal cells located on the floor of the 3rd ventricle and are part of the hypothalamus

124
Q

What are Choroidal epithelial cells and where are they located?

A

ependymal cells and are located in the choroid plexus and are responsible for CSF production

125
Q

What are Ependymocytes and where are they located?

A

Ependymocytes are ependymal cells and are located in ventricles and the central canal the of spinal cord

126
Q

cells that produce neurotrophic factors such as NGF

2 listed

A
  • Oligodendrocytes
  • Astrocytes
127
Q

Cell that may contribute to the pathophysiology of neurodegenerative disorders such as Alzheimers disease

A

Microglia

128
Q

Fuse as multinucleated giant cells in HIV

A

Microglia

129
Q

Insulin transport across the BBB

A

Active transport that requires energy

130
Q

Transferrin transport across the BBB

A

uses active transport and requires energy

131
Q

glucose transport across the BBB

A

Facilitated transport and does not require energy

132
Q

Amino Acid transport across the BBB

A

Facilitated transport and does not require energy

133
Q

organum vasculosum lamina terminalis (OVLT) function and caveat

2 listed

A
  • for osmolarity regulation, and neurohypophysis for antidiuretic hormone secretion
  • not covered by the BBB
134
Q

What is nuclear pyknosis?

A

(irreversible chromatin condensation)

135
Q

What is lipofuscin?

A
  • lipofuscin is a nuclear inclusion in the CNS as a result of aging
  • more precisely, fine yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. It is considered to be one of the aging or “wear-and-tear” pigments, found in the liver, kidney, heart muscle, retina, adrenals, nerve cells, and ganglion cells.
136
Q

What are ependymal granulations and where are they located?

A

When ependymal cells are damaged they do not regenerate and a scar is formed by subependymal astrocytes (forming ependymal granulations)

137
Q

Neurapraxia prognosis

A

An excellent recovery is expected and may occur within hours, days, weeks, or at the maximum, a few months

138
Q

Axonotmesis prognosis

A

Overall, partial recovery is the expected outcome, but the time course is significantly protracted as compared with neurapraxia.

139
Q

Wallerian degeneration description and involved in?

A
  • Involved in Axonotmesis
  • Proximal to the lesion, the cell body undergoes changes including swelling and chromatolysis, which resolves with time. Distal to the lesion, the axon degenerates, and the myelin sheath involutes; this process is known as Wallerian degeneration.
140
Q

Neurotmesis prognosis

A
  • No significant regeneration occurs with such a lesion, unless surgical re-anastomosis is performed.
  • Spontaneous reversal of the changes is impossible as the nerve regenerates in a disorganized proliferation of axons, Schwann cells, and perineural cells within a collagenous stroma called a neuroma.
  • With surgical intervention (scarring debridement and approximation of the nerve ends or interposing of a nerve graft), the axon may grow along the endoneurial tubes of the distal segments.
  • This process may take months to years until a useful function is achieved. In neurotmesis, muscle recovery can only occur by axonal regeneration.
141
Q

Action potential ion channels: Resting state

A

all gated ion channels are closed

142
Q

Action potential ion channels: Depolarization

A
  • Na+ channels open
  • K+ channels closed
143
Q

Action potential ion channels: Repolarization

A
  • Na+ channels inactivated
  • K+ channels open
144
Q

Action potential ion channels: Hyperpolarization

A
  • Na+ channels reset and closed
  • K+ channels still open

Neuroscience (96 decks)

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