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PSYCH 371 > Chapter 2: Essential Neurobiology > Flashcards

Chapter 2: Essential Neurobiology Flashcards

1
Q

What is the basic activity pathway in the brain that underlies behavior?

A
  1. ionic channels
  2. membrane current
  3. neuronal activity
  4. local network activity
  5. systems activity
  6. cerebral activity
  7. behavior
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2
Q

What is the soma (cell body)?

A

rounded, centrally located structure

control and energy house of the neuron

contains the cell’s nucleus (DNA), controls protein manufacturing, directs metabolism

also receives input from other neurons

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3
Q

What are the dendrites?

A

branched appendages off the soma

input structure of a neuron (information collectors)

receives outputs of other neurons, dendritic spines, input filtering

inputs number in the thousands

if excitatory input large enough, cell may generate an output (action potential)

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4
Q

What is the axon?

A

the cell’s output structure (directional propagation)

one (major) axon per cell

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5
Q

What are the three distinct parts of the axon?

A

initial segment
main axon
axonal branches

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6
Q

What is the initial segment in the axon?

A

beginning of axon (at soma)

where AP initiated

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7
Q

What is the main axon?

A

tube-like structure arising from soma

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8
Q

What are the axonal branches in the axon?

A

bifurcating “mini axons” at end of main axon

connect to dendrites/somas of other cells at the synaptic terminal/button

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9
Q

What is the synaptic terminal or bouton?

A

present at termination of axon

connects to dendrite of another neuron

contains transmitter substance

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10
Q

How do neurons signal within neurons?

A

conduction: transmembrane current

electrotonic (passive)
active (electrogenic)

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11
Q

How do neurons signal between neurons?

A

transmission (chemical neuro-transmission)

ionotropic: excitatory (post-synaptic closer to threshold), inhibitory (less likely to excite)

metabotropic: influence the metabolism of a cell

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12
Q

What is the resting membrane potential?

A

the resting membrane potential is the drive for all neuronal signaling

inside of the cell is negative because of the unequal distribution of charged molecules

potassium (K+) is permeable

sodium (Na+), calcium (Ca2+), and chloride (Cl-), are much less permeable

organic anions are impermeable

large driving forces working to push Na+ and Cl- inside but the membrane won’t let them

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13
Q

What is the difference between cells such as nerve & muscle and all other cells?

A

excitable - voltage/ligand gated channels

membrane potentials

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14
Q

What direction does the resting potential drive ions through membrane channels?

A

K+ inside to out (hyperpolarization)
Na+ outside to in (depolarization)
Cl- outside to in (hyperpolarization)
Ca2+ outside to in (depolarization)

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15
Q

What is the all-or-none response in action potentials?

A

always the same amplitude & duration

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16
Q

What is the refractory response in action potentials?

A

two APs cannot overlap in time

inactive for a period of time based sodium channels voltage a time restraints

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17
Q

What is the sequence of events in an action potentials?

A
  1. resting membrane potential
  2. electrotonic depolarization to threshold (Na channels open)
  3. depolarizing phase of AP (Na+ entry, more Na+ channels open, more Na+ entry)
  4. repolarization phase of AP (Na channels close, no more Na entry, K+ channels open, K+ exits)
  5. hyperpolarizing phase of AP (delay before K+ channels close, K+ continues to exit)
  6. back to resting potential (K+ channels closed, redistribution of ions and charge)
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18
Q

What occurs in the propagation of the action potential?

A

the action potential is directionally passed down the axon like a traveling wave

once triggered at the axon hillock, it acts to depolarize the adjacent segment (away from the cell body) to threshold, forms leading edge of wave

this next segment then generates an action potential which acts to depolarize the next adjacent segment (leading edge) to threshold)

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19
Q

What is synaptic transmission?

A

at the synapse, the action potential opens Ca channels, allowing Ca2+ entry

Ca2+ acts as both a charge carrier AND a 2nd messenger

causes neurotransmitter vesicles to fuse with the membrane

release of neurotransmitter into synaptic cleft

binding of neurotransmitter to postsynaptic receptors, opening ligand-gating channels, post-synaptic currents, voltage changes

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20
Q

What is ionotropic neurotransmission?

A

“fast” - current/voltage changes

ligand-gated channels: excitatory (opening of depolarizing channels), inhibitory (opening of hyperpolarizing channels)

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21
Q

What is metabotropic neurotransmission?

A

“slow” - 2nd messengers, changes of “metabolism” of cell

modulation of future responsiveness

ligand binding, change that takes multiple chemical steps, effects last longer

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22
Q

What is the integration of synaptic activity?

A

synaptic potentials can summate

electrotonic propagation to the cell body/axon hillock

convergent activity has an opportunity o “add up” or “subtract”

excitatory and inhibitory inputs can cancel each other

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23
Q

What is temporal summation?

A

two or more APs from same presynaptic cell occurring close together in time

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24
Q

What is spatial summation?

A

two or more APs from different presynaptic cells occurring close together in space

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25
Q

What are sensory neurons?

A

sensory organs to CNS

“receptors”

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26
Q

What are motor neurons?

A

CNS to muscles and organs

“effectors”

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27
Q

What are interneurons?

A

connections within CNS

“processors”

principal cells and local circuit neurons

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28
Q

What is the “stretch” reflex?

A

tap on your knee, you kick “knee jerk”, making sure your spinal cord is intact

sensory neuron directly to motor neuron

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29
Q

What is the “withdrawal” reflex?

A

away from painful stimulus, involves interneuron

sensory neuron to interneuron to motor neuron

30
Q

Why might an interposed interneuron be important to a reflex?

A

indirect connection between sensory and motor

there to modify the reflex

fundamental but the flexion might injure you more, understand what the situation is and modify it to prevent other injury or bad outcomes

31
Q

How are changes in synaptic efficacy involved in learning and memory?

A

both short and long-term changes in simple behaviors result from changes in the strength of synaptic connections at specific sites in the nervous system

suggested by Ramon y Cajal (1894)
theorized by Donald Hebb (1949)
shown by Eric Kandel (2001)

32
Q

What are simple systems in learning and memory?

A

in order to systematically characterize changes in the nervous system that underlie changes in behavior (learning) and the retention of those behaviors (memory), one requires a simple system, both in terms of the behavior, its modification, and the organism demonstrating it

simple behaviors: reflexes
simple learning: habituation, sensitization, classical conditioning
simple organisms: invertebrates

33
Q

What is Aristotle’s idea of association by contiguity?

A

stimuli that occur together tend to form an association where the thought of one leads to the thought of the other

34
Q

What are some examples of non-associative learning?

A

habituation
sensitization

35
Q

What is an example of associative learning?

A

classical conditioning

36
Q

What is the definition of habituation?

A

repetitive stimulation gradually produces less and less of a response

37
Q

What is the definition of sensitization?

A

a noxious or strong stimulus increases the amplitude of a response to any other stimulus

38
Q

What is the definition of classical conditioning?

A

a process by which a “neutral” stimulus that previously did not elicit a specific behavioral response comes to elicit that response (in a reflex-like fashion) after it has been paired once or more times together with a stimulus that already elicits this response

39
Q

What are the reasons that Aplysia is convenient as an animal model?

A
  1. it engages in simple adaptive behaviors that are easy to study
  2. the total number of CNS neurons is small (~20,000), possible to trace neuronal circuitry involved in behavior
  3. neuronal soma are large and located on outside of ganglia, ease of recording and manipulation, even during behavior
  4. identifiable neurons due to invariant position, shape, and size within ganglia, between and within experimental consistency
40
Q

How is habituation shown in the gill withdrawal reflex?

A

progressive decrease in gill withdrawal to siphon taps when the siphon taps are repeated

41
Q

How is sensitization shown in the gill withdrawal reflex?

A

sudden enhancement of gill withdrawal to siphon tap after a tail shock is given alone

42
Q

How is classical (alpha) conditioning shown in the gill withdrawal reflex?

A

repeated paired presentations of light siphon taps (that do not elicit gill withdrawal) with tail shock (that do induce gill withdrawal) leads to the development of gill withdrawal to the light siphon taps alone

43
Q

What is the neural control of the gill withdrawal reflex?

A

the circuit has a direct sensory to motor connection

it also has interposed sensory - motor interneurons

44
Q

How was sensory adaptation shown to NOT be the neural site of habituation?

A

like getting habituated to smells, olfactory sensors shut down

reduction in responsiveness of sensory neurons to stimulus

sensory neurons also stop responding to tap

but neuron always responds the same way through the whole process, so not true

45
Q

How was motor fatigue shown to NOT be the neural site of habituation?

A

reduction of muscular responsiveness to motor drive

it can’t keep retracting

get some motor response every time, so not true

46
Q

How was sensory - motor depression (homosynaptic) shown to be the neural site of habituation?

A

reduction of sensory drive to motor neuron (presynaptic)

reduction of responsiveness of motor neuron (postsynaptic)

motor neuron eventually stops responding to the sensory neuron

47
Q

What was the experiment to determine whether synaptic change occurred pre- or post-synaptically in habituation?

A
  1. pharmacological receptivity of motor neuron to NT: if modification is postsynaptic, receptivity should go down, not the case, therefore not postsynaptic
  2. release of NT (Quantal analysis): analyze the “packets” (quanta) of NT released, separate the number of quanta from the quantal size
    changes in number of quanta = change in presynaptic release
    changes in quantal size = changes in postsynaptic receptivity
  3. number of quanta decrease, therefore the change is presynaptic, homosynaptic depression
48
Q

What does homosynaptic depression mean?

A

only have to effect one synapse (the one between sensory and motor)

49
Q

What are the functional changes in presynaptic currents during habituation?

A

changes in numbers of quanta typically reflect changes in presynaptic entry of calcium

pharmacological and electrophysiological isolation of Ca2+ currents contributing to sensory neuron AP in habituated Aplysia: reduction in width of spike and Ca2+ currents reduced

result: decrease in EPSP in motor neuron

50
Q

What are the anatomical changes in number of contacts during habituation?

A

less physical connections

  1. fewer sensory to motor synapses
  2. same number of vesicles, but less docked
51
Q

What is habituation in relation to the gill withdrawal response?

A

habituation mediated by a decrease in synaptic efficacy: homosynaptic depression

intracellular mechanisms controlling NT release: decrease in number of presynaptic vesicles released, decrease in presynaptic Ca2+ currents, decrease in docking of presynaptic vesicles

changes in anatomical connectivity: fewer sensory - motor neuron synapses

52
Q

How was sensory facilitation shown to NOT be the neural site of sensitization?

A

increase in responsiveness of sensory neurons to stimulus

responding more to the tap

response doesn’t change, so isn’t the site

53
Q

How was motor facilitation shown to NOT be the neural site of sensitization?

A

increase of muscular responsiveness to motor drive

stimulate motor neuron response doesn’t change

54
Q

How was sensory - motor facilitation (heterosynaptic) shown to be the neural site of sensitization?

A

increase of sensory drive to motor neuron (presynaptic)

increase of responsiveness of motor neuron (postsynaptic)

response of the motor neuron from the sensory neuron signal goes up

55
Q

What was the experiment to determine whether synaptic change occurred pre- or post-synaptically in sensitization?

A
  1. pharmacological receptivity of motor neuron to NT: if modification is postsynaptic, receptivity should go up, no increase, therefore not postsynaptic
  2. release of NT (Quantal analysis): analyze the “packets” (quanta) of NT released, separate the number of quanta from the quantal size
    changes in number of quanta = change in presynaptic release
    changes in quantal size = changes in postsynaptic receptivity
  3. number of quanta increase, therefore the change is presynaptic, heterosynaptic facilitation
56
Q

What are the functional changes in presynaptic currents in heterosynaptic facilitation?

A

changes in numbers of quanta typically reflect changes in presynaptic entry of calcium

pharmacological and electrophysiological isolation of Ca2+ current contributing to sensory neuron AP in sensitized Aplysia
increase on width of spike
Ca2+ currents increased

result: increased EPSP in motor neuron

57
Q

What are the anatomical changes in number of contacts in heterosynaptic facilitation?

A

more physical connections

more sensory to motor synapses
more docking of vesicles

58
Q

What is the circuit mediating heterosynaptic facilitation?

A

tail sensory neurons - modulatory (facilitating) interneurons – axo-axonic synapse on presynaptic bouton of siphon sensory neurons

increase in NT release of siphon sensory neurons

transmitter: serotonin (5-HT) & other biogenic amines

59
Q

How does 5-HT lead to presynaptic facilitation?

A

serotonin activates a metabotropic receptor to effectuate three biochemical results:

Gs protein/Adenyl cyclase/cAMP/PKA
phosphorylation (inactivation) of K+ channels (decrease K+ current)
activation of Ca2+ channels (increase Ca2+ current)
NT vesicles mobilized, exocytosis enhanced

prolongation of the presynaptic AP, increase Ca2+ entry, increase NT release, increase postsynaptic effect on motor neuron

60
Q

What are the steps in the mechanism of heterosynaptic facilitation?

A
  1. 5-HT
  2. Gs protein
  3. Adenyl cyclase (ATP to cAMP)
  4. PKA (decrease K+ current, increase Ca2+ current, increase vesicle mobilization)

net effect: increase NT release

61
Q

What is the mechanism of long term heterosynaptic facilitation?

A

consolidation of short term memory for sensitization into long term memory for sensitization: requirement of protein synthesis, anisomyocin blocked long-term but not short term facilitation

long term sensitization due to: maintenance of presynaptic facilitation (persistent PKA activation), growth of new synaptic connections

intimately related to biochemical pathways activated for short-term changes

62
Q

What are the steps of the mechanism of long term presynaptic facilitation?

A
  1. PKA
  2. MAPK
  3. translocation to nucleus
  4. activation of CREB, CRE gene expression

early: ubiquitin, persistent activity of PKA
later: activation of proteins necessary for synaptic growth?

net effect: maintenance of increase NT release

63
Q

What is sensitization in relation to the gill withdrawal response?

A

increase in synaptic efficacy mediated by heterosynaptic facilitation

intracellular mechanisms controlling NT release: increase in number of presynaptic vesicles released, increase in presynaptic Ca2+ currents, increase in docking of presynaptic vesicles

changes in anatomical connectivity: greater sensory - motor neuron synapses

64
Q

What is “true” classical conditioning?

A

production of a behavioral response to a previously neutral stimulus due to its pairing with another stimulus that evokes the response

65
Q

What is alpha conditioning?

A

enhancement of a behavioral response to a weak stimulus when it is paired with a strong or noxious stimulus

66
Q

What is pseudoconditioning?

A

conditioning obtained without contiguity between neutral and unconditioned stimuli (noxious UCS = sensitization)

67
Q

What is differential conditioning?

A

greater conditioning to stimulus paired with UCS than another stimulus unpaired with UCS

68
Q

What is the mechanism of classical conditioning in the gill withdrawal reflex?

A

GWR shows both alpha and differential conditioning

UCS = tail shock
paired (CS + mantle tap)
unpaired (CS - siphon) tap
greater enhancement of CR to CS+ than CS-

69
Q

What are the cellular correlated of classical conditioning?

A

circuit: similar to sensitization

mechanism: similar to sensitization, activity dependent (differential) heterosynaptic facilitation

70
Q

How is activity dependence a mechanism of classical conditioning?

A

coincidence of activity in sensory neuron and modulatory interneuron evokes greater facilitation

temporal contiguity & contingency: AP in sensory neuron, influx of Ca2+ (Ca2+ binding protein calmodulin, Ca2+/calmodulin binds adenyl cyclase)

amplification of 5-HT activation of adenyl cyclase - greater increase of cAMP

greater facilitation

71
Q

What are the steps involved in the mechanism of activity-dependent heterosynaptic facilitation?

A
  1. AP allows Ca2+ facilitation of adenyl cyclase
  2. 5-HT-Gs protein
  3. Adenyl cyclase (increase ATP to cAMP)
  4. increase in PKA (decrease in K+ current, increase in Ca2+ current, increase vesicle mobilization)

net effect: big increase in NT release

72
Q

What is classical conditioning in relation to the gill withdrawal response?

A

increase in synaptic efficacy mediated by activity-dependent heterosynaptic facilitation

mechanism of presynaptic facilitation similar to sensitization, additionally requiring contingent activation of sensory and facilitating interneuron

post-synaptic activity-dependent changes: retrograde signaling - presynaptic changes (NT release), postsynaptic changes (NT sensitivity)

PSYCH 371 (17 decks)

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