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z. Neuro Class > Cellular Neuro Science ppt 5-6 > Flashcards

Cellular Neuro Science ppt 5-6 Flashcards

1
Q

What does the structure of the neuron consist of?

A

Soma
Dendrites
Axon

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2
Q

What is the soma?

A 
Consists of nucleus & cytoplasm (ER, GA, Mito, cytoskeleton and microtubules)
NISSL bodies (modified RER)
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3
Q

What are the dendrites?

A

It is a tapering process from the soma that forms the receiving zone of the neuron, conduct electricity toward the body. Contain Nissl bodies and GA.

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4
Q

What is the axon?

A

Longest Process arrises from the axon hillock (continues as the unmyelinated proximal part called initial segment.
Initial segment (spike initiation some) where the action potential arises.
NO NISSL, ER or GA.
Does contain- vesicles, mitochondria and neurofibrils.

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5
Q

How are neurons classified based on number of processes?

A

Multipolar- many from soma (spinal motor)
bipolar- two processes (retinal)
Unipolar- single process (ANS)

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6
Q

How are neurons classified based on length of the axon?

A

Golgi type 1- LONG (cortical motor neurons)

Golgi type 2- short (cortical inhibitory)

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7
Q

What are glial cells?

Types and functions?

A

Supporting cells.
smaller but more numerous than neurons.

  1. Astrocytes- BBB
  2. Ependymal cells- lining of ventricles CSF
  3. Oligodendrocytes- CNS myelin sheath
  4. Microglia- immune cells.
    Schwann cells – PNS-myelin sheath
    Satellite- PNS support
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8
Q

What is the myelin sheath?

A

A multilayer lipid and protein covering that electrically insulates the axon of a neuron and increases the speed of impulse conduction.
Reduces energy expanses and protects the axon.

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9
Q

Schwann vs oligodendrocytes

A

Schwann- wrap around a single axon

Oligodendrocyte- nucleus in the middle wraps a number of axons

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10
Q

What is demyelination?

A

Damage to the myelin sheath caused by INFLAMMATION, viral infections, physical compression or demyelinating disorders

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11
Q

What are the demyelinating disorders?

A 
MS
Guillain Barre
Charcot Marie
Progressive multifocal leukoencephalopathy
Central Potine myelionylsis
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12
Q

What is MS?

A

Multiple Sclerosis.
inflammatory autominute disorder. Autoantibodies vainest the myelin basic protein of OLIGODENDROCYTES.
CNS demyelination.

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13
Q

Clinical features of MS?

A

Scanning Speech
Intentional tremor
Nystagmus
Positive Babinski

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14
Q

Diagnos of MS

A

Increased polyclonal IgG
Myelin Basic protein
MRI: multifocal pages of periventricular demyelination in white matter.

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15
Q

What is Guillain Barre Syndrome?

A

Inflammatory autoimmune demylination of the peripheral motor ventral roots.
Associated with infection. (campylobacter jejuni)

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16
Q

Clinical features of Guillain Barre?

A

no fever.
Areflexic (hyporeflexive). Symmetric ascending muscle weakness. (begins lower extremities)
Paresthesia in the distal lower extremities

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17
Q

Diagnosis of Guillain Barre.

Treatment and Prognosis

A

Elevated CSF protein with normal cell count.
papilledema and clinical presentations.

Treatment- respiratory support. plasmapheresis and IV immunoglobulins.
Prognosis- Death ue to secondary pulmonary complications. Full recovery with supportive care

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18
Q

What is Charcot Marie Tooth Disease?

A

demyelination, which is caused by a mutation in one of the connexin genes expressed in the Schwann cells. (no functional gap junctions)

affect both motor and sensory nerves.

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19
Q

Clinical Features of Charcot Marie?

A
  • Weakness of the foot and lower leg muscles
  • foot drop and a high-stepped gait
  • Foot deformities, such as high arches and hammertoes
  • The lower legs may appear like an “inverted champagne bottle”
  • Weakness and muscle atrophy can occur in the hands
  • Mild or severe neuropathic pain
  • Hypo-reflexia
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20
Q

Treatment and Prognosis of Charcot Marie

A

No cure. PT. leg braces

Normal Life Expectancy

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21
Q

What are the two types of axonal transport?

A
  • Anteriograde- Kinesin ( fast transport microtubule dependent)
  • Retrograde- Dynein (microtubule dependent)
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22
Q

What can Retrograde transport carry?

A

Transports nerve growth factor and neurotropic viruses and toxins (herpes simplex, rabies, polioviruses, and tetanus toxin).


23
Q

What does Anteriograde transport carry?

A

transporting newly synthesized membranous organelles (vesicles) and precursors of neurotransmitters.
cytoskeletal and cytoplasmic elements

24
Q

What is Neuropraxia?

A

A transient block. The paralysis is incomplete, recovery is rapid and complete, and there is no microscopic evidence of nerve degeneration.

25
Q

What is Axonotemesis?

A

Axons are damaged but the surrounding connective tissue sheaths remain more or less intact. Wallerian degeneration occurs peripherally

26
Q

What is neurotmesis?

A

Complete section of the nerve trunk

27
Q

What is Wallerian Degeneration?

A

Changes that occur distally to the site of damage on an axon. Loses tail piece.

28
Q

What is chromatolysis?

A

The cell body swells up due to edema and becomes round in appearance, and the Nissl substance gets distributed throughout the cytoplasm. nucleus moves from its central position to the periphery due to edema.

29
Q

What is Anteriograde Transneuronal Degenration?

A

CNS: degeneration of another postsynaptic neuron closely associated with the same function

30
Q

What is Retrograde Transneuronal Degenration?

A

Terminals of the neuron synapsing with a chromatolytic neuron withdraw and are replaced by processes of glial cells.

31
Q

What are the steps of degeneration?

A

Step 1: Degeneration of the synaptic terminals distal to the lesion.
Step 2: Wallerian degeneration.
Step 3: Myelin degeneration.
Step 4: Scavenging of debris. (Microglia breakdown the axon and its myelin. This step is more rapid in the PNS than the CNS.)
Step 5: Chromatolysis.
Step 6: Retrograde transneuronal degeneration.
Step 7: Anterograde transneuronal degeneration.

32
Q

Where is regeneration of nerve fibers more effective?

A

In thePNS.

Effective regeneration does not occur in the CNS

33
Q

1st degree nerve injury

A

Transient loss of function that occurs due to mild pressure on the nerve. Recovers hrs-weeks

34
Q

2nd degree nerve injury

A

Severe nerve damage with intact edoneural tube. Delayed recovery

35
Q

3rd degree nerve injury

A

severe nerve damage that interrupt edoneural tube.

36
Q

4th degree nerve injury

A

severe damage to nerve associated with disorganization of nerve fasciculi.

37
Q

5th degree nerve injury

A

complete transection of nerve

38
Q

How do neurons communicate?

A

Via synapse that are the neuro-neuronal junctions through which information from one neuron passes to the other.
On average each neuron forms about 2000 synapses.

39
Q

What are Axo-dendritic synapses?

A

Most common 80 of cerebral cortex. Axon of presynaptic neuron connects with dendrite of postsynaptic neuron.

40
Q

Axo-Somatic Synapse

A

15% in cerebral cortex.

Axon of presynaptic neuron synapse with soma of postsynaptic neuron.

41
Q

Axo-axonic Synapse

A

Axon of presynaptic neuron synapse with axon of postsynaptic neuron

42
Q

Dendro-dentritic Synapse

A

Rare

Dendrite of presynaptic neuron synapse with dendrite of postsynaptic neuron.

43
Q

Classification of synapses (transmission)

A

Chemical
Electrical
Conjoint

44
Q

Chemical Synapse

A
  • Impulse occurs through release of neurotransmitters.
  • One way conduction
  • CNS
  • Slower conduction.
45
Q

Electrical Synapse

A
  • Impulse occurs through gap junctions.
  • Conduction in either direction
  • Predominant in smooth and cardiac muscles
  • Faster conduction
46
Q

Conjoint Synapse

A

Partly electrical & partly chemical.

47
Q

What are the 3 types of synaptic vesicles?

Wha

A
  • Small clear: Ach, GABA, glycine, glutamate
  • Small dense-core: Catecholamines
  • Large dense core: Neuropeptide
48
Q

What is a synaptic cleft?

A
  • Gap between pre- & post-synaptic membrane
  • Neurotransmitter released from presynaptic terminal diffuse across the cleft to reach post-synaptic receptors
  • Neurexins (proteins attached to presynaptic membrane) provide structural stability to synapse.
49
Q

Describe the post synaptic membrane

A
  • Postsynaptic density: modified area for synaptic transmission
  • Receptors are clustered in postsynaptic density
50
Q

What are the steps in a synaptic transmission?

A
  1. An action potential depolarizes the axon terminal
  2. the depolarization opens voltage gated Ca2+ channels and ca2+ enters the cell.
  3. Calcium entry triggers exocytosis of the synaptic vesicle contents.
  4. Neurons transmitter diffuses across the synaptic cleft and binds with receptor on the postsynaptic cells.
51
Q

What is the presynaptic mechanism of a synaptic transmission?

A

n-sec-1: a neural-specific syntaxin-binding protein

NSF: N-ethylmaleimide sensitive fusion proteins,

52
Q

What are the two types of postsynaptic mechanisms?

A

Excitatory postsynaptic potential (EPSP)

Inhibitory postsynaptic potential (IPSP)

53
Q

What do EPSP do?

What neurotransmitters are involved?

A

-Depolarization of postsynapticmembrane

  • Neurotransmitters: Acetylcholine, Nor-adrenaline
  • opening of Na+ or Ca2+ ion channels or closure of K+ ion channels
54
Q

What do IPSP do?

What neurotransmitters are involved?

A
  • Hyperpolarization of the postsynaptic membrane
  • GABA, Glycine
  • opening of Cl- ion channels, Opening of K+ ion channels, Closure of Na+ or Ca2+ ion channels

z. Neuro Class (19 decks)

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