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Neuropsych > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Hormones

A

Chemicals produced by endocrine glands that travel to target cells via bloodstream

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2
Q

Pituitary Gland (“Master Gland”)

A
  • Controls other glands (adrenal, thyroid, gonads, mammary) and has systemic affects through release of hormones:
  • Reproductive hormones:
  • *Affect mood, cognition, behavior in both sexes
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3
Q

Hormones and Emotions

A
  • Testosterone increases libido in males, females.
  • Oxytocin- Promotes bonding; released during labor (uterine contractions), during breast feeding (milk letdown), during coitus in females, males
  • Prolactin released during breast feeding (milk production)
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4
Q

Estrogen and Emotions

A
  • Estrogen levels shift significantly during female’s life.
  • Depression mirrors these changes in estrogen.
  • Estrogen (estradiol) has profound effects on body & brain.
  • It activates genes to synthesize gene products, including trophic factors & enzymes that synthesize & metabolize neurotransmitters & receptors in females.
  • Affects the 3 main neurotransmitters involved in depression: Serotonin, Norepinephrine and Dopamine
  • Dysregulation during estrogen fluctuations may cause somatic and brain abnormalities.
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5
Q

Estrogen levels & Depression over the lifespan

A

Estrogen levels shift significantly during female’s life.
• Rise and cycle from puberty until menopause
• Rise dramatically during pregnancy
• Plummet postpartum
• Erratic during perimenopause (37-55)
• Minimal during menopause
• Depression mirrors these changes in estrogen.

Depression increases significantly during puberty.
• May worsen during luteal phase (14 days before) of cycle
• Major risk during postpartum after abrupt fall in estrogen
• Risk for depression, psychosis, mania
• Risk during perimenopause

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6
Q

Estrogen: effects on body & brain

A
  • It activates genes to synthesize gene products, including trophic factors & enzymes that synthesize & metabolize neurotransmitters & receptors in females.
  • Affects the 3 main neurotransmitters involved in depression: Seratonin, Norepinephrine, and Dopamine
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7
Q

Dysregulation during estrogen fluctuations may cause somatic and brain abnormalities.

A
  • During perimenopause:
  • Vasomotor sx’s (hot flashes, sweating) caused by dysregulation of hypothalamic thermoregulatory centers modulated by 5-HT, NE
  • Sxs of depression
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8
Q

Hormones and Cognitive Function

A
  • Studies comparing premenopausal and postmenopausal women, women in various stages of pregnancy, and females and males with varying levels of hormones indicate that hormones affect cognitive function.
  • Ultimately, cognition is determined by complex interaction of hormones and experience.
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9
Q

Stressor

A

Event that has an arousing effect

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10
Q

Stress responses

A

Behavioral and physiological responses to cope with stressor

•Exciting, sad, or frightening events elicit essentially same acute stress responses.

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11
Q

Chronicity (of stress hormones)

A

Major problem today in humans

-we experience such high and long-lasting stress reactions (i.e. work, school).

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12
Q

Stress Hormones: 2 biochemical pathways

A

“Fast response” by norepinephrine/epinephrine
•Prepares body for sudden burst of activity

“Slow response” by cortisol
•Prepares body for longer-lasting adaptations
•Activated in minutes to hours
•Helps body resist stressors
•Prepares body for longer-lasting adaptations (e.g., restoring energy that has been expended and making more available)
•Essential to life – without it you die; it’s how we deal with stress

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13
Q

High cortisol causes =

A

•Increased appetite
•Weight gain
•Increased abdominal fat
•Increased risk of cardiovascular disease and insulin-resistant diabetes
•Glucose intolerance
•Increased risk of insulin-resistant diabetes (NIDDM)
•Damaged arteries leading to atherosclerosis
•Hypertension/water retention
•Muscle weakness
•*Causes depression
•Cortisol level that does not decrease in
diurnal (through urine) fashion throughout day may be a marker for major depression.

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14
Q

*Cortisol and memory

A
  • Chronic stress results in continued high level of cortisol, which destroys hippocampal cells.
  • Impairs ability to provide negative feedback (which is when the brain is told to stop producing cortisol).
  • Keeps levels high, etc. in a pathological, vicious circle.
  • May impair memory
  • PTSD (e.g., early sexual abuse) may decrease glucocorticoid-receptor density in hippocampus.
  • Impairs ability of hippocampus to control cortisol
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15
Q

Sleep Deprivation Consequences

A

•Even one night of < 7-8 hrs shows impairments in: mental acuity, memory (40% poorer after one night under 7-8 hrs) ,learning, reasoning, reaction time, executive functioning

Note:
•Effects are accumulative.
•Many times people are not aware of deficits and think they have “adapted.”

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16
Q

Primary insomnia

A
  • Difficulty initiating or maintaining sleep or having non-restorative sleep for at least one month
  • Causes clinically significant distress or impairment in functioning
  • No clear underlying cause and not due to another sleep disorder, psychiatric disorder, medical condition, medications, or other substances

Note:

  • Insomnia can be transient, acute, or chronic
  • **The most common sleep disorder; over 30% of primary care patients
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17
Q

Secondary insomnia

A

•Underlying medical or psychiatric condition causing or significantly contributing to insomnia (e.g., psychiatric disorder, pain, medications, obstructive sleep apnea)

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18
Q

Rule Out Causes of Insomnia

A
  • Psychiatric conditions: MDD, Bipolar, Anx

* Medical conditions: chronic pain, hypertension, hyperthyroidism, diabetes, etc.

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19
Q

*Hypothalamus & Sleep

A

The hypothalamus has a “sleep-wake switch.”
• Throughout day, various chemicals gradually increase, making a person feel increasingly tired.
• At bedtime, these combine w/ the “sleep” component of the “sleep-wake switch,” which releases GABA. – “puts the cortex to sleep”; Brain is inhibited and put to sleep.
• In AM, the “wake” component of the “sleep-wake switch” releases histamine, which “wakes up” the brain.

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20
Q

Various factors interfere with slow-wave sleep:

A
  • Apnea
  • Periodic leg movement disorder
  • Chronic pain
  • *Corticotropic-releasing hormone (CRH), cortisol (stress) prevent slow-wave sleep.
  • *Lack of exercise
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21
Q

Drugs that interfere with NREM sleep:

A 
• Most sedatives/hypnotics:
• All benzodiazepines (BZDs), including ones used for sleep
• Alcohol
• Many antihistamines 
• Caffeine
• EXCEPTIONS
     -The “Z” drugs: Ambien, Sonata, Lunesta
     -Rozerem
     -Melatonin Supplement
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22
Q

Cognitive-Behavioral Therapy for Insomnia

A
  • *Efficacy research has shown that cognitive and behavioral treatments, collectively called cognitive-behavioral therapy (CBT) are more efficacious than hypnotics - both in the short and long term.
  • Although well accepted by pts, these techniques remain generally unknown and under-utilized by health-care practitioners.
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23
Q

CBT for insomnia targets one or more of the following:

A
  • Cognitive and psychological factors - Beliefs, expectations, appraisal, worry
  • Behaviorally based factors that perpetuate insomnia - Maladaptive sleep habits, irregular sleep schedule
  • Arousal reduction - Relaxation, meditation, biofeedback
  • Didactic sleep hygiene education - Targeting factors interfering and promoting sleep
  • Sleep restriction
  • Stimulus-control therapy - Reduce anxiety or conditioned arousal pts may feel when attempting to go to bed and give a set of instructions designed to re-associate bed/bedroom w/ sleep
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24
Q

The most efficacious/effective treatment for primary insomnia is:
A) Hypnotic drugs
B) Treating the underlying medical condition
C) CBT
D) These are all equally efficacious/effective.

A

C) CBT

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25
Q

The most common sleep disorder is chronic primary insomnia. (True or False)

A

True

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26
Q
  1. Neuroplasticity:
    A) Occurs primarily during the first few years of life but very little after that
    B) Is involved in learning and memory
    C) Is a key phenomenon in the rehabilitation of patients suffering from TBI
    D) Both B and C
A

D) Both B and C

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27
Q 
2.	Which form of memory is most improved by “top-down” organizing of information?
A)	Implicit memory
B)	Procedural memory
C)	Prospective
D)	Declarative memory
A

D) Declarative memory

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28
Q

Neuroplasticity

A

The ability of the brain to change physically and chemically in response to neurodevelopment, behavior, environment
•Involved in learning, memory, adapting to lesions
•Occurs throughout lifetime, primarily stimulated by experience

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29
Q

Neurodevelopment starts on day __ of gestation

A

18

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30
Q

Neurogenesis

A
  • Growth of new neurons

* Mostly complete by end of 2nd trimester

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31
Q

Neuronal selection

A
  • Selection of best neurons

* Mostly complete by end of 2nd trimester

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32
Q

Migration

A
  • Move to destinations

* Starts by 8 wks and mostly complete by birth

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33
Q

Most myelination of prefrontal cortex is not complete until _______________.

A
  • early adulthood
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34
Q

Competitive elimination

A

Reorganization, restructuring, pruning:

•Intense during late childhood & adolescence

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35
Q

What age do the following processes stop? Neurogenesis, differentiation (specialization), myelination (formation of myelin), synaptogensis (formation of synapses), arborization (extension of dendrites), and competitive elimination.

A

•Continue throughout lifetime to some degree

Note:

  • mostly occurs before birth
  • most myelination of prefrontal cortex is not complete until early adulthood
36
Q

Habituation

A

– Decreased response to stimulus

Specifically:
-influx of calcium ions in response to action potential decreases –> less NT’s released at postsynaptic membrane & less depolarization of postsynaptic membrane

37
Q

Sensitization

A

– Enhanced response

-Serotonin reduces K+ effluc through potassium channels, prolonging action potential on neuron –> more Ca2+ influx and increased transmitter release

38
Q

*Long-term potentiation (LTP)

A

A change in amplitude of EPSP, which lasts from hours to days or longer, in response to stimulation of a synapse
•Occurs especially in hippocampus
•In hippocampus, LTP may be particularly likely due to high number of NMDA receptors on a type of pyramidal neuron in area CA1
•If at the same time, a stimulus B causes presynaptic neuron to release glutamate into the dendrites of this same postsynaptic neuron, the NMDA receptors can be activated, which leads to LTP.
•Thus, A and B can become associated in this neuron.
•Helps explain why “neurons that fire together wire together.”

39
Q

AMPA-Glu receptor:

A
  • When Glu binds, channel opens, allowing Na+ to enter and K+ to exit, causing an EPSP.
  • Is the main receptor mediating fast excitation in CNS

MAIN DIFFERENCE FROM NMDA?

40
Q

NMDA-Glu receptor

A
  • A “coincidence detector” in that it opens its channel for Ca2+ influx if 3 events occur:
  • Membrane has depolarized sufficiently to remove Mg2+ from blocking the pore.
  • Glutamate has bound to NMDA receptor.
  • Glycine (or serine) has bound to NMDA receptor (at a different site than Glu).

MAIN DIFFERENCE FROM AMPA?

41
Q

Associative learning

A

– A form of learning in which unrelated stimuli become associated to produce a behavioral response. Ex: Classical conditioning

Note:
-different stimuli may cause different events required for “coincidence detector” (NMDA) to fire –> causing neuron to learn association.

42
Q

SYNAPTIC CHANGES

A

• If procedures that produce habituation, sensitization, LTP, or associative learning are repeated a number of times, the behavioral changes can last much longer (days, months, life-time).
• Increased dendritic connections increase the number of synapses, thereby allowing more complex communication among a network of neurons
-Dendritic Spines: extensions of membrane that allows many more synapses

43
Q

Dendritic Branching

A

• Complexity of dendritic branching (arborization) is associated with complexity of task being performed and changes by experience.

MORE COMPLEX TASK = HIGHER COMPLEXITY OF DENDRITIC BRANCHING

44
Q

Neurotrophic factors:

A
  • Stimulate growth of neurons, aid in repair
  • Experience stimulates production.

Examples:

  • Nerve growth factor (NGF)
  • Brain derived neurotrophic factor (BDNF)
  • Glial-derived neurotrophic factor (GDNF)
  • Epidermal growth factor (EGF)
45
Q

Neurogenesis

A

– Creation of new neurons
• Occurs when animals learn, especially in hippocampus
• Occurs in enriched environments
• New neurons found in complex-housed (with stimulation), compared to cage-housed animals
• Enhances latter learning (led to Head Start)

46
Q

Explicit memory

A

Ability to store and retrieve a memory and know that one has retrieved the correct one:

  • Declarative memory
  • Conscious memory
  • “Knowing that”
  • Are specific modules specializing in specific explicit memories
  • critically dependent on working memory

Examples:

  • Semantic memory – Facts, general knowledge
  • Episodic memory – Autobiographic
  • Incidental memory
  • Verbal/Nonverbal memory
  • Words vs. pictures
  • recent memory and remote memory
  • Memorizing information from this course
47
Q

3 processes/stages of Explicit memory

A
  • Encoding
  • Consolidation/storage
  • Retrieval
48
Q

Encoding

A
  • Short-term storage, initial processing, working memory (short-term memory)
  • limited capacity and decays quickly
49
Q

Four components of working memory:

A
  • “Phonological loop” for auditory
  • “Visuospatial sketchpad” for visuospatial
  • “Central executive”
  • “Episodic buffer” for interaction of semantic memory on working memory (for gist)
50
Q

Consolidation/storage

A

• Expression of genes, protein synthesis (for long-term memory), alteration & strengthening of synapses

51
Q

Retrieval

A
  • recalling information from long-term memory
52
Q

Explicit memory & Hippocampal formation

A
  • Involved in forming, maintaining, & retrieving new and fairly recent memories
  • Left for verbal
  • Right for nonverbal (e.g., faces, spatial information, melodies)
53
Q

Explicit memory & Frontal lobes:

A
  • Memory for temporal order of events (“recency memory,” “temporal memory”)
  • Episodic memory of place & time of autobiographical information
  • Executive component of working memory (ability to manipulate information being held briefly)
54
Q

Memory storage

A
  • Memories are stored in specific association cortices although storing requires above structures.
  • Semantic knowledge is distributed throughout neocortex.
55
Q

Memory deficits in explicit memory (but with implicit memory intact):

A
  • Anterograde amnesia, confabulation, especially w/ lesions in hippocampal formation
  • Anoxia/hypoxia – Oxygen deprivation
  • Alzheimer’s disease (initial dysfunction of hippocampus, followed by more extensive cortical damage)
  • Amnesia may be time-limited (ECT, head injury, transient global amnesia)
  • Anterograde amnesia – Impaired ability to learn new information after a lesion
  • Retrograde amnesia – Impaired ability to recall memories prior to lesion
  • Minutes to years
  • A temporal gradient often exists (e.g., Alzheimer’s).
  • Recent lost before remote
56
Q

Implicit memory

A

Individual can demonstrate knowledge (memory) but cannot explicitly retrieve the information:
• “Knowing how”
• “Procedural memory”
• Encoded in similar way as it was perceived
• Passive role during encoding (although repetition over many trials is usually required)

  • Examples:
  • Classical conditioning (Pavlovian) - Neutral stimulus becomes paired with response
  • Operant conditioning (instrumental) – Consequences of a response increase or decrease probability of that response
57
Q

Principles of neuroplasticity:

A
  • “Behavioral change reflects brain change.”*
  • “All nervous systems are plastic in the same general way.”*
  • “Plastic changes are age-specific.”*
58
Q 
1.	Neurotransmitters may: 
A)	Inhibit neurons
B)	Excite neurons
C)	Alter DNA function
D)	All of the above
A

D) All of the above

59
Q
  1. Relative to excitation or inhibition, a neurotransmitter’s effect on the DNA of the postsynaptic neuron is delayed and lasts longer. (True of False)
A

A) True

60
Q

Neurons

A

• Basic signaling units, information processors, computational devices, CPU’s

61
Q

Glia (glial cells)

A

• the support cells (structural and functional support)

62
Q

Resting Membrane Potential

A
  • At rest, neuron has electrical potential (charge across its membrane) of -70 mV (inside negative relative to outside) due to unequal distribution of charged particles (ions, proteins)
  • It is said to be “polarized.”
63
Q

Resting potential created by:

A
  • Semipermeability of membrane

* Hard for Na+ to pass into neuron, and proteins (mostly negative charge) are kept inside due to size & charge

64
Q

Synapse

A

– Site of functional contact

65
Q

Graded Potentials

A

If Na+ or Ca++ channels open, Na+ or Ca++ can enter.
• Charge on membrane becomes less negative, or depolarized (excited).
• It is now closer to its firing threshold of -50 mV.
• Is an excitatory post-synaptic potential (EPSP)

If Cl- or K+ channels open, Cl- or K+ can exit.
• Charge on membrane becomes more negative, or hyperpolarized (inhibited).
• It is now further from its firing threshold of -50 mV.
• Is an inhibitory post-synaptic potential (IPSP)

66
Q

Firing is termed

A
  • an “action potential”

• The amplitude is constant for all action potentials (“all-or-none”)

67
Q

Saltatory conduction

A

Action potential “jumps” from node to node
• Is possible because of myelin (prevents ions from crossing membrane - so no action potential)
• Through myelinated portions, current is passively transmitted extremely fast.
• At nodes of Ranvier, there is no myelin but rich in voltage-sensitive channels
• Where action potential is re-generated
• Greatly increases speed

68
Q

Action potentials

A
  • Amplitude of action potential is constant and cannot provide information about intensity.
  • Intensity is provided by frequency of action potentials because more intense stimulus increases probability that firing thresholds will be reached and that action potentials will be generated.
  • Duration of stimulus is reflected in period over which action potentials occur (total number).
  • Brain processes patterns of these action potentials.
69
Q

Multiple sclerosis (MS)

A
  • Episodic, inflammatory, multifocal disease
  • Likely is an autoimmune response against myelin antigens in CNS
  • Less myelin slows speed of propagation and causes “cross-talk” (“short-circuiting”) in motor, sensory axons.
  • Affects optic nerves, cerebral hemispheres, brainstem, cerebellum, spinal cord
  • Most types have mood & affective instability, alterations in behavior or personality, which usually occur throughout illness.
  • Mild-moderate cognitive deficits (e.g., attention, speed of information processing, memory recall, executive functioning) in > 50%
  • Severe cognitive decline in 20-30%
70
Q

Two most common types of MS

A
  1. Relapsing-remitting (RRMS)
    • Accounts for 80-85% of new cases of MS
    • After 15 yrs, most evolve into secondary progressive MS (SPMS)
    • Most will require assistance w/ ambulation; some will become totally dependent for ADL’s
  2. Primary progressive MS – 15-20% of new cases
71
Q

Glutamate (Glu)

A
  • generally excites neurons.

* Most common excitatory NT

72
Q

Gamma-aminobutyric acid (GABA)

A
  • generally inhibits neurons.

* Most common inhibitory NT

73
Q

Acetylcholine (ACh)

A
  • the NT used for neuromuscular transmission.

* When ACh is released at neuromuscular junction, it leads to muscular contraction.

74
Q

Histamine (H)

A
  • From the tuberomammillary nucleus (of the hypothalamus) is the NT in the “wake” nucleus of the “sleep-wake switch” of the hypothalamus.
  • When released, it wakes up the cortex and inhibits the “sleep” nucleus of the hypothalamus.
75
Q

Dopemine (DA)

A
  • DA cell bodies in substantia nigra project primarily to striatum of BG (nigrostriatal pathway)
  • When 90% of DA neurons die here, get Parkinson’s disease
76
Q

NE cell bodies in the locus coeruleus project to entire cortex:

A
  • Activates cortex for alertness, responsiveness to novel stimuli, response to stressful stimuli (especially fear)
  • At times, produces positive feelings of reward, helps maintain emotional tone, inhibits pain
77
Q

Neurotransmitter synthesis & storage:

A

• Most neurotransmitters are synthesized in axon terminal and stored in synaptic vesicles until needed.

78
Q

Steps of neurocommunication?

A
  • Release of NT
  • Activation occurs when neurotransmitter binds to specific binding site on specific receptor (protein in postsynaptic membrane). This causes:
  • Excitation or
  • Inhibition or
  • Initiation of other chemical reactions
  • Deactivation of neurotransmitter:
  • Reuptake:
  • Neurotransmitter or its degraded end-product taken up by presynaptic membrane via transporter proteins (“reuptake pumps”)
  • Most common type of deactivation
  • Enzymatic degradation (e.g., monoamine oxidase)
  • Simple diffusion
  • Taken up by glia, which may degrade or store neurotransmitter for re-export to axon terminal
79
Q

Transmembrane Signaling

A
  • Problem: For a neurotransmitter to affect a cell, its “signal” must pass that neuron’s lipid-bilayer membrane.
  • Most molecules, including ions, cannot cross because they are charged or not sufficiently lipophillic.

Two families of receptors for circumventing barrier posed by the membrane.
• 1st family is comprised of ionotropic receptors (ligand-gated channels)
- Allow movement of ions across membrane through a gate that opens when neurotransmitter binds
- Rapid change in membrane potential (msec’s)
- Mediate fast behavior
- May be excitatory or inhibitory

• 2nd family is comprised of metabotropic receptors

  • Alter internal chemistry, including altering ion channels and activating enzyme
  • Enzyme can activate a “second messenger,” which in turn can activate other enzymes that can affect many chemical reactions (2nd messenger cascade)…
80
Q

Metabotropic

A
  • “2nd messenger” can travel to nucleus and affect DNA resulting in change in production of proteins (gene transcription)
  • Formation of new receptors, enzymes, trophic factors
  • Up-regulation – Increase in number or sensitivity of receptors
  • Down-regulation – Decrease in number or sensitivity of receptors
81
Q

Neurotransmitters that generally alter the internal chemistry of neurons:

A
  • Acetylcholine (ACh) when binding to muscarinic receptors
  • Dopamine (DA)
  • Norepinephrine (NE)
  • Epinephrine (E)
  • Serotonin (5-HT)
  • Glutamate (Glu) when binding to specific subtypes of receptors
82
Q

Metabotropic Receptors

A

Modulate synaptic actions & behavior by altering excitability of neurons, strength of synapses and efficiency of neurocommunication.
• Such modulatory synaptic pathways can act as crucial reinforcing pathways during process of learning. (Neuroplasticity)
• Hormones bind to metabotropic receptors.

83
Q

Characteristics of metabotropic receptors:

A
  • Tremendous amplification of signal
  • Flexibility & diversity of responses
  • Can affect ion channels, membrane potentials, enzyme activity, gene transcription (protein production)
  • Diversity of receptor subtypes
  • When protein synthesis is involved:
  • Onset of action will be delayed 30 minutes to hours.
  • Effects will persist hours to days (or longer) after concentration of neurotransmitter has been reduced to zero due to slow turnover of proteins.
84
Q

Cortisol

A
  • Promotes protein breakdown (which can lead to muscle weakness/wasting)
  • Shuts down systems that aren’t immediately necessary
    • immune system - which can lead to infections,
    • reproductive system - which can lead to infertility, decreased libido, and amenorrhea
  • inhibits inflammatory response
  • inhibits slow wave sleep
85
Q

CRH or CRF

A

Corticotrophin-Releasing Hormone or Corticotrophin Releasing Factor

  • released by hypothalamus in response to stress
  • increased ACTH - which increases cortisol
  • May cause: depression/anxiety, brain dysfunction/damage

Neuropsych (5 decks)

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