Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the axon?

A

the cell’s output structure (directional propagation)

one (major) axon per cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the three distinct parts of the axon?

A

initial segment
main axon
axonal branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the initial segment in the axon?

A

beginning of axon (at soma)

where AP initiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the main axon?

A

tube-like structure arising from soma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the synaptic terminal or bouton?

A

present at termination of axon

connects to dendrite of another neuron

contains transmitter substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do neurons signal within neurons?

A

conduction: transmembrane current

electrotonic (passive)
active (electrogenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

excitable - voltage/ligand gated channels

membrane potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

always the same amplitude & duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is ionotropic neurotransmission?

A

“fast” - current/voltage changes

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is temporal summation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is spatial summation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are sensory neurons?
sensory organs to CNS "receptors"
26
What are motor neurons?
CNS to muscles and organs "effectors"
27
What are interneurons?
connections within CNS "processors" principal cells and local circuit neurons
28
What is the "stretch" reflex?
tap on your knee, you kick "knee jerk", making sure your spinal cord is intact sensory neuron directly to motor neuron
29
What is the "withdrawal" reflex?
away from painful stimulus, involves interneuron sensory neuron to interneuron to motor neuron
30
Why might an interposed interneuron be important to a reflex?
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
How are changes in synaptic efficacy involved in learning and memory?
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
What are simple systems in learning and memory?
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
What is Aristotle's idea of association by contiguity?
stimuli that occur together tend to form an association where the thought of one leads to the thought of the other
34
What are some examples of non-associative learning?
habituation sensitization
35
What is an example of associative learning?
classical conditioning
36
What is the definition of habituation?
repetitive stimulation gradually produces less and less of a response
37
What is the definition of sensitization?
a noxious or strong stimulus increases the amplitude of a response to any other stimulus
38
What is the definition of classical conditioning?
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
What are the reasons that Aplysia is convenient as an animal model?
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
How is habituation shown in the gill withdrawal reflex?
progressive decrease in gill withdrawal to siphon taps when the siphon taps are repeated
41
How is sensitization shown in the gill withdrawal reflex?
sudden enhancement of gill withdrawal to siphon tap after a tail shock is given alone
42
How is classical (alpha) conditioning shown in the gill withdrawal reflex?
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
What is the neural control of the gill withdrawal reflex?
the circuit has a direct sensory to motor connection it also has interposed sensory - motor interneurons
44
How was sensory adaptation shown to NOT be the neural site of habituation?
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
How was motor fatigue shown to NOT be the neural site of habituation?
reduction of muscular responsiveness to motor drive it can't keep retracting get some motor response every time, so not true
46
How was sensory - motor depression (homosynaptic) shown to be the neural site of habituation?
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
What was the experiment to determine whether synaptic change occurred pre- or post-synaptically in habituation?
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
What does homosynaptic depression mean?
only have to effect one synapse (the one between sensory and motor)
49
What are the functional changes in presynaptic currents during habituation?
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
What are the anatomical changes in number of contacts during habituation?
less physical connections 1. fewer sensory to motor synapses 2. same number of vesicles, but less docked
51
What is habituation in relation to the gill withdrawal response?
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
How was sensory facilitation shown to NOT be the neural site of sensitization?
increase in responsiveness of sensory neurons to stimulus responding more to the tap response doesn't change, so isn't the site
53
How was motor facilitation shown to NOT be the neural site of sensitization?
increase of muscular responsiveness to motor drive stimulate motor neuron response doesn't change
54
How was sensory - motor facilitation (heterosynaptic) shown to be the neural site of sensitization?
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
What was the experiment to determine whether synaptic change occurred pre- or post-synaptically in sensitization?
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
What are the functional changes in presynaptic currents in heterosynaptic facilitation?
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
What are the anatomical changes in number of contacts in heterosynaptic facilitation?
more physical connections more sensory to motor synapses more docking of vesicles
58
What is the circuit mediating heterosynaptic facilitation?
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
How does 5-HT lead to presynaptic facilitation?
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
What are the steps in the mechanism of heterosynaptic facilitation?
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
What is the mechanism of long term heterosynaptic facilitation?
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
What are the steps of the mechanism of long term presynaptic facilitation?
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
What is sensitization in relation to the gill withdrawal response?
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
What is "true" classical conditioning?
production of a behavioral response to a previously neutral stimulus due to its pairing with another stimulus that evokes the response
65
What is alpha conditioning?
enhancement of a behavioral response to a weak stimulus when it is paired with a strong or noxious stimulus
66
What is pseudoconditioning?
conditioning obtained without contiguity between neutral and unconditioned stimuli (noxious UCS = sensitization)
67
What is differential conditioning?
greater conditioning to stimulus paired with UCS than another stimulus unpaired with UCS
68
What is the mechanism of classical conditioning in the gill withdrawal reflex?
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
What are the cellular correlated of classical conditioning?
circuit: similar to sensitization mechanism: similar to sensitization, activity dependent (differential) heterosynaptic facilitation
70
How is activity dependence a mechanism of classical conditioning?
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
What are the steps involved in the mechanism of activity-dependent heterosynaptic facilitation?
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
What is classical conditioning in relation to the gill withdrawal response?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions