neural basis - matt roser, L2 Flashcards

1
Q

Who measured the speed of axon potentials and what was the speed?

A

Von Helmholtz measured the speed of axon potentials at 90 ft/sec

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

What hypothesis did Von Helmholtz refute?

A

The hypothesis of ‘vitalism’ which suggested that neural signals were a vital force of nature

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

Who is credited with the invention of the method for staining neurons?

A

Camillo Golgi invented the method of staining neurons with silver nitrate, known as the ‘Golgi’ method

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

What concept did Santiago Ramón y Cajal discover regarding neurons?

A

Cajal discovered the synapse and the functional polarity of neurons

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

What was the disagreement between Golgi and Cajal?

A

Golgi believed the nervous system was a continuous mass, while Cajal believed it was composed of individual units

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

What significant publication did Donald Hebb release in 1949?

A

The Organization of Behaviour

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

What does Hebb’s theory propose about brain activity?

A

It proposes that complex psychological phenomena might be produced by brain activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are neurons considered in the nervous system?

A

Neurons are the basic, distinct units of the nervous system

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

What is the resting potential of a neuron?

A

-70mV

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

What is the role of astrocytes in the central nervous system?

A

Astrocytes supply nutrients, structural support, clean-up, and chemical protection for neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two primary types of glial cells in the peripheral nervous system?

A

Schwann cells and satellite cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the function of the sodium-potassium pump?

A

It exchanges 3 Na+ (sodium) ions for 2 K+ (potassium) ions to maintain ion concentrations
-sodium ions must be kept in greater concentration outside the cell by low permeability

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

What happens when depolarization reaches a threshold in a neuron?

A

An action potential is generated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the synaptic cleft?

A

The space separating pre- and post-synaptic membranes

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

What are excitatory post-synaptic potentials (EPSPs) caused by?

A

Opening Na+ channels leading to depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do inhibitory post-synaptic potentials (IPSPs) do?

A

Hyperpolarize the neuron and move the potential away from the firing threshold
-K+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is temporal summation in neural processing?

A

PSPs in close succession overlap and add together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the most common excitatory neurotransmitter in the brain?

A

Glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the role of GABA in the brain?

A

It acts as the most common inhibitory neurotransmitter

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

What effect does dopamine have in the brain?

A

It can be excitatory, inhibitory, or modulatory depending on the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the mesolimbic system associated with?

A

Reward and learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the difference between agonists and antagonists in drug action?

A

Agonists facilitate post-synaptic effects, while antagonists inhibit them

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

What is positive reinforcement?

A

The presentation of an appetitive stimulus in association with a behavior

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

What is the result of anterograde amnesia?

A

Inability to form new long-term memories following injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What did Cajal propose about synaptic connections?

A

They are modified by learning and can persist as memory

strength can be increased by sensitisation and classical conditioning -> reduced by habituation -> storage of non declarative memory is embedded in the neural circuit that produces the behaviour -> unconscious memories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the effect of dopamine antagonists on reinforcement learning?

A

They block reinforcement learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the role of the hippocampus in memory?

A

It is involved in memory consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Fill in the blank: The brain’s most common inhibitory transmitter is _______.

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

True or False: The synapse is the junction where neurons communicate with each other.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the process of classical conditioning?

A

Association between two stimuli and an automatic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Anterograde amnesia?

A

Inability to form new long term memories following insult / injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is retrograde amnesia?

A

Inability to recall memories preceding insult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which brain structures are primarily involved in memory consolidation?

A

Medial Temporal Lobe & Hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does ECT stand for?

A

Electroconvulsive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Who is Henry Molaison commonly referred to in studies of memory?

36
Q

What type of surgery did H.M. undergo?

A

Bilateral resection of medial temporal lobe including the hippocampus

37
Q

What type of memory remained intact after H.M.’s surgery?

A

Previous declarative memory (digit span, perceptual learning, instrumental & classical conditioning)

38
Q

What type of amnesia did H.M. experience?

A

Dense anterograde amnesia

39
Q

Is the hippocampus necessary for short term memory?

40
Q

What is the critical function of the hippocampus?

A

Consolidation of new memories

41
Q

What principle explains the strengthening of synapses through simultaneous input?

A

Hebbian learning

42
Q

What must occur for long-term potentiation (LTP) to be induced?

A

*The postsynaptic cell must be depolarized (by strong input)
*The postsynaptic cell must receive additional input (weak input)

43
Q

When was long-term synaptic potentiation (LTP) first observed?

44
Q

What is the cellular basis of all long-term learning?

A

Use-dependent strengthening of synaptic connections

45
Q

What does Hebb’s law state?

A

‘Cells that fire together wire together’

46
Q

What neurotransmitter is involved in long-term potentiation?

47
Q

What type of receptors are NMDA receptors?

A

Double gated – transmitter & voltage
contain transmembrane channel for Ca2+

48
Q

What happens when glutamate binds to NMDA receptors?

A

receptors depolarise the cell (remove the MG+ block), Opens Ca2+ channel, activating enzyme

49
Q

What triggers the insertion of more AMPA receptors into the membrane?

A

Activation of enzyme by Ca2+, insertion of more AMPA receptors into the membrance, retrograde messenger leads to increased presynaptic glutamate release -> leading to bigger excitatory sensory potentials

50
Q

What is the result of low-frequency stimulation of a synapse?

A

Long-Term Depression

51
Q

What happens to inputs that do not contribute to postsynaptic firing?

A

They are weakened

52
Q

What do neurons work as in processing information?

A

A network of units

53
Q

How do drugs affect synaptic transmission?

A

In many ways

54
Q

What is reinforced behavior likely to do?

A

Increase the likelihood of reoccurring

55
Q

How are learned behaviors, experience, and memory instantiated in the brain?

A

As patterns of synaptic strength

56
Q

what does the cell body contain?

A

nucleus - DNA coding production of proteins which serve functions within the cell
mitochondria - produce adenosine phosphate - energry
-both used in processes within dendrites, axon and terminal buttons

57
Q

what are the supporting cells?

A

neuroglia
-half of brains volume
-central ns glia cells are astrocytes and oligodendrocytes
-peripheral ns glia cells are schwann and satelitte cells

58
Q

what is the role of oligodendrocytes in the central nervous system?

A

form processes which produce the myelin sheath

59
Q

how neurons work?

A

transmission - one direction, dendrites -> terminals
-dendrites & soma recieve input from previous neurons
-input changes potential of the neuron
-resting potential is the charge across the membrance at rest - membrane is polarized
-charge is caused by differences in ion concentractions and maintained by diffusive & electrostatic pressures

60
Q

what is the process of depolarization?

A
depolarisation
61
Q

what happens in the process of neural transmission?

A

NT molecule binds with a receptor -> opens ion channels and changes to the polarisation of the post synaptic membrane
-effects depend on ion channel opened: excitatory and inhibitory

62
Q

what happens in neural processing?

A
  1. ion channels open and PSPs decay over time
  2. several EPSPs needed to meet threshold
  3. allows inputs from temporal and spatial summation -> IPSP & EPSPs CANCEL EO
63
Q

what effect do the primary transmitters have?

A

-exicatory & inhibitory effects
-effects on post synaptic neuron is determined by the receptors present, the state of the neuron and the presence of other transmitter substances -> complex modulation of neural processing

64
Q

what does glutamate do?

A

increases the membrance potential of the post synaptic cell
-is an amino acid produced by neurons metabolism
-activates types of receptors e.g. NMDA receptors control Na+ and Ca2+ gates
-Ca2+ involved in changes to AMPA receptors -> long term potentiation

65
Q

what is GABA?

A

Gamma-AminoButyric Acid
-most common inhibitory transmitter

66
Q

what does GABA do?

A

-decreases membrance potential of the postsynaptic cell
-prevents excessive excitation, inhibitory interneurons increase the flexibility of the nervous system

67
Q

what does dopamine do?

A

-dopaminergic projections from substansia nigra and ventral tegmental area modulate activity in striate, limbic and contrical areas.

68
Q

what does dopaminergic projections from substantia nigra cause?

A

modulates input areas of the basal ganglia
-degenerations causes parkinsons disease

69
Q

what do dopaminergic projections from ventral tegmental areas modulate?

A

reward and learning,
changing behaviour to unexpected or highly salient stimuli
-stimuli associated are percieved as exciting or rewarding

70
Q

what do drugs have to cross in order to have an effect?

A

the blood-brain barrier
-aids regualtion of brains chemical enivronment

71
Q

what does drug action impact?

A

-precursor for AGO
-prevents storage of NT in vesicles
-inhibits release of NT (ant)
-stimulates release of NT (AGO)
-stimulates postsynptic receptors (AGO)
-blocks postsynaptic receptors (ANT)

72
Q

what are examples of drug action?

A

cocaine - a catecholamine agonist, blocks reuptake of dopamine and norepinephrine

73
Q

why are drugs addictive?

A

drug-taking behaviour is reinforced
-thru positive and negative reinforcement
-linked to release of dopamine in the nucleus accumbens - part of the mesolimbic dopaminergic system

74
Q

what is negative reinforcement?

A

the removal of an aversive stimulus
(e.g. anxiety) in association with a behavior

75
Q

why is temporal proximity important in addiction?

A

-both herion and morphine convert into dopamine in the brain but heriod is more addictive -> crosses the blood brain barrrier faster so is an effective reinforcer

76
Q

what is learning?

A

the acquisition of information

77
Q

what is memory?

A

the retention of information

78
Q

what is operant conditioning?

A

Involves an association between a learned response and a stimulus

Reinforcement, through presentation of an appetitive stimulus, and successive refinements of a complex behaviour leads to strengthening of associations between a stimulus and a response (the behaviour)

79
Q

what is hebbs rule?

A

a synapse that is repeatedly active when the post synpatic neuron is firing will become strengthened
-classical conditioning

80
Q

how is operant conditioning shown within the brain?

A

Basal ganglia integrates perception and action planning
-> Destruction leads to failure of instrumental conditioning

81
Q

what brain areas are included in reinforcement?

A

-main: ventral tegmentum and dopamine

82
Q

how is the ventral tegmentum reinforced?

A

-electircal microstimulation of VT have reinforcing effects on behaviours -> projects to nucleus accumbens, prefrontal cortex, hippocampu and the amygdala - the **mesolimbic dopaminergic system **
-extracellular dopamine concentraction and FMRI activation increased in Nucleus accumbens after stimulation

83
Q

how is dopamine reinforced?

A

-DA responds to the reward durinf the period when the monkey is learning a task -> reward is unexpected until performed reliably
-dopamine in nucleus accumbens surges in response to the predictive stimulus
-response of midbrain dopaminergic neurons represents a learning signal that codes for errors in prediction of reward

84
Q

what is the mesolimbinc dopamine system involved in?

A

modulation of associative learning in general, not only that involving reinforcement

85
Q

why is long term depression caused by low frequency stimulation of a synapse?

A

weakened neurons, after inputs which aren’t involved -> learning becomes insatiated