Neurophys W4D2 H3&4 Flashcards

1
Q

Astrocytes

A

a. transport materials between neurons and blood vessels, b. give structural rigidity to the CNS, c. regulate the composition of the extracellular space around neurons, d. store energy (mainly as glycogen), e. secrete growth factors Astrocyte cytoskeleton is primarily microtubules and intermediate filament proteins made up of “glial-fibrillary acidic protein” or GFAP; astrocytes increase GFAP expression with damage or when nearby neurons are under stress and so this can be an early marker of neural damage.

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2
Q

Oligodendrocytes

A

Form myelin sheaths around axons in CNS Have many arms, so just a single oligodendrocytes can myelinate short stretches in up to 50 different nerves! Gaps between myelinations = Nodes of Ranvier

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3
Q

These cells in the CNS results in salutatory propagation and increase in overall nerve conductance velocity.

A

Oligodendrocytes

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4
Q

Epithelial-like cells lining brain ventricles and central canal where CSF is stored.

A

Ependymal Cells **fun fact: neuronal stem cells mixed in with ependymal cells. in certain parts of brain, these stem cells are responsible for the making of new memories!

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5
Q

What are these folds???

A

Ependymal cells of the choroid plexus in the ventricles of the brain – site of CSF production.

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6
Q

What are the two types of cells that can produce myelin? How are they different/

A

Oligodendrocytes = CNS, multiple legs

Schwann cells = PNS, wrap around single axon and has ability to produce myeline, but doesn’t necessarily

Nodes of Ranvier = gaps between myelinated bits in CNS and PNS and results in salutatory conduction

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7
Q

The number of these cells increases after brain damage to clearn dying neurons.

A

Microglia! The macrophages of the brain that mediate immune defense activity within CNS.

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8
Q

What the heck is the zonula occludens?

A

Zone of tight junctions between the capillary epithelia cells of the brain. Establishes BBB between blood and CSF.

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9
Q

You are a doc in the ER and concerned that a patient of yours has meningitis. You must do a spinal tap to determine the state of the CSF. You prepare the patient for needle injection into their spine. Where should you poke this poor patient to ensure that you don’t hit the spinal cord? What layer of the meninges must you collect the fluid from? What levels of meninges will you pierce when traveling to this space?

A

Below L3 vertebra.

The conus medullaris is usually at the level of the intervertebral disk between L1 and L2. Below this level is the cauda equina, and these fibers are suspended in the CSF. The possibility of injuring the spinal cord or rootlets is low if a needles is introduced below L3 vertebra.

You will pierce the dura mater and arachnoid mater and draw fluid from the subarachnoid space.

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10
Q

What type of neuron is this? Where do we find it in the body?

A

Pseudo-unipolar.

We see them in the DRG!

The axon has a peripheral branch (from the cell body to the periphery: skin, joint and muscle) and a central branch (from the cell body to spinal cord)

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11
Q

Unlike the DRG neurons, the __________ neurons are multipolar neurons with dendrites and a _________ axon.

A

Sympathetic neurons are multipolar with a single axon.

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12
Q

As compared to the sympathetic ganglia, the parasympathetic ganglia are _______ to the organs which they innervate.

A

Closer! Parasympathetic system has long pre-ganglionic nerve and short post-ganglionic nerve.

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13
Q

These cells are the glia of the ganglia.

A

Satellite Cells.

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14
Q

What are the three types of nerve connective sheaths? What do each cover?

A

Endonerium = surrounds individual Schwann cells and the nerves they cover

Perineurium = surrounds bundle of nerve fibers; fasicles

Endoneurium = outermost layer enclosing a bundle of nerve bundles

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15
Q

Myelin increases the speed of an action potential by primarly _________ ________.

A

Decreasing capacitance.

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16
Q

What best describes why action potentials are unidirectional?

A

Inactivation of sodium channels.

17
Q

If an action potential is initiated in the middle of an axon, in which direction will it travel?

A

To both the soma and axon terminal.

18
Q

A particular type of scorpion toxin interacts with the pore of the K+ channel, blocking its activity. How would this change the action potential?

A

K+ channels repolarize the cell. The downward repolarization, which is mediated by K+ channels, would be less rapid.

19
Q

What the hey is a refractory period?

A

This is the time during which another stimulus given to the neuron (no matter how strong) will not lead to a second action potential. Thus, because Na+ channels are inactivated during this time, additional depolarizing stimuli do not lead to new action potentials. The absolute refractory period takes about 1-2 ms

20
Q

Which of the following is not a main factor that influences the speed of action potential propagation along an axon:

a. the degree of myelination of the axon.
b. the length of the axon.
c. the diameter of the axon.
d. the kinetics of the voltage-gated channels.

A

The length don’t do a thang!

21
Q

A black cat scratched ya up real nice and you need a couple stitches. At the ER, the doc preps you with some Lidocaine in order to spare you further pain. Use your knowledge of action potentials to propse a course of action of this god-send local anaesthetic.

A

Lidocaine, and other local anesthetics (LAs) bind to a particular domain of the voltage-gated sodium channels which are located primarily in the axon hillock. By inactivating Na+ channels, the threshold for axonal excitation becomes more unattainable and the refractory period is increased. Consequence= no nerve transduction of sensory axons to the CNS.

22
Q

Success! The doc stitched ya up real nice. The black cat attack wounds should heal up quickly. Your hand is still extremely numb from the Lidocaine but you are able to move your hand muscles just fine. Why is it that nerves carrying pain signals are more susceptible to the effects of local anesthetics as compared to nerves that perform proprioception or motor function?

A

Local anesthetics preferentially target pain and temperature neurons because they are smaller and lack myelination. Neurons that are small in diameter have a large internal resistance, so currents do not travel as quickly down the axon.

23
Q

You start with a narrow, unmyelinated neuron and transform it into a wide, myelinated neuron. What has changed?

A

Decreased internal resistance. Decreased capacitance. Increased membrane resistance. All 3 mean faster action potential propagation conductance!

24
Q

A patient presents with nerve-associated symptoms that leads you to believe she may have MS. You order an MRI to get a visual of what is going on. If your suspicion is correct, where may you expect to see lesions? What are these due to?

A

Lesions in the CNS due to inflammation and scarring involving oligodendrocyte glia cells.

25
Q

What is the relationship between K “leak channels” and capacitance?

A

Loss of current through K “leak” channels decreases speed and distance that the electrical current can travel. “Insulation” of axon with myelin decreases membrane capcitance, thus less charge leak and thus faster action potential.

26
Q

Why does an action potential originated at the axon hillock travel down the axon in a unidirectionl manner?

A

Refractory period!

27
Q

Tell me the basic sequence of events in a neuromuscular junction, por favor.

A

1) An action potential propagates down the axon of the motoneuron and depolarizes its synaptic terminal
2) Depolarization causes voltage-gated Ca channels to open and extracellular Ca floods the synaptic terminal
3) Ca entry leads to exocytosis of vesicles filled with acetylcholine (ACh)
4) ACh diffuses across the synaptic cleft to the muscle where it binds to nicotinic ACh receptors, which opens the cation channels, leading to a depolarization of the muscle (**Inability to elicit an action potential in muscle can manifest as muscle weakness)
5) ACh is removed from the synaptic cleft by enzymatic degradation (by acetylcholinesterase) and by diffusion

28
Q

__________ receptors act via second messengers to open a gated ion channel.

A

Metabotropic

29
Q

___________ receptors lead to ______ synaptic potentials because the transmitter binds to and activates receptors that also function as ion channels.

A

Ionotropic receptors lead to fast synaptic potentials because the transmitter binds to and activates receptors that also function as ion channels.

The absence of intermediate steps leads to a rapid change in conductance, as compared to metabotropic receptors.

30
Q

What is spatial integration?

A

Integration of synaptic potentials from different synaptic inputs. Synaptic potentials produced at similar times from different synapses will be combined in the dendrites or at the soma of the postsynaptic cell and thus produce a larger response than that produced at a single synapse.

31
Q

What is temporal integration?

A

Integration of synaptic potentials from repetitive activation of one synaptic input. If the time between action potentials in the presynaptic cell is shorter than the duration of the synaptic potential produced in response to a single presynaptic action potential, the synaptic potentials produced by each action potential will begin to pile up and cause a larger response than that produced by a single presynaptic action potential.

32
Q

These structures play an especially important role in synchronizing groups of cells once a chemical signal is recieved.

A

Gap junctions! Allow for electrical signal communication between cells. No need for translation between electrical and chemical signals, and thus a more focused, quick communication style between cells designed to communicate with one another.

33
Q

Of these neurotransmitters, which are typically excitatory and which are typically inhibitory?

Glutamate, GABA, Glycine, Acetylcholine

A

Excitatory: Glutamate and Acetylcholine

Inhibitory: GABA and Glycine

34
Q

A metabotropic glutamate receptor can act in __________ __________, by hyperpolarizing a neuron.

A

A metabotropic glutamate receptor can act in presynaptic inhibition by hyperpolarizing a neuron.

35
Q

Electrical synapse junctions are made up of these gap proteins.

A

Connexins.

36
Q

Neurotransmitter release is often stimulated by changes in conductance of which ion?

A

Calcium, duh!

37
Q

Which ion can act in an inhibitory fashion when coupled to metabotropic receptors?

A

K+

Could act to effectively hyperpolarize the cell, making it difficult to reach threshold for AP.

38
Q

Below is a list of chemical transmitters. How are each removed from the synaptic cleft?

Peptide neurotransmitters, GABA, ACh, Glycine, Biogenic amines, glutamate

A

GABA, glycine, glutamate: primary role of glia in reuptake

ACh: acetylcholine esterase

Biogenic amines: COMT in cleft and cell, MAO in cell and reuptake

Peptide neurotransmitters: diffusion and proteases

39
Q

The EPSP and IPSP is small; about 1 mV. In order for this to reach threshold some type of summation is often necessary. What are the types of summation?

A

Temporal: Multiple closely timed sequential activation at the same synapse

Spatial: Multiple concurrent inputs at different sites