Histology #2 Flashcards

1
Q

Dendritic Spins

A

Involoved in learning and memory
- Dynamic structure

Axon terminal = cinnects to dedritic spines

Image - Perkinjie nuerons

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2
Q

Brainstem

A

Segway from the brain to the spinal cord

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3
Q

CNS function vs. PNS function

A

CNS - Recives and processes sensory infomration + responds to sensory input with motor output

PNS functioon - Sense sensory to CNS + transmitts motor output from the brain to the muscles/glands

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4
Q

Autonomic vs. Somatic

A

Somatic - voletray movement
Automanic - involentray movement (Ex. breathing)

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5
Q

Types of cells in nervous systems

A
  1. Nurons
  2. Glial Cells
  3. Mylinating cells
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6
Q

Nuerons

A

Function processes signals (receives input or sends out commonas) + conduct AP

Types:
1. Motor (effernet) - control effctor organs
- Located in CNS
2. Sesory (afferent) - receive snesory information
- Cell body located in CNS or ganaglia
3. Projection nuerons - connects regions that are far away (located in CNS)
4. Iterneurons - creates circuts by connecting nuerns
- Can be inhibitor or excitatory
- Located in CNS or glanglia

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7
Q

Glial cells

A

Supoort and protect nuerons
- Froms mylin sheeth + removes cellular debris + structural support
- Don’t generate electrical impuluses

Types:
1. Astocytes
2. Satalite cells
3. Mylinating cells (Oligiodenricytes + Schwann cells)
4. Microglia
5. Ependymal cells

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8
Q

Astrocytes

A

Located in CNS

Start shaped

Come in contact with capilaries - set up structure frameowrk in CNS (provide structural support)

Image - see branches that project + come into contaxt with capilaryes or nuerons

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9
Q

Satilited cell

A

Surround the cell bodies in the ganglia

Function - suport and protext nuerons

Image - Satilire cels surrounding teh cell body of teh nueron

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10
Q

Oligiodendrites

A

CNS - uses Olgiodentries –> forms and maintains mylin sheeth aorund axons
- Can interact with several nerons

Image - oligiodenidtes forms myline sheeth of two nuerons

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11
Q

Shcwann cells

A

Surrounds one axon at a time

Image - see axon in center - myline sheeth is the thick black coating
- See shwan cells envelopes around the axon

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12
Q

Microglia

A

Immune function in CNS (immune survalence)
- Only found in CNS

Reponde to site of danage or enjury + phagocytose debris + dying cells + immune survenlace

Image - see microglia stained in brown

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13
Q

Are glial cells mobile

A

Glial cells = can be mobiled (move aorund to pganocytes but teh structiral ones are more static

Immune system = mobile
Dedritic proccess = mobile

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14
Q

Ependlymal cell

A

Found as cuboidal or columnar epithelial cells

Forms a singe layer that line ventricles or central canal of the spinal cord

produces CSF in ventricles

Have cilia that prkect form apical memebrane - faclitates movement of CSF

Image -
Top = columnar
Bottom - crss section of ventricle - epdymal are cuboidal - have cilia coming out of epical memebrane

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15
Q

Common cell types in the Cerebrum

A
  1. Nueorns
  2. Nueroglial cells (Atrocytes + Oligiodendricytes + Microglia)

Have different types of nuerons divided based on functions or morphological patters

There are 5 tyoes of neurons in the cerebral cortext

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16
Q

Types of nuerons in the Cerebral cortex (Grey matter)

A
  1. Pyridmidal cells
  2. Fusiform cells
  3. Cells of Matinotti
  4. Horizontal cells of Cajal
  5. Stellate cells
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17
Q

Common cell types in Cerebrum (immage)

A

See -
White matter- atsrocyte + microglia + Oligiodendricyte + Axon

Grey Matter - Nueron + oligiodendricute + microglia + Astrocyte

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18
Q

Where are the protoplasmic astrocytes located

A

Protoplasmic astrocytes = located in grey matter

Oligiodendricytes + Microglia + Astrocytes = in both grey and white matter (but the astrocytes are different in grey vs. white)

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19
Q

Division of the Cerebellum

A

Cerebellar cortext (grey Matter) + white matter core

ALSO divided into two halves

Image - see the white matter core

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20
Q

Function of the cerebellum

A

Function - maintain balance + maintain equilibrium + controls volentary movements (fine and smooth movements) + cgnitive functions (Attention + language + memeory) + controls posture chnages (muscle tone)

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21
Q

Layers of teh cerebelum

A
  1. Molecular - nuerons are more dispersed
  2. Purkinnje layer
  3. Granual layer - niuerons are small and numerous and closley packed
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22
Q

Common cell types in cerebelum

A
  1. Nuerons (in cortxt)
  2. Nueronal glial cells (in cortext + white matter
    • Astrocytes
    • Oligiodendrytes
    • Micorglia

There are 6 tyes of nuerons in the celebelum cortext

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23
Q

Types of nuerons in cerebelum cortext

A

There are 6 types of nuerons in the cerebelum cortext
1. Sallete cells + basketes cels (in moelcular layer)
2. Pukinjie cells (forms a layer)
3 Granual cells (smaller) + golgi cells (in granular layer)
4. Have unpolar brish cells = granual layer but primary floccunodular lobe and vermis

Some cells are inhibitory + some are exciatory (IN SLIDES)

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24
Q

Spinal cord

A

Column of nerves within the vertabra that goes from the Brainstem to the lumbar region

Function - communcates infomration form the PNS and the brain

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25
Nuimver of nerves in the Spinal cord
8 Cervical nerves 12 Thoracies nerves 5 Sacral nerces 1. Cocygeal nerve Total - 31 pairs of nerves
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Function of Grey matter
Process infomration Found in center of the spinal cord + in cerebral cortext
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White matter
Contains mylinated and unpmylinated axons Has few nueronalc ell bodies Function - Transmits information
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Structures in CNS
1. Cerebrum 2. Cerebelum 3. Brain stem 4. Spinal cord
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Cerebrum
Largets part of teh brain Grey matter in cortext + white matter in center Composed of two hemisphere (divided by the medial longitudnal fissure) Function - controls concious thoughts and finction Most common cell types - nuerons + glial cells (Ex Astrocytes)
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Cell body of Nueron
Function - metabolic and synthetic machinery Stains positive for Nissle stain because of teh riygh ER Has variation in shape (round, oval, triangular (pyrimidal)) and size - Larger in motor nuerons and smaller in granial cells
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Axon in Nueron
Function - Transmits signals Axon = constant diameer + usually unbranched - Only branched in Psudounipolar
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Axon hillock
Boundery between the soma and axon - site of AP initiation IF you have enough depolarizaton in the axon hillock = can open volatge gated Na chanels = depolarizes cells THEN Na chanels will close and delayed K chanels will open K going into the cell and repolarize the cells - end at a hyperpolarization/ refractory period
33
Why is white matter white
White matter is white because it is rich in mylinated axons = rich in lipids
34
Schwann cells mechanism
Glial cells = preform mylination Schwann cells wtatch to axins --> wind plasma memebranes around teh axon in a helical fashion until it deposites ultiple layers of myline THEn the layers will fuse together to make one myline sheeth Image - can see cross section of mylinated axon (can see layers of myline)
35
Initiations of mylination
Before Oligiodentries mature they are Oligiodendricyte progentor cells - OPCs ca sense attarrctive and repulsive cues on teh axons IF there is an attarctive cue then the OPCs will extend a limb from the cell body to the cue and begin the wrapping process - Can mylinate multiple nearby axons IF there is a repulsive cue then the OPCs won't extend Product - end with nodes of unmylinated regions = have nodes of Ranvier
36
Nodes of Ranvier image
Nodes - unmylinated regions of the axon Image 1 - See where the mylin sinches inwards = have nodes of Ranvier Image 2 (right) - myline is blue - see layers and see that myline terminates at the nodes of ranvier
37
How does mylination work
Overall - speeds up the action potential because it is rich in lipids Lipids - not polar = avoids electrical charge = poor conductors of electricty BUT good insulators = retains the strength of the AP doen the axon + creates salatdor conductions were the AP jumps between the nodes - Speed is 100X faster compared to unmylined
38
Synapse
Region were electrical or chemical signals are transmitted between nuerons and dendrites How it works - At the presnapse there are vesicles with NT --> NT fuse with the presynamptic membrane --> NT are released into the synaptic cleft --> NT bind with receptors on the post synaptic cleft
39
Synapse histology
Nueron = blue - has vesicles that contain NT (purple circles) + arrow shows teh NT are going to the green + black line is the cleft
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Nueromuscular junction mechanism
Motor nueron connects to the muscle - AP causes the volatged gated Ca chanels to open - Ca causes teh Actylcholine to bind to the presynaptic memebrane - AcH goe sto the cleft --> AcH binds to the ligand gated Na chanels - flow of Na cuases an AP - AP causes the T-tubules to open --> T-tubules opening causes teh SR to release Ca --> Ca binds to the tropinin complex --> casues a confirmation change - actin binds to myosin - During relaxaton = Ca is absorbed and mysine binding sites close
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NMJ histology (Image 1)
Image 1 - Axon in blue - vesclicles in ellow with AcH --> going to the skelatal muscle on the right Image 2 - See motor nueron connecting to muscle fibers
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NMJ image 2
Image 2 - See motor nueron connecting to muscle fibers
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Post synaptic receptors
Overall - receotors mediate the membrane Types: 1. Volatge gated chnages 2. Ligand gated chanels 3. GPCRs ALL receptors on post synaptic = result in depolarization or hyperpolarization of the memebrane - Difference = if excitatory or inhibitory
44
Voltage gated vs. Ligand Gated vs. GPCRs
Voltage gated - reulst in local immedtae affect by alowing ions into the membrane Ligand gates ion chanels - Local immediate affect GPCRs - Widesoread affect - Often coupled to effector proteins + produces second messengers
45
Excitatory signal
Overall - positive charge flows to the post synpatic = causes depolarization = more likley to generate an AP Example - Glutamate (most common EPSB NT) - Glutamate fuses with the presynaptic memenrane --> GLU goes to the cleft --> Glu binds to the ligand gated chanel (NMDR) --> NMDR allows Na and Ca to post synaptic cell --> Na will depolarize the cell + Ca acts as a secondary messenger ---> because have depolarization you van have AP in ysnapse or in subsquent synpases -
46
What happens with High Glu
High Glutamate = overactivation of nuerons = get seizures
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Inhibitory sugnals
Overall - influx of negativley charged ions = get hyperpolarization --> less likley to fire AP = inhibits cell Example - GABA fuses to the preseynapyic emmebrane --> GABA goes to the cleft ---> Ligang gated chanels A and C --> Chnages let Cl into the cell --> Cell becomes hyperpolarized --> cell is less likley to have AP
48
What happens with low GABA
Low GABA = no inhibition of nervous system = can get seizures
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Functions of nervous system
Overall - muscle control + sensory preception + cogntion + homeostatss 1. Sensory input 2. Infomration processnig 3. Coordination of repsnes 4. Enabling complex behaviors 5. Maintaining homeostasis
50
Overview of disoerders
MG - Have disruption of the NMJ ALS (nuerodegentive disorder) - Have degeneration of the motor nueron that impairs motor control Alzheimers -Accumilation of amyloid plaques and tai tangles that lead to cognitive disfunctions
51
Myostena Gravis (MG)
Overall - Autoimmune disorder - affects the connection between nerves and muscles Progressive = volentary muscle weakness gets worse over time
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Symptoms of MG
Overall - Muscle weakness + tired Affects the eye muscles (causes drooping of eylid + double vision) Can have chnages in facial + diffuclty swallowing + weakness in upper and lower limbs - If affcets diaphram = can lead to difficulty breathing
53
Cuases of MG
Overall Issues in teh NMJ --> leads to muscle weakness - Caused by production of antibodies againt AcH receports + overactive compartment pathway + Disruption of the thalymus Have AcH and AcH recpotores in NMJ + have Mask in NMJ (stimulates epxression of AcH receptors) In MG - immune syste prdoduces AB that destor or block teh AcH receptors = AcH can't bind - ALSO have AB that will go to Mask receptor - ALSO can have overactive complement protein = promotes immune function + enhances function of AB Complement protein + mask receptors = reduces AcH
54
Histopathology of MG (Image 1)
See Normal vs. Nuscles in MG MG - sixe and shape of muscle are vraible vs. normal are very unifrom + MG has space between muscle fibers + accumularion of nucleo
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Histopathology of MG (Image 2)
MG = have chnages in the junctional folds (more wide + shallow + few folds) + have widening of the synaptic cleft
56
ASL
Overall - causes degernation of motor nuerons in the CNS = have muscle twitching + issues chewing/swallowing + pain in feet andhands + eye movement abnormailities + progressive weakness + issues speack + trouble with daily acitivities + cognoive and behavioral imporment Leads to death 2-5 years upon onset of symptoms due to failure of basic activities (failure to move + breath + swallow)
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Genetic cause of ASL
5% = family history --> has some genetic compenent 95% = No family history --> could be due to protein degredation + oxidarve distress + glial cell disfunction
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ALS histology
Have loss of motor nuerons in motor cortxt + spinal anterior horn _ loss of mulination in spine Image 1 - Thoracis and lumbar spin in normal vs. ALS - Top = blue dye for nuerons --> ALS have loss of normal compared to normal
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ALS histology #2
Motor nuerons in control is defined vs. less in ALS and deformed and stain differentley in ALS Have purple dots around ALS - glial cells come to supoirt the nueron but fail = marker of nuerodenegeration
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Dimentia
Umbreela term for groups of symotms that affect conginotive abilities + memeory + thinkning + behavior
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Alzheimers
Most common cause of dimmensioa (casues 60-70% of cases) progressive nuerdegenerative disorder that affecst memory and cognitive functions - Progressive for 3-11 years
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Types of Alzheimers symptoms
Symptoms: 1. Mild - little memery loss (lose ability to cound + cognotive difficulties + might get lost + personlaity/ behavioral chnages 2. Moderate = affects concious thoughts + worse ememory loss + can't mutli task + might have halicenous 3. Severe - lose bodily functions + can't talk/walk/swallow + bedridden
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Cause of Alzheimers
Unknown - combination of age related chnages in the brain + genetic alterations + envrinemnts and life sytel factors Can have below age of 65 - have genetic alterations ( Genetic alteractons = APP + PSEN1 + PSEN2)
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Pathology of Alzheimers
1. See formation of amaloid plaques (biildup and clumps of amaplod beta fragmnets between nuerons 2. Nuerofibulary taregts - twisted strand of tau inside nuerons = stick together 3. Loss of nuerons - loss of function and connections to otehr nuerons 3. Brain atrophy - brain tissue srhinks Loss of nuerons - due to plaques + tangles --> lose communication + nuerons die Plaqus and tangles form in happocampus first --> then spread to other areas as disease progress Image - Top right - see plaques and tangles Lower left - see different tyoes of plaques in brain (not all plaques look the same) Lower right = tangles and plaques in frontal lobe
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Brain size on Alzheimers
Have Brain atrophy - Brain shrinks as age BUT shrinks dramatically in alzheimers Image - see atrophy in brian oin the left vs. healthy brain on the right
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Alzhemiers image 2
A and B on left = single amploid plauqes Bottom = tangles Bottom left = pretangles that lead to tangles
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