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Neuroscience > Learning/Memory and Reward, dopamine, and addiction > Flashcards

Learning/Memory and Reward, dopamine, and addiction Flashcards

1
Q

learning

A

process of encoding new information

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2
Q

memory

A

the newly encoded information ⇒ formalizing with physiological and biological change
- Can be stored/present in the brain across short seconds to long years over timescales
- The expression of learned memories allows for new behavior, decision making, and adaptation

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3
Q

long term potentiation (LTP)

A

strengthening of synaptic connections (potentiation) as a consequence of repeated activation
- Cells that fire together wire together
- Initially discovered in rabbit hippocampus

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4
Q

what does balance of synaptic strengthening/weakening across brain regions reflect?

A

the storage and decay of information during learning and forgetting

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5
Q

what is memory consolidation necessary for? When does it happen?

A

stability; sleep

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6
Q

what does LTP stimulate?

A

an input neuron and get output activity

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7
Q

components of LTP? (5)

A
  • LTP is a change in the baseline strength of a synaptic connection
  • Durability depends on how the stimulus is induced ⇒ most often it is not permanent for a given synapse
  • The collective cells underlie learning
  • There are also depressions across synapses after the experience
  • You can demonstrate an increase in the connection strength
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8
Q

how does repeated activation change neurons? (3)

A
  • morphology
  • membrane receptor makeup and concentration
  • gene expression
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9
Q

how does morphology change from repeated activity of neurons?

A

If the protrusions change in shape/multiply at the synapse this can change morphology of neurons in striatum

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10
Q

what does morphology refer to?

A

dendritic spines/synaptic contact points

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11
Q

how does membrane receptor makeup and concentration change from repeated activation?

A

The pre learning state has less vesicles and less receptors but after LTP both are increased
- Neurotransmitter release
- Neurotransmitter receptors

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12
Q

how does gene expression change from repeated neural activation?

A

epigenetics or gene alterations

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13
Q

Non-declarative/Procedural memory

A

automatic, motor, and skill based learning ⇒ sequences of action we engage in a lot
- Also things with background associations such as pavlovian

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14
Q

Nondeclarative types of memory (3)

A
  • Skills and habits ⇒ basal ganglia, cerebellum, neocortex
  • Emotional associations ⇒ amygdala
  • Adjusting reflexes ⇒ cerebellum
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15
Q

declarative memory

A

what and where memories that are explicit ⇒ encyclopedia information

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16
Q

types of declarative memory?

A
  • episodic
  • semantic
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17
Q

episodic memory

A

remembering events
- Autobiographical
- Spatial

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18
Q

semantic memory

A

knowing facts

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19
Q

what lobe is involved in declarative memory?

A

the medial temporal lobe

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20
Q

associative learning

A

pavlovian conditioning and operant conditions results in non declarative or implicit memories
- Forming unconscious associations and expectations about the world
- Procedural memories ⇒ motor plans and skills

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21
Q

HM

A

treated for temporal lobe epilepsy with a bilateral lesion of part of his medial temporal lobe
- removal/disconnection of the hippocampus and amygdala

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22
Q

what happened after HM’s surgery?

A

He was unable to form new declarative memories after ⇒ facts, events, people

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23
Q

which memories were intact after HM’s surgery?

A

Procedural memories were intact (aka motor memories)

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24
Q

what happens when people without declarative memory are repeatedly asked to draw a star?

A
  • The same people can do a procedural task where they draw lines between the two stars and stay in between the lines
  • After multiple days of working on this they get better at it even though they don’t remember doing it prior
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25
Q

what brain regions are involved in procedural memory?

A

cortex, basal ganglia, thalamus loop

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26
Q

what type of phenomenon does procedural memory allow? (3)

A

Associative learning, motor skills, habits
- damage impairs motor control and skill learning

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27
Q

Huntington; what don’t they have deficits in?

A

medium spiny neurons die off in the striatum and people often have motor impairments
- Happens progressively based on striatal damage
- Don’t have deficits in declarative memories

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28
Q

medial temporal lobe damage results

A

leads to disruption of declarative and emotional memory formation

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29
Q

Hippocampus

A

“C” shaped that wraps around the thalamus and has an output track called the fornix

30
Q

Papez circuit

A

responsible for declarative memory formation
- Hippocampus ⇒ fornix tract ⇒ mammillary bodies ⇒ mammillothalamic tract ⇒ anterior thalamus ⇒ cingulate gyrus ⇒ hippocampus

31
Q

what does the hippocampus give us in terms of information?

A

the what and where of information

32
Q

spatial memory cells (2)

A
  • place cells
  • grid cells
33
Q

place cells

A

where specific location encoding is done by individual neurons in the hippocampus ⇒ fire at a specific location

34
Q

grid cells

A

spatial geometry encoding by individual neurons in entorhinal cortex
- represented by action potentials for a single grid cell based on space

35
Q

how does the hippocampus reflect where you are in space?

A

they change the activity of neurons

36
Q

amygdala

A

key for linking emotional experience to events during memory formation

37
Q

where does memory formation generally occur?

A

largely in subcortical structures

38
Q

where does memory storage generally occur?

A

distributed across cortical areas

39
Q

what does the frontal cortex encode?

A

episodic/semantic

40
Q

what does the motor cortex and cerebellum encode?

A

procedural

41
Q

what do sensory specific cortices and association cortices encode?

A

audio or visual memory

42
Q

T/F the medial temporal lobe is where memories are long term stored?

A

no, we know this from HM

43
Q

reward circuit

A

direct behavior toward advantageous stimuli
- promote future acquisition

44
Q

examples of reward circuits

A

Food, sex, exercise, social interaction ⇒ evolutionarily advantageous that we seek out for survival

45
Q

what are reward circuits important for? (3)

A
  • signaling value of rewards
  • directing learning about them
  • producing the motivation to obtain them
46
Q

how are rewards experienced?

A

as positive emotions

47
Q

what are negative effects of reward circuits?

A

can also produce disadvantageous reward seeking behavior, as happens in addiction

48
Q

major brain regions that control reward seeking and are affected by drugs (2)

A
  • basal ganglia
  • limbic system
49
Q

what parts of the basal ganglia are involved in reward seeking (2- structure and neurotransmitter)

A

dopamine, striatum

50
Q

what parts of the limbic system are involved in reward seeking (4)

A

prefrontal cortex, amygdala, insula, hippocampus

51
Q

what areas of dopamine neuron cell bodies are in the midbrain? (2)

A
  1. substantia nigra pars comopacta
  2. ventral tegmental area
52
Q

what pathway is involved with the substantia nigra pars compacta?

A

nigrostriatal pathway
- Motor systems, control of movement, etc.
- projects to striatum

53
Q

what are the pathways of the ventral tegmental area?

A
  • mesostriatal/mesolimbic pathway
  • mesocortical pathway
54
Q

what does the mesostriatal/mesolimbic pathway do?

A

engaged during reward related behaviors
- projects to the nucleus accumbens

55
Q

what does the mesocortical pathway do?

A

project to frontal and nucleus accumbens
- Make and release dopamine but project to different parts of the forebrain in prefrontal area

56
Q

what do all parts of the striatum receive?

A

strong axon inputs from dopamine neurons located in the different parts of the midbrain

57
Q

where are dopamine neurons concentrated? Where do they project to?

A

SNc; dorsal striatum (caudate/putamen) and VTA
- from there they project to the nucleus accumbent to make a W shape

58
Q

Brain stimulation reward (BSR)

A

animals will work very hard to receive electrical stimulation of certain brain regions
- You can stimulate certain parts of the brain to demonstrate it will create a value of a reward signal

59
Q

what species was BSR done with?

A

with mice by implanting a stimulation device and animals will work really hard to get stimulation delivered to parts of the brain
- the rat learned that if it presses the bar there will be a zap of stimulation into its brain via the electrode placed there
- this is possible for feelings of reward when we engage in experiences

60
Q

what regions support BSR? (5)

A
  • VTA/SNc
  • Medial forebrain bundle
  • Septum
  • PFC
  • Striatum
61
Q

what brain areas support the strongest reward?

A

VTA and medial forebrain area

62
Q

what dampens BSR and blunts reward seeking?

A

dopamine neuron lesions or pharmacological inactivation of dopamine signaling
- these studies established that dopamine is critical for a core feature of behavior ⇒ positive reinforcement

63
Q

Rewarding stimuli

A

things that feel good and are wanted
- Stimulate dopamine release in the nucleus accumbens and striatum
- Eating, sex, exercise, social activities, etc.
- This signal is needed for learning and motivational drive for survival, but is co-opted by drugs

64
Q

how do drugs compare to normal rewards?

A

most drugs produce much greater dopamine levels, compared to food rewards ⇒ have an impact on the brain that promote things non-essential for survival
- drug effects extend longer over time than food which engaged neuronal mechanisms even more

65
Q

T/F all drugs increase dopamine signaling?

A

(T) drug classes/types like stimulants vs opioids have the same effect
- Increase dopamine signaling in the striatum
- Like natural rewards of different modalities, these classes also increase dopamine

66
Q

what does drug exposure do to genes?

A

rapidly alters gene expression in reward systems
- May change expression in reward circuits ⇒ increase or reduce

67
Q

what happens with drug tolerance?

A

chronic administration creates tolerance for what that drug does
- Often other parts are sensitized
- The two things can happen at once => This is what makes addiction cycles viscous

68
Q

what does repeated drug exposure do to the dopamine system?

A

they sensitize and overactivate reward systems
- The same experience promotes a greater response in the brain than it does originally

69
Q

what does drug exposure do to stratal neuron structure?

A

by increasing the density and thickness of the spines on the neurons, the synaptic connectivity is stronger and signaling at the synapses is stronger
- changes the physical makeup

70
Q

T/F drugs damage brain tissue?

A

most drug use does not damage brain tissue, but produces changes in gene expression, morphology, and neurotransmission that affect learning, decision making, and motivation

71
Q

how does sucrose compare to amphetamine?

A

sucrose has much less of a plasticity increase as amphetamine does
- Shows the drugs activate things in an exaggerated way

72
Q

addiction

A

a medical condition, based on drug effects on brain systems that support normal reward seeking and motivation
- Continued drug use despite negative consequences
- Persistent drug craving and compulsive use
- Relapse

Neuroscience (18 decks)

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