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Human Body > Histology #2 > Flashcards

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
Q

Nuimver of nerves in the Spinal cord

A

8 Cervical nerves
12 Thoracies nerves
5 Sacral nerces
1. Cocygeal nerve

Total - 31 pairs of nerves

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26
Q

Function of Grey matter

A

Process infomration

Found in center of the spinal cord + in cerebral cortext

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27
Q

White matter

A

Contains mylinated and unpmylinated axons

Has few nueronalc ell bodies

Function - Transmits information

28
Q

Structures in CNS

A
  1. Cerebrum
  2. Cerebelum
  3. Brain stem
  4. Spinal cord
29
Q

Cerebrum

A

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)

30
Q

Cell body of Nueron

A

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

31
Q

Axon in Nueron

A

Function - Transmits signals

Axon = constant diameer + usually unbranched
- Only branched in Psudounipolar

32
Q

Axon hillock

A

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
Q

Why is white matter white

A

White matter is white because it is rich in mylinated axons = rich in lipids

34
Q

Schwann cells mechanism

A

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
Q

Initiations of mylination

A

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
Q

Nodes of Ranvier image

A

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
Q

How does mylination work

A

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
Q

Synapse

A

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
Q

Synapse histology

A

Nueron = blue - has vesicles that contain NT (purple circles) + arrow shows teh NT are going to the green + black line is the cleft

40
Q

Nueromuscular junction mechanism

A

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

41
Q

NMJ histology (Image 1)

A

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

42
Q

NMJ image 2

A

Image 2 - See motor nueron connecting to muscle fibers

43
Q

Post synaptic receptors

A

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
Q

Voltage gated vs. Ligand Gated vs. GPCRs

A

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
Q

Excitatory signal

A

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
Q

What happens with High Glu

A

High Glutamate = overactivation of nuerons = get seizures

47
Q

Inhibitory sugnals

A

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
Q

What happens with low GABA

A

Low GABA = no inhibition of nervous system = can get seizures

49
Q

Functions of nervous system

A

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
Q

Overview of disoerders

A

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
Q

Myostena Gravis (MG)

A

Overall - Autoimmune disorder - affects the connection between nerves and muscles

Progressive = volentary muscle weakness gets worse over time

52
Q

Symptoms of MG

A

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
Q

Cuases of MG

A

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
Q

Histopathology of MG (Image 1)

A

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

55
Q

Histopathology of MG (Image 2)

A

MG = have chnages in the junctional folds (more wide + shallow + few folds) + have widening of the synaptic cleft

56
Q

ASL

A

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)

57
Q

Genetic cause of ASL

A

5% = family history –> has some genetic compenent

95% = No family history –> could be due to protein degredation + oxidarve distress + glial cell disfunction

58
Q

ALS histology

A

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

59
Q

ALS histology #2

A

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

60
Q

Dimentia

A

Umbreela term for groups of symotms that affect conginotive abilities + memeory + thinkning + behavior

61
Q

Alzheimers

A

Most common cause of dimmensioa (casues 60-70% of cases)

progressive nuerdegenerative disorder that affecst memory and cognitive functions
- Progressive for 3-11 years

62
Q

Types of Alzheimers symptoms

A

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

63
Q

Cause of Alzheimers

A

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)

64
Q

Pathology of Alzheimers

A
  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
  4. 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

65
Q

Brain size on Alzheimers

A

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

66
Q

Alzhemiers image 2

A

A and B on left = single amploid plauqes

Bottom = tangles
Bottom left = pretangles that lead to tangles

67
Q
A

Human Body (31 decks)

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