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Module 4: Neuro > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the three types of neurons? Where are they most often found (CNS vs PNS)?

A

Bipolar (PNS)

Multipolar (CNS)

Pseudounipolar (PNS)

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2
Q

What are glial cells?

A

Non-neuronal cells that maintan homeostasis, form myelin, and provide structural and metabolic support for neurons in the developing and mature nervous system

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3
Q

What do astrocytes do?

A

they are cells in the CNS that:

  • Provide scaffolds for growing axons and migrating neurons during development
  • have numerous projections that anchor neurons to their blood supply
  • maintain appropriate extracellular ion concentration
  • contribute to the formation of the BBB
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4
Q

What do microglia do?

A

They are specialized cells in the CNS that:

  • are capable of phagocytosis
  • protect neurons in CNS
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5
Q

What do ependymal cells do?

A

Line fluid-filled cavities (ventricles) of the brain and spinal cord

  • These cells create and secrete CSF and beat their cilia to help circulate CSF
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6
Q

What do oligodendrocytes do?

A
  • Coat axons in the CNS with their cell membrane, forming a specialized membrane differentiation called myelin ==> produces the myelin sheath
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7
Q

What is myelin sheath?

A

Insulation to the axon that allows electrical signals to propagate more efficienty

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8
Q

What are Schwann cells?

A

Myelin producing cells of the PNS

  • they also play a rone in nerve regeneration following injury
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9
Q

What do satellite cells do?

A

surround and support nerve cell podies in peripheral ganglia (in PNS)

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10
Q

What is unique about neurons in the CNS vs PNS?

A
  • *CNS:**
  • many presynaptic inputs to the postsynptic cell are required to activate a neuron
  • Excitatory and inhibitory inputs
  • various neurotransmitters (NT)
  • Many APs firing sychronously to attain an AP in the target neuron
  • *PNS:**
  • 1 prensynaptic input to 1 postsynaptic cell
  • Excitatory inputs ONLY
  • One NT
  • 1 AP in a motor neuron fires to attain an AP in target cell
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11
Q

How are CNS synapses mediated?

A

chemically

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12
Q

Where can neuron-neuron intereaction occur in CNS cells?

A
  1. Axon-dendrite interaction
  2. Axon-soma
  3. Axon-axon
  4. Dendrite-dendrite (rare)
  5. Soma-soma (rare)
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13
Q

What are factors influencing the size of the graded AP in the CNS?

A
  • Amount of neurotransmitter released into synaptic cleft
  • Density of receptors on postsynaptic membrane
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14
Q

How does integration of synaptic inputs occur in CNS neurons?

A
  • Graded postsynaptic potentials (both IPSP and EPSP) spread passively through the cell and decay over time and space
  • As the PSPs reach the axon hillock, the potentials are integrated and decision is made to trigger (or not trigger) an AP
  • PSPs are integrated by summation
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15
Q

What is temporal summation?

A

Conseutive EPSPs at the same site sum to depolarized the membrane toward the AP threshold

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16
Q

What is spatial summation?

A

Simultaneous EPSPs at different synapses on the same neuron sum to depolarize the membrane toward the AP threshold

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17
Q

What is it meant by divergence of local synaptic connections?

A

One neuron is able to influence many postsynaptic neurons

  • information is spread out to many cells
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18
Q

What is it meant by convergence of local synaptic connections?

A

Many presynaptic neurons converge and influence a single postsynaptic neuron

  • Increases influence and possibiltiy of postsynaptic cell’s abilty to fire
    (increase spatial summation)
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19
Q

What is an Axoaxonic Synapse Type 1?

A

When the presynaptic neuron influences the voltage at the axon hillock and alters the likelihood of generating an AP on the postsynaptic neuron

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20
Q

What is an Axoaxonic Synapse Type 2?

A

When the presynaptic neuron influences the voltage at the postsynaptic neuron at the axon terminal and alters the amount of Ca2+ present in the axon terminal of the postsynaptic cell

  • This results in altered amount of NT released by the postsynaptic cell (onto its postsynaptic cell)
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21
Q

How can an Axoaxonic Synapse Type 2 lead to presynaptic facilitation?

A

The “facilitating” neuron’s axon terminal activity results in increased Ca2+ in the axon terminal of the other neuron –> Increased NT release –> Increased EPSP or IPSP size in the final postsynaptic cell

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22
Q

How can Axoaxonic Synapse Type 2 result in presynaptic Inhibition?

A

The “inhibiting” neuron’s axon terminal activity results in decreased Ca2+ in the axon terminal of the other neuron –> Decreased NT release –> Decreased EPSP or IPSP size in the final postsynaptic cell

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23
Q

What is a feedforward excitation?

A

A –> B –> C

Neuron A Excites Neuron B –> Neuron B excites Neuron C

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24
Q

What is a feedforward inhibition?

A

A –> B –> C

Neuron A excites Neuron B –> Neuron B inhibits Neuron C

25
Q

What is disinhibition?

A

A –> B –> C –> D

Neuron A excites Neuron B –> Neuron B inhibits Neuron C –> Neuron C is inhibited from inhibiting Neuron D

26
Q

What Amino Acids are used as Neurotransmitters?

A

GABA

Glutamate (main excitatory NT in brain)

Glycine

27
Q

What amines are used as neurotransmitters?

A

Acetylcholine

Dopamine

Noepinephrine

Histamine

Serotonin

28
Q

What neuropeptides are used as neurotransmitter?

A

Enkephalins

Substance P

(also endophins and dynorphins)

29
Q

What is co-localization and how does it affect the postsynaptic neuron?

A

Many peptides like Substance P are co-localized with classical NTs in vesicles

  • Co-localization modulates the action of the NT on the PS cell
30
Q

How do the CNS and PNS differ in healing and repair?

A

PNS has an intrinsic ability for repair and regeneration

CNS is, for the most part, incapable of self-repair and regeneration

31
Q

What is an anterograde reaction to injury?

A

If the axon is cut, the part distal to the cut degenerates (wallerian degeneration)

  • This is because materials for maintaining the axon are formed in hte ccell body and can no longer be transported down the axon
  • *PNS:** Schwann cells in the region dedifferentiate and divide
  • Schwann cells and macrophages phagocytose the degenerative debris

CNS: Microglia , astrocytes, and macrophages phagocytose the degenerative debris

32
Q

What is a retrograde reaction to injury?

A

Swelling of the cell body and nucleus

  • degredation of neuron opposite to AP propogation direction
  • Displacement of the nucleus from the center of the cell to an eccentric location
  • Dispersion of the Nissl substance into fine, homogenous particles of decreased basophilia
  • ribosome-studded ER are dispersed and replaced with polyribosomes
33
Q

How does the PNS regenerate peripheral nerves?

A

Sprouting: tips of the proximal stumps form enlargements or growth cones

  • Growth cose sprout at nearest Node of Ranvier of the proximal segment, and must grow across teh injury site and into the schwann cell guidance tunnels
  • When the growing axons contact Schwann cells, a second wave of Schwann cell proliferation occurs
  • These Schwann cells form guidance tunnesl along the former course of the axon
  • Elongating axons innervate target tissue, myelinate, and functional recovery occurs
34
Q

What is a neuroma?

A

Failure of regenerating axonal sprouts to cross the injury site (possibly due to formation of scarring or loss of large segement of nerve) results in a neuroma

  • the permanently denervagted muscle fibers demonstrate severe atrophy
35
Q

How does the CNS regenerate its neurons?

A

Axonal regeneration is typically abortive

–> no regeneration occurs

36
Q

How can a crush injury affect PNS regeneration?

A

Endoneurial sheaths remain intact, making it an easier injury to repair

37
Q

How can a transection injury affect PNS regeneration?

A

Continuit of axoplasm is lost

  • misalignment of axons with original pathway can occur
  • if suture ends of nerve together, the chance of recoery increases
38
Q

How can the site of injury affect PNS regeneration?

A

The closer to target site the nervev is damaged, the greater the likelihood for regeneration

39
Q

How can age affect PNS regeneration?

A

Younger = Greater regenerative activity

40
Q

Why are CNS neurons unable to regenerate?

A

Many factors:

  • loss of molecules that promote axonal growth
  • Expression of molecules taht inhibit axonal growth
  • Oligodendroglia do not form “guidance tunnels”
  • Development of glial scar at injury site impedes growth of axons due to proteoglycan production that inhibits sprouting
41
Q

What is Cerebral Spinal Fluid?

A

Clear, colorless fluid that forms a crucial component of the CNS environment

  • Bathes the brain and spinal cord
  • CSF production, circulation, and absorption affect the homeostasis of CNS
  • Percolates through ventricles and out into subarachnoid space
42
Q

Where is CSF produced?

A

It is actively secred into ventricles by the choiroid plexus epithelium

43
Q

How does CSF leave the subarachnoid space and enter the veinous system?

A

Through Arachnoid granulations

44
Q

What is the subarachnoid space?

A

Space between the arachnoid and pia mater

  • filled with CSF
  • in certain regions, subarachnoid space is expanded to form cisterns, which contain a considerable volume of CSF
45
Q

What is the choroid plexus?

A

Area in the ventricles that form and secrete 70-75% of CSF

Consists of:

  • Capillary network core lined with fenestrated endothelium
  • Choroid epithelium, (simple cuboidal), surrounding the interstitial fluid and vascular core

Separates CSF in the ventricles from blood of the vascular plexus

46
Q

What are extrachoroidal sources of CSF?

A

Cerebral capillary walls

Metabolic generation of water by teh complete oxidation of glucose

47
Q

What are the functions of CSF?

A
  • Maintains constant external environment for neurons and glia
  • Removes harmful brain metabolites

- Distributes neuroactive hormones throughout the nervous system

  • Protects CNS from trauma via the bouyant effect
48
Q

How does CSF composition differ from blood in:

Protein

Glucose, K+, Ca2+, pH

Mg2+, Cl-, lactate, H20

Na+

A

less protein (200x less)

less glucose, K+, Ca2+, pH

More Mg2+, Cl-, lactate, H20

Equal Na+

49
Q

What do you have to take into account when doing a lumbar puncture to assess cranial CSF?

A

Lower spine CSF is slightly different from cranial CSF

50
Q

What are the blood-brain-CSF barriers?

A
  • the communication/transport of chemical substances between these compartments occurs through specific barrieres:
  • Blood Brain Barrier
  • Blood-CSF barrier
  • CSF-brain barrier
51
Q

What is the purpose of the blood brain barrier?

A

To maintain the microenvirontment of the brain and CNS

52
Q

What is transported across the BBB?

A

Glucose

Certain Amino Acids

Ribonucleotides

*Note: two different transporters are often required for most molecules:

  1. from blood –> brain
  2. from brain –> blood
53
Q

What are transport mechanisms across the BBB?

A
  1. Diffusion for lipid soluble, hydrophobic compounds
  2. passive and actie carrier-type transporters
  3. Ion channels and ion-exchangers for ions and other lipid insoluble hydrophilic compounds
54
Q

What are general features of carrier-type transporters of the BBB?

A
  • saturability
  • stereospecificity
  • enhancement of transport velocity
55
Q

What are circumventricular organs?

A

Areas of specialized tissue that lack a BBB located in close proximity to the ventricular system

Include:
Subfornical organ
Subcommissural organ
Pineal
Area postrema
Median eminance
Neuropypophysis
Organum vasculosum of the lamina terminalis

56
Q

What is brain edema?

A

Increased brain volume due to increased water content

Two Types:
vasogenic
cytotoxic

57
Q

What is vasogenic edema?

A

Cause: ischemia, head trauma, meningitis

** Mechanism:** Increased permeability of BBB and capillary walls

Manifestations: Increase in brain interstitial fluid
increased intracranial pressure
Smaller ventricles

58
Q

What is Cytotoxic edema?

A

Cause: Drug poisoning, hyponatremia, water intoxication, hypoxia from asphyxia

Mechanism: net shift of water from extracellular space to the interior of brain cells

Manifestations: cell swelling, decrease in brain interstitail fluid and water diffusion, increased intracranial pressure, marked reduction of ventricles

Module 4: Neuro (17 decks)

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