Section 2 - Cell Biology of Neurons and Glial Cells Flashcards

1
Q

_____ injection follows neurons retrogradely (back to cell body)

A

HRP (horseradish peroxidase) (which is, i’m sure, carly’s favorite peroxidase)

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2
Q

Lipophilic dyes: ____ label postsynaptic neurons ____ label presynaptic neurons

A

DiO DiI (stain living or dead)

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3
Q

_____ travel anterogradely; can cross synapses to label distribution patterns of neurons

A

Radioactive amino acids

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4
Q

_____ virus transports retrogradely and then _____ adjacent cells, go to CNS; eventually go anterograde to _____

A

Rabies virus; produces and sheds copies of virus to; salivary glands

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5
Q

_____ is transported retrogradely from axon terminals at site of infection. What is a big difference from rabies?

A

Tetanus toxin (from clostridium tetani). It is a bacteria and is DILUTED cell-to-cell (no replication).

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6
Q

What is the supposed pathology of bipolar disorder?

A

Imbalances in phosphatidyl inositol (PI) (which is linked to neurotransmitters acetylcholine, serotonin, norepinephrine, histamine)–> mood changes

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7
Q

How do we treat bipolar disorder?

A

Drug: lithium carbonate (stabilizes PI turnover and stabilizes mood)

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8
Q

What is the pathology of Alzheimer’s disease?

A

Degeneration of neurons in basal forebrain nuclei, loss of synapses in cerebral cortex and hippocampus, presence of neurofibrillary tangles and senile plaques. Cortical cells lose cholinergic terminals and choline acteyltransferase levels in cortex/hippocampus are VERY LOW.

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9
Q

What is myasthenia gravis?

A

Patient’s immune system produces antibodies to nicotinic acetylcholine receptors –> destruction of neuromuscular junctions

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10
Q

What is an astrocytic scar?

A

Destruction of cells in CNS due to injury creates space filled with proliferation/hypertrophy of astrocytes (they retain ability to divide in the brain, so they are very common for CNS tumor)

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11
Q

Astrocytic tumors are most often in _____

A

the frontal and temporal lobes

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12
Q

What mediates the CNS inflammatory response?

A

Cytokine, (IL)-1, tumor necrosis factor alpha, and prostaglandin release from microglia and astrocytes

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13
Q

What is neurovascular coupling?

A

Blood flow increases to areas of increased neuronal activity

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14
Q

What is functional hyperemia?

A

A consequence of neurovascular coupling (increase in blood to accommodate tissue activity). It is defective in conditions such as migraine, stroke, hypertension, spinal cord injury, and Alzheimer’s.

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15
Q

What is spreading depression?

A

Wave of suppressed neuronal activity, spreading across regions of gray matter –> decreased blood flow that could damage neurons and lead to potential negative feedback (low oxygen leads to reduced NO, leads to further reduced oxygen). NO dilates vessels.

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16
Q

What is multiple sclerosis (MS)?

A

Loss of myelin results in interrupted propagation of APs down axons. Remyelination is possible.

17
Q

What is this?

A

Dawson fingers are a radiographic feature depicting demyelinating plaques through the corpus callosum, arranged at right angles along medullary veins. Characteristic of MS.

18
Q

What is microglial withdrawal?

A

Microglia reshape processes to form long rod cells apposed to afferent neurons; can become motile (phagocytes) in tissue injury and migrate to site for phagocytosis. Happens in viral encephalitis, neurosyphilis, etc.

19
Q

How to microglia act following peripheral nerve damage?

A

Surround motor neuron cell bodies in brainstem, displace all synapses. Once targets are re-established, new synapses can form. This is synaptic stripping.

20
Q

Microglia can be harmful when they’re trying to help…how?

A

When phagocytosing bacteria, release IL-1B –> loosens tight junctions (allows leukocytes and plasma to enter CNS –> bacterial meningitis)

21
Q

What is an astrocytoma?

A

Glial tumors encountered most often.

22
Q

Describe a Grade 1 astrocytoma

A

Resemble differentiated astrocytes reacting to injury, growing slowly, gradually enlarging

23
Q

Describe Grade 2 astrocytoma

A

Prominent processes filled with glial filaments, recur afer surgery where they may become more aggressive (become higher grade). They are vengeful little bastards.

24
Q

Describe Grade 3 astrocytoma

A

Nuclei that are enlarged with increasing chromatin density, nuclear uniformity lost, blood vessel density increased and growith is rapid. Malignant.

25
Q

Describe Grade 4 astrocytoma

A

Glioblastoma multiforme.

HIGHLY MALIGNANT. Astrocytes spindled, elongated, mitotic figures present. Invade leptomeninges, spread from continuos gyri, cross corpus callosum.

26
Q

What is an oligodendroglioma?

A

Slow growing tumor in brain lobes; dark, round nuclei with clear cytoplasm. Enlarged clusters around neurons and nodules of tumor cells beneath pia.

27
Q

Where are ependyomas located?

A

Spinal cord (cervical), any ventricle, spaces of posterior fossa. Not very aggressive and can be dissected away.

28
Q

Ependyomas can cause supratentorial lesions, leading to ______

A

hydrocephalus or seizures; nausea, vomiting, headaches, cranial nerve signs

29
Q

What differentiates ependyomas from choroid papillomas?

A

Presence of basal bodies.

30
Q

What is a microglioma?

A

Lymphoma of brain consisting of B and T cells.

31
Q

Child tumors are primarily ______

A

Medulloblastomas (retain embryonic unrestrained growth and rapidly spread along surface of brain and spinal cord)

32
Q

What are common benign primary tumors?

A

Meningiomas or schwannomas. Covered by fibrous vascularized capsule. Can compress normal tissue.

33
Q

How do prostate carcinomas tend to metastasize to the CNS?

A

To spinal cord via the Batson venous plexus

34
Q

Compare/contrast schwannomas and neurofibromas. (Tumors of PNS)

A

Schwannoma: encapsulated, no nerve fiber involvement, easitly excised

Neurofibroma: difficult to remove, unencapsulated, invade nerve fibers

35
Q

When is the best chance of recovery for axonal damage?

A

Crushed axon in PNS - focal demyelination expected to recover

36
Q

What is axonotmesis?

A

Compression of axon (proximal axon sprouts, distal Schwann stays, so regeneration can occur in the same position)

37
Q

What is neurotmesis?

A

Nerve is severed (regeneration less likely because it may not go to the right place)

38
Q

What is neurapraxia?

A

Nerve conduction failure (focal demyelination without axonal degeneration)

39
Q

What is the process that ends up causing “phantom pain”? (as in limb amputation)

A

Axons fail to enter Schwann cell tubes and can end blindly in connective tissue, form neuromas. Stimulation of these fibers leads to phantom pain.