Unit 2 Week 4 Flashcards

1
Q

What is learning?

A

acquisition of new knowledge or skills

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2
Q

What is memory?

A

retention of learned information

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3
Q

What are the two broad categories of memory?

A

Declarative (explicit)
-memory of facts and events
Nondeclarative (implicit)
-memory for skills, habits and others that don’t have a conscious component

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4
Q

Describe the flow of sensory information into long-term memory

A

sensory experience, memory acquisition, short-term memory, memory consolidation, long-term memory

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5
Q

Where is memory stored in neural circuits?

A

Distributed Memory Storage: a neural network model
-unique pattern or ratio of neuronal activity
-distributed memory
-no single neuron represents specific memory

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6
Q

What is the cellular basis of memory?

A

modification of synaptic strengths that change the input-output relations of neurons within neural circuits

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7
Q

Where do memories reside?

A

in synaptic modification

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8
Q

What is synaptic pasticity?

A

describe changes in the strengths of synaptic connections in response to experience and neuronal activity

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9
Q

What is synaptic strengthening?

A

-synaptic potentiation
-formation of new synapses

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10
Q

What is synaptic weakening?

A

-synaptic depression
-elimination of exiting synapses

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11
Q

What is the Hippocampus?

A

a brain region that is important for memory formation

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12
Q

What is LTP?

A

Long Term Potentiation
A long-lasting increase of the effectiveness of synaptic transmission
Shown by increased EPSP amplitude

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13
Q

What is Hebb’s rule?

A

synaptic potentiation results when presynaptic activity correlated with strong activation of the postsynaptic neuron

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14
Q

What does NMDA receptor activation depend on?

A

both glutamate and voltage
-Mg2+ blocks the channel at certain negative Vm, even if glutamate binds
-Need depolarization and glutamate for activation and let in lots of Ca2+

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15
Q

What does the NMDA receptor act as?

A

coincidence detector
-Ca2+ entry through NMDA receptor specifically signals presynaptic and postsynaptic neurons are active at the same time

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16
Q

What are the mechanisms of LTP in CA1?

A

Ca2+ through NMDA receptors activate protein kinases (CaMKII)
Achieve LTP by:
1. increasing the effectiveness of existing AMPA receptors on the membrane via phosphorylation of CaMKII
2. inserting new AMPA receptors into the membrane

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17
Q

What is the BCM theory?

A

An extension of Hebb’s rule…
Synaptic depression results when presynaptic activity is correlated with a weak depolarization of a postsynaptic neuron

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18
Q

What is LTD?

A

Long-Term Despression

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19
Q

What is the mechanism of LTD in CA1?

A

-increase protein phosphatase activity
-de-phosophorylate AMPA receptors on the membrane
-remove existing AMPA receptors

20
Q

What is the difference between LTD and LTP?

A

opposite change of AMPA receptors

21
Q

What accounts for bidirectional synaptic changes?

A

When the postsynaptic cell is weakly depolarized by other inputs: active synapses undergo LTP instead of LTP

22
Q

Bidirectional plasticity is governed by two simple rules. What are they?

A

Synapses during strong depolarization of postsynaptic neuron causes LTP (Hebb’s rule)
Synapses during weak depolarization of postsynaptic neuron causes LTD (BCM theory)

23
Q

Describe memory consolidation

A

Phosphorylation insufficient as long-term memory consolidation mechanism
-phosphorylation of a protein is not permanent
-memories would be erased
Protein molecules themselves are not permanent

24
Q

Describe the regulation of CaMKII

A

-once activated, autophosphorylation will keep kinases stay “on” permanently
-which may hold LTP and memory for a long time

25
Q

Describe how protein synthesis relations to memory consolidation

A

-new protein synthesis required during the period of memory consolidation and for formation of long-term memory

26
Q

What is CREB? Why is it relevant?

A

cyclic AMP response element binding protein (a transcription factor)
-bind to cAMP response elements (CREs) to regulate expression of specific genes, which ultimately leads to new protein synthesis

27
Q

Describe the regulation of gene expression by CREB

A

CREB-2: a repressor of gene expression
CREB-1: an activator of gene expression

28
Q

What is synaptic remodeling?

A

formation of new synapses during learning or memory and demolition of old synapses during learning and memory

29
Q

What are Channelrehodopsins (ChRs):

A
  • a subfamily of light-gated cation channels
    -they serve as sensory photoreceptors in unicellular green algae, controlled phototaxis
30
Q

What is Halordopsin?

A

-a yellow-light-activated Cl- pump, found in archaea
-to move chloride ions into the cell, reducing the membrane potential

31
Q

What can optogenetics be used for?

A

to control neural activity with light
positive ions = neuron activation
negative ions = neuron inhibition

32
Q

What happens to the brain during sleep?

A

the brain is “disconnected” from both input and output ends

33
Q

What is the Electroencephalogram (EEG)?

A

-measurement of generalized activity of cerebral cortex
-helps diagnose neurological conditions, such as epilepsy and sleep disorders, and for research

34
Q

How are large EEG signals activated?

A

synchronous acitivy

35
Q

What are the three functional brain states in humans?

A

awake
REM sleep (rapid eye movement)
Non-REM sleep (slow-wave)

36
Q

What type of sleep is known as paradoxical sleep? Why?

A

REM sleep, EEG of REM sleep is very similar to EEG of an awake state

37
Q

What is happening during non-REM sleep?

A

an idling brain with moveable body, also called slow-wave sleep

38
Q

What is happening during REM sleeo?

A

an active, hallucinating brain with a paralyzed body, where dreams occur

39
Q

What are the Sleep promoting neurons?

A

acetylcholine in the midbrain/pons

40
Q

What do GABAergic neurons in the preoptic area (POA) promote?

41
Q

What activates GABAergic POA neurons?

42
Q

What do neuropeptide hypocretin (Hcrt) and Hcrt neurons promote?

A

wakefulness

43
Q

What causes narcolepsy?

A

mutations of Hcrt

44
Q

What are the sleep-promoting factors?

A

Adenosine: released by neurons; may have inhibitory effects of diffuse modulatory systems
Nitric Acid (NO): triggers release of adenosine
Muramyl Dipeptide: isolated from the CSF of sleep-deprived goats, facilitates non-REM sleep
Interleukin-1 (cytokine): synthesized in brain, stimulates immune system, induces fatigue and sleepiness
Melatonin: released at night, inhibited during daylight; helps initiate and maintain sleep- used to treat symptoms of jet lag and insomnia

45
Q

What is the broad behavioral definition of sleep?

A

Sleep is readily reversible quiescence state that is associated with reduced responsiveness to the environment and under homeostatic control

46
Q

Why do we sleep?

A

Restoration
-sleep to rest and recover and prepare for when we wake again
- conserve energy, repair and clear metabolic
waste in the brain, facilitate memory and
synaptic plasticity
Adaptation
-sleep to keep out of trouble, hide from predators