Histology #2 Flashcards
Dendritic Spins
Involoved in learning and memory
- Dynamic structure
Axon terminal = cinnects to dedritic spines
Image - Perkinjie nuerons
Brainstem
Segway from the brain to the spinal cord
CNS function vs. PNS function
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
Autonomic vs. Somatic
Somatic - voletray movement
Automanic - involentray movement (Ex. breathing)
Types of cells in nervous systems
- Nurons
- Glial Cells
- Mylinating cells
Nuerons
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
Glial cells
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
Astrocytes
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
Satilited cell
Surround the cell bodies in the ganglia
Function - suport and protext nuerons
Image - Satilire cels surrounding teh cell body of teh nueron
Oligiodendrites
CNS - uses Olgiodentries –> forms and maintains mylin sheeth aorund axons
- Can interact with several nerons
Image - oligiodenidtes forms myline sheeth of two nuerons
Shcwann cells
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
Microglia
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
Are glial cells mobile
Glial cells = can be mobiled (move aorund to pganocytes but teh structiral ones are more static
Immune system = mobile
Dedritic proccess = mobile
Ependlymal cell
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
Common cell types in the Cerebrum
- Nueorns
- 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
Types of nuerons in the Cerebral cortex (Grey matter)
- Pyridmidal cells
- Fusiform cells
- Cells of Matinotti
- Horizontal cells of Cajal
- Stellate cells
Common cell types in Cerebrum (immage)
See -
White matter- atsrocyte + microglia + Oligiodendricyte + Axon
Grey Matter - Nueron + oligiodendricute + microglia + Astrocyte
Where are the protoplasmic astrocytes located
Protoplasmic astrocytes = located in grey matter
Oligiodendricytes + Microglia + Astrocytes = in both grey and white matter (but the astrocytes are different in grey vs. white)
Division of the Cerebellum
Cerebellar cortext (grey Matter) + white matter core
ALSO divided into two halves
Image - see the white matter core
Function of the cerebellum
Function - maintain balance + maintain equilibrium + controls volentary movements (fine and smooth movements) + cgnitive functions (Attention + language + memeory) + controls posture chnages (muscle tone)
Layers of teh cerebelum
- Molecular - nuerons are more dispersed
- Purkinnje layer
- Granual layer - niuerons are small and numerous and closley packed
Common cell types in cerebelum
- Nuerons (in cortxt)
- Nueronal glial cells (in cortext + white matter
- Astrocytes
- Oligiodendrytes
- Micorglia
There are 6 tyes of nuerons in the celebelum cortext
Types of nuerons in cerebelum cortext
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)
Spinal cord
Column of nerves within the vertabra that goes from the Brainstem to the lumbar region
Function - communcates infomration form the PNS and the brain
Nuimver of nerves in the Spinal cord
8 Cervical nerves
12 Thoracies nerves
5 Sacral nerces
1. Cocygeal nerve
Total - 31 pairs of nerves
Function of Grey matter
Process infomration
Found in center of the spinal cord + in cerebral cortext
White matter
Contains mylinated and unpmylinated axons
Has few nueronalc ell bodies
Function - Transmits information
Structures in CNS
- Cerebrum
- Cerebelum
- Brain stem
- Spinal cord
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)
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
Axon in Nueron
Function - Transmits signals
Axon = constant diameer + usually unbranched
- Only branched in Psudounipolar
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
Why is white matter white
White matter is white because it is rich in mylinated axons = rich in lipids
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)
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
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
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
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
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
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
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
NMJ image 2
Image 2 - See motor nueron connecting to muscle fibers
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
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
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
-
What happens with High Glu
High Glutamate = overactivation of nuerons = get seizures
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
What happens with low GABA
Low GABA = no inhibition of nervous system = can get seizures
Functions of nervous system
Overall - muscle control + sensory preception + cogntion + homeostatss
- Sensory input
- Infomration processnig
- Coordination of repsnes
- Enabling complex behaviors
- Maintaining homeostasis
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
Myostena Gravis (MG)
Overall - Autoimmune disorder - affects the connection between nerves and muscles
Progressive = volentary muscle weakness gets worse over time
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
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
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
Histopathology of MG (Image 2)
MG = have chnages in the junctional folds (more wide + shallow + few folds) + have widening of the synaptic cleft
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)
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
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
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
Dimentia
Umbreela term for groups of symotms that affect conginotive abilities + memeory + thinkning + behavior
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
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
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)
Pathology of Alzheimers
- See formation of amaloid plaques (biildup and clumps of amaplod beta fragmnets between nuerons
- Nuerofibulary taregts - twisted strand of tau inside nuerons = stick together
- Loss of nuerons - loss of function and connections to otehr nuerons
- 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
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
Alzhemiers image 2
A and B on left = single amploid plauqes
Bottom = tangles
Bottom left = pretangles that lead to tangles
