Astrocyte

CNS support cell (glial cell type)

Large oval light staining nuclei

Form perivascular foot processes that apply to blood vessel wall (and pia-glial membrane)

Cajal's gold sublimate stain

CNS support cells (glial cell)

 Small spherical nuclei with densely stained nucleoplasm

Hortega's Silver Carbonate stain

CNS support cell (glial cell)

fusiform shaped nucleus with densely stained nucleoplasm

 Spindle shaped

Hortega's Silver Carbonate stain

Rxn occurs in direction of conduction distal to site of injury

Wallerian Degeneration

Anterograde reaction to injury

• Shwann cell proteases degrade injured site
• Diffusible factor released from fragments to induce MACS
• Debris picked up by supporting cells and MACS
• MACS induce shwann cell proliferation at distal stump
• PNS: shwann cells line up to form guidance tunnel
• growth cones sprout at nearest N.O.R. and axon grows across injury site through guindance tunnels to reach its target.  Shwann cells continue to proliferate.

PNS damage vs CNS damage

PNS damage more likely to recover well.

PNS has proteins to promote recovery and guidance tunnels

• CNS has inhibitory cytokines and glycoproteins
• CNS does not form guidance tunnels

1. Crush vs transection. Crush is better because endoneurial sheaths remain intact
2. Closer to cell body the regeneration potential is less than an injury close to target
3. Young better than Old

1. Nauta: stain degenerating axons and axon terminals
2. Marchi: stain degenerating myelin sheaths
3. Weil or Weigert: degenerating myelin sheaths are not stained while normal myelin is stained blue/black

Cell body is located in higher brain centers and axons descend down (i.e brain-->spinal cord)

Anterograde degeneration/demyelination will occur below the injury

Neuronal cell bodies are locate in the lower part; ascend into higher brain centers

(i.e. spinal cord-->terhalamus)

Anterograde degeneration and demyelination will occur above the injury (on other side from cell body)

rarely seen.

damage to axons that provide the majority of input to a neuron

i.e lesion in retin; transneuronal degeneration occurs in cells of lateral geniculate body

Efferent projections

Amino Acids taken up by cell body; products transported down the axon to the axon terminals. Can be fast or slow

Retrograde Axoplasmic Transport

Affernt projections to a neuron

HRP taken up by axon terminals and transported down axon towards cell body.

HRP LOCALIZED IN CELL BODY=RETROGRADE TRANSPORT

Consecutive EPSPs from the same site add together to produce an AP

Long Time Constant: longer it takes for an synapse to decay-makes it earsier to reach threshold.

Simultaneous EPSPs from different synapses add to produce an AP

Long Lenth Constant: an EPSP will travel farther (passively) in the neuron making it more likely to produce an AP 

Presynaptic neuron axon terminal synapses on the axon terminal of the post synaptic neuron.

Example. Presynaptic neuron A synapses on the axon terminal of post synaptic neuron B to modulate its calcium release.  Calcium release modulates the amount of NTs released which in turn modulates the excitatory/inhibitory potential of the next neuron.

Neuron 1 excites Neuron 2

THe excited Neuron to acts to inhibit Neuron 3.

 Neuron 3 (an inhibitory neuron) activity is now decreased.

Decreased Neuron 3 activity leads to the increased activity of neuron 4 leading to activation/excitation of neuron 5, etc.

Two pencil touches activate several DORSAL ROOT GANGLION cells.

In the MEDULLA, these neurons make excitatory synapses with MEDULLARY neurons. Firing of adjacent medullary neurons is inhibited using medullary inhibitory interneurons.

Stimuli percieved is better localized; however overall neuronal activity and percieved stimulation is decreased 

the filum terminale invested by dura within the lumbar cistern below S2. Attaches to te tip of the coccyx.

(2) posterior spinal arteries-supply the posterior third of the spinal cord

 (1) anterior spinal artery-supplies the anterior two thirds of the spinal cord

Posteromarginal nucleus

Dorsal Horn

Somatosensory recipient

Thin band separating the substantia gelatinosa (clear stain) and the Lasseur Zone (light purple stain)

Substantia Gelatinosa

Dorsal Horn

Somatosensory Recipient

Claw like shape cervical/thoracic

Clear (white) stain

Lamina 3 & 4

Nucleus Proprius

Dorsal Horn

Processing of somatosensory information

Aquamarine and darker blue stain below claw (L2)

Dorsal Horn

Processing of somatosensory information

Below L3&4-no defined boundaries

Clarke's Nucleus

Lateral Horn

light area-nucleus does not stain well

Recieve muscle spindle information

 C8-L2-only seen well in lower thoracic to upper lumbar

Interomediolateral nucleus

Lateral Horn

T1-L2,3

the myelinated ascending fibers enter into the spinal cord medial to the zone of lissauer

the small thinly myelinated and unmyelinated fibers enter through the zone of Lissauer (why this area is lightly stained)

Ascend ipsilaterally

Do not synapse in the spinal cord

Examples: posterior column 

ascend ipsilaterally and contralaterally

synpase on relay neurons of the spinal cord

Examples: ALSTS, PSCT, ASCT

anterolateral spinothalamic system/tract

lamina II neurons synapse on dendrites of lamina I, IV, and V neurons.  These form the ALSTT. Travel contralaterally across the anterior white commisure. Tract ascends through spinal cord in the latral funiculus to the thalamus on the contralateral side

UMN damage symptom

Initial spastic muscle reflex then sudden collapse of resistance

Babinski Sign (bilateral)

spastic paralysis

clasp knife

Hypertonia

loss of cremasteric reflex

increased resistance to passive movement

late muscle atrophy

Flaccid Paralysis

HypOtonia

reduced myotatic reflexes

fasciculations

RAPID muscle atrophy