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002 - 6120 - Vet Neurobiology > (03) Cellular Neurobiology > Flashcards

(03) Cellular Neurobiology Flashcards

1
Q

The mechanisms of neuronal signaling are based on what? What are these properties determined by? What is the clinical relevance of this?

A
  • excitability, functional polarity, and specific connectivity
  • ion channels and receptors withing the plasma membrane of neurons and by signaling messengers (neurotransmitters) released from neurons
  • channels and receptors involved in neuronal signaling are important drug targets
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2
Q

arrows left to right (with regards to singal)

A
  • input, integration, conduction, output
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3
Q

What is the state of the charge across the membrane at resting membrane potential? What does this create? What is the membrane potential at rest?

A
  • there is a separation of charge across the membrane
  • creates an electrical potential
  • ~ -60 to -70 mV
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4
Q

Which ions are unevenly distributed across the membrane? What does movement of these through channels in the membrane create?

A
  • K+, Na+, Ca2+, Cl-
  • current
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5
Q

What is a transmembrane protein that forms a pore in the membrane? Is it gated or non-gated?

A
  • channel
  • can be either
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6
Q

What is the direction of current?

A
  • same as the direction of the movement of positive ions
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7
Q

What determines if ions are flowing in or out of cells? For any ion, the potential at which the chemical driving force equals the electrical driving force is defined as what? Which equation is used to determine this?

A
  • by chemical driving force (concentration gradient) and electrical driving force (potential difference)
  • Equilibrium potential
  • Nernst equation
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8
Q

Which direction do ions move in?

A
  • ions move in the direction that drives the membrane potential closer to their equilibrium potential
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9
Q

If the membrane potential is -60 mV and the equilibrium potential of K+ is -90 mV, which direction will K+ ions be flowing? What does this make it? What will Na+ ions be doing? What will this make it?

A
  • out of the cell (outward current)
  • hyperpolarized
  • flowing into the cells,
  • depolarized
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10
Q

What are the only channels open at rest?

A
  • K+ channgels (leak channels)
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11
Q

What maintains the distribution
of ions across the membrane?

A

Carrier (transport) proteins:
Na+/K+ ATPase (pump) moves
Na+ out of and K+ into the cell

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12
Q

The electrical activity of neurons is based on:

A
  • separation of charge across the membrane
    (membrane potential, Vm)
  • distribution of ions across the membrane
    (concentration gradients)
  • availability of open channels (permeability)
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13
Q

The resting membrane potential (Vr) is determined
predominantly by:

A
  • K+ current flowing through resting (leak) K+ channels
  • the activity of the Na+/K+ ATPase
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14
Q

If Vm < Vr, the cell is ____________.
If Vm >Vr, the cell is ____________.

A
  • hyperpolarized
  • depolarized
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15
Q

Opening of K+ channels
leads to _________

Opening of Na+ or Ca2+
channels leads to ____________

A
  • outward current,
    hyperpolarization, and less
    excitability.

inward
current, depolarization,
and more excitability.

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16
Q

What is a membrane depolarization that propagates along the axon and conducts the electrical signal from the cell body to the axon terminals? The “threshold” for action potential generation is what? What happens at this point?

A
  • an action potential
  • the depolarization
  • voltage gated Na+ channels are activated
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17
Q

Suprathreshold depolarization of the membrane initiates what? What are at the basis of the action potential?

A
  • an action potential
  • voltage gated channels
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18
Q

Give me what happens after suprathreshold depolarization?

A
19
Q

Use-dependent blockers of voltage-gated Na+ channels are used as what?

In demyelinating disorders, voltage gated K+ channels are along the ______. What does this cause?

A
  • anti-epileptic drugs (phenytoin, carbamazepine, lamotrigine)
  • internodes of the axons, causing conduction abnormalities
20
Q

What is a specialized point of functional contact between neurons or between a neuron and a target organ that allows communication?

The synapse is a site of apposition between a ________ and a __________.

What happens here?

A
  • The synapse
  • presynaptic element of one neuron, postsynaptic membrane of a target neuron (or an effector organ)
  • a presynaptic axon enlargement releases transmitter molecules that diffuse across a synaptic cleft and bind to receptor channels in the postsynaptic membrane
21
Q

Adult human brain has been estimated to contain how many synapses?

A
  • 100 to 500 trillion
22
Q

What three elements are synapses composed of?

A
  • pre-synaptic nerve terminal
  • synaptic cleft
  • postsynaptic element
23
Q

What does the pre-syanptic nerve terminal (presynaptic enlargement) contain?

What else is it called?

How are the vesicles anchored in?

What do they fuse with upon stimulation?

A
  • neurotransmitters in synaptic vessels
  • bouton, varicosity, or end plate
  • by actin microfilaments
  • plasma membrane
24
Q

What are the pre and postsynaptic membranes separated by?

What gets released into here?

What does the cleft contain? What surrounds these?

A
  • a synaptic cleft (20 nm wide)
  • neurotransmitters
  • glycoprotein linking material, glial cell proceses
25
Q

What is a dendrite, cell body, or target cell receiving the synaptic input?

What are embedded in the postsynaptic plasma membrane? What do they bind to?

How thick is the postsynaptic plasma membrane?

A
  • postsynaptic element
  • receptor proteins (typically ligan-gated channels), neurotransmitter molecules
  • may appear unremarkable or thickened (electron dense)
26
Q

What are the three common presynaptic arrangements?

A
  1. axon terminal branches have terminal enlargements (called boutons or bulbs)
  2. axon terminal branches feature varicosities (for synapses “in passing”)
  3. Neuromuscular synapse: axon branches have ramifications that form motor end plates on skeletal muscle fibers
27
Q

What are the four classifications of synaptic types? (+ explain each!)

A
  • axodendritic - axon terminal branch (presynaptic element) synapses on a dendrite
  • axosomatic - axon terminal branch synapses on a soma (cell body)
  • axoaxonic - axon terminal branch synapses on another axon terminal branch (for presynaptic inhibition) or beside the initial segment of an axon
  • Dendrodendritic - dendrite synapsing on another dendrite (very localized effect)
28
Q

What are the presynaptic events?

A
  1. action potential arrives at end of axon - presynaptic membrane passively depolarized (towards 0 transmembrane potential) - Ca++ channels open - influx of Ca++
  2. elevated CA++ triggers vesicle mobilization and docking with PM where vesicles fuse with presynaptic PM and release neurotransmitter (5,000 per vesicle) by exocytosis
  3. Transmitter molecules diffuse across cleft and bind with postsynaptic receptor proteins
  4. neurotransmitters eliminated from synaptic clefts via uptake by presynaptic or glial processes and/or via enzymatic degradation at postsynaptic membrane (molecules are recycled)
  5. presynaptic PM repolarizes and synaptic vesicles are recycled
29
Q

What are the clinical correlations that deal with presynaptic events?

A
  • Inhibition of release (Ca2++ channel inhibitors), (bacterial toxins: botulinium, tetanus)
  • inhibition of clearance (reuptake inhibitors (eg serotonin)
  • inhibition of degradation (MAO)
  • Deficits in synaptic vesicle recycling
30
Q

What are the post-synaptic events? (The first two let’s say)

(for end of 1 - what does activation of [Na and K] channels lead to? - activation of Cl - or K+ channgels)

For the end of 2 - what does the magnitude of a PSP depend on? What are the two types of PSP’s?

A
  1. neurotransmitter molecules bind briefly/repeatedly to ligand-gated receptors - opens ion channels directly (or by means of second messengers) - neurotransmitter binding results in proportional ion flux across post-synaptic membrane - excitability effect depends on nature of the ion channels in the particular postsynaptic membrane (ie in the resting state, postsynaptic PM is polarized (resting K+ channels dominate conductance)
    - activation of [Na and K] channels leads to depolarization toward zero potential
    - activation of Cl- or K+ channels leads to hyperpolarization of postsynaptic membrane
  2. postsynaptic potential (PSP) results from altered membrane conductance. PSPs constitute electrotonic conduction, a passive voltage spread (in contrast to regenerative conduction of which axons are capable). PSPs decay exponentially, over distance and with time
    - magnitude of a PSP depends on number of open ion channels depend on the amount of neurotransmitter released
    - EPSP = excitatory PSP = depolarization toward zero potential, excites the postsynaptic cell
    - IPSP = inhibitory PSP = hyperpolarization (serves to cancel EPSPs), inhibits the postsynaptic cell
31
Q

What are part 3 and 4 of the postsynaptic events?

A
  1. Following removal/degradation of neurotransmitter molecules, the postsynaptic membrane is repolarized (K+ channel conductance again dominates)
  2. Integration of PSP: Neurons receive thousands of synapses. The changes in membrane potential at active synapses sum together in space and time. An Action potential is generated if the summed charge in membrane potential is suprathreshold.
32
Q

What are the four types of synaptic transmission? (+ each of their effect on membrane potential + time course)?

Fast transmission is mediated by what?

Slow transmission in mediated by what?

What is a receptor?

A
  • fast excitatory, depolarization, ms
  • fast inhibitory, hyperpolarization, ms
  • slow excitatory, depolarization (increased excitability), s
  • slow inhibitory, hyperpolarization (decreased excitability), s
  • ligan-gated ion channels (ionotropic receptors)
  • G-protein coupled receptors (GPCR, metabotropic receptors)
  • receptor: protein that transmits a signal upon the binding of a ligand
33
Q

What is neuromodulation?

A

slow synaptic transmission,
extrasynaptic transmission

34
Q

Is synaptic transmission unidirectional? if so, why?

A
  • yes
  • vesicles are located on one side
35
Q

What is the major excitatory neurotransmitter in the nervous system? What are the major inhibitory neurotransmitters?

A
  • glutamate
  • GABA and glycine
36
Q

Which is slower - synaptic transmission or axonal conduction?

What does each synapse introduce into the neural pathway? how much?

A
  • synaptic transmission
  • a delay (0.5 msec/synapse)
37
Q

What are more susceptible to fatigue, hypoxia, and drug effects - axons or synapses? What does this mean?

A
  • synapses
  • pathways fail first at synapses
38
Q

How do different kinds of drugs work (tranquilizers, anesthetics, narcotics, anticonvulsants, muscle relaxants)?

A
  • by modifying activity selectively among the differnent kinds of chemical synapses
39
Q

What diseases are manifestations of selective synaptic dysfunction?

A
  • Parkinson’s, tetanus, myasthenia gravis, various intoxications, etc
40
Q

Neuropeptides (eg opiod peptides, the neurokinin substance P)….

how are they released?

How do they modulate the excitability of the postsynaptic cells?

Does release of neuropeptides requires stronger presynaptic depolarization than small synaptic vesicles?

Extrasynaptic transmission also occurs between ______ and __________.

A
  • from large-dense core vesicles (rather than small synaptic vesicles) outside of the synaptic cleft
  • through activation of extrasynaptic G-protein coupled receptors.
  • yes
  • neurons, adjacent glial cells (astrocytes, microglia)
41
Q

How do astrocytes supporst synaptic transmission (4 ways)?

A
  • recycle neurotransmitters
  • secrete neurotrophic factors (eg neural growth factor) that stimulate the growth and maintenance of neurons
  • dictate number of synapses formed on neuronal surfaces and modulate synapses in adult brain
  • maintain appropriate ionic composition of extracellular fluid surrounding neurons, by absorbing excess potassium and other larger molecules
42
Q

What is the net movement of substances along the axon?

What are the two rates?

What are the two directions?

A
  • axonal transport
  • fast axonal transport (100-500 mm/day)
  • slow axonal transport (1-10 mm/day)
  • Anterograde transport and retrograde transport
43
Q

What is the transport of materials down the axon away from the cell body? What is this important for?

A
  • anterograde transport
  • for renewing proteins along the axon and thus maintain the axon
44
Q

What is transport from the axon terminal toward the cell body?

How do viruses (rabies) and neurotoxins (tetanus toxin) take advantage of this?

What do tetanus and Botulinum toxins do?

A
  • retrograde transport
  • This is the mechanism by which they gain access to the CNS
  • they are proteases which cleave neuronal SNARE-proteins

002 - 6120 - Vet Neurobiology (23 decks)

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