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Bio Bases Of Bx > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Hormones

A

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

Hierarchical control:
Sensory stimuli–>Hypothalamus–>Pituitary gland–>Endocrine glands–> Target cells affected by hormones

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2
Q

3 controls over hypothalamic-hormone activity

A
  1. Feedback- detects level of hormone to see if it needs to be shut down if making too much
  2. Regulation by limbic system, frontal lobes- Ex. Sight, sound, thought of baby can trigger oxytocin release & milk ejection, but anxiety and stress can inhibit release.
  3. Experience- example: neurons that release oxytocin increase in size in mother
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3
Q

Pituitary Gland (Master Gland)

A
  • Controls other glands (Adrenal (on top of kidneys), thyroid, gonads, mammary)
  • Has systemic affects through release of hormones: (e.g. Adrenal Cortex- secretes cortisol and adrenal medulla secretes adrenaline during sympathetic NS activation)
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4
Q

Adrenocorticotropic hormone (ACTH)

A

Critical to understand stress

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5
Q

Reproductive hormones

A

Affect mood, cognition, behavior in both sexes

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6
Q

Testosterone

A

Increases libido in males and females.

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7
Q

Oxytocin

A
  • Promotes bonding

- Released during labor (uterine contractions), during breast feeding (milk letdown), during coitus in females and males

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8
Q

Prolactin

A
  • Released during breast feeding (milk production)
  • Inhibits testosterone
  • Males are more aggressive, females more nurturing (?)
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9
Q

Estrogen

A

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)- due to exposure to estrogenic molecules
Minimal during menopause

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10
Q

Estrogen and depression

A

Depression mirrors these changes in estrogen.

Increase in female depression doesn’t begin until adolescence and after menopause the level of depression between females and males becomes equal- due to cycle of estrogen not increase or decrease

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11
Q

Estrogen and the brain

A

Has profound effects on body & brain

Activates genes to synthesize gene products, (trophic factors & enzymes) that synthesize & metabolize neurotransmitters & receptors in females.

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12
Q

Estrogen, emotions and trophic factors

A
  • Change breasts, uterus
  • Preserve bone mineralization
  • Reduce cholesterol
  • Facilitate growth of new synapses
  • Prevent apoptosis (planned cell death) and neurodegeneration – trophic factors keep it from being excessive
  • Nerve growth factor (NGF)
  • Brain-derived neurotrophic factor (BDNF)
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13
Q

Estrogen and emotions

A

Affects the 3 main neurotransmitters involved in depression (5-HT, NE, DA (and ACh) systems

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14
Q

Estrogen fluctuations

A

Dysregulation during estrogen fluctuations may cause somatic and brain abnormalities.

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15
Q

Hormones and cognitive function

A

Cognition is determined by complex interaction of hormones and experience

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16
Q

Stressor

A

event that has an arousing effect

  • Context and degree of control matter
  • Physical stressors exist- surgery and excessive exercise
  • Chronicity of stress today is a problem
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17
Q

Stress response

A

Behavioral and physiological responses to cope with stressor

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18
Q

2 biochemical pathways

A
  1. “Fast response” by norepinephrine/epinephrine- Prepares body for sudden burst of activity; sympathetic NS
  2. “Slow response” by cortisol. Prepares body for longer-lasting adaptations (more info in next card)
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19
Q

Slow response by cortisol

A
  • 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
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20
Q

Chronic cortisol output

A

Turns off insulin, which causes liver to begin releasing glucose
- But chronic output may increase risk of insulin-resistant diabetes (Type II- insulin is secreted in normal amounts but receptors become resistant because of too much glucose)

Promotes lypolysis (breaking down of fat) for increased energy
- But increases abdominal fat that is particularly dangerous for cardiovascular system and that predisposes body to insulin-resistant diabetes
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21
Q

Cortisol and protein

A

Promotes protein breakdown (catabolism), but excessive output can lead to muscle weakness/wasting.

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22
Q

Cortisol and immune system

A

Cortisol shuts down systems not immediately needed to deal with stressor
Inhibits immune system
- Can lead to infections
- Glucocorticoids are used to treat autoimmune diseases and decrease tissue rejection.

Inhibits inflammatory response
Inhibits reproductive system

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23
Q

Cortisol and sleep

A

Inhibits slow-wave sleep (deep sleep)

  • Decreased synthesis of 5-HT, DA, NE
  • Predisposition to depression/mania
  • Decreased synthesis of growth hormone
  • Can lead to osteoporosis
  • Stunted growth and failure to thrive

Cortisol from stressed mother passes placental barrier and into infant’s blood and brain

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24
Q

High cortisol causes…

A
  • Increased appetite
  • Weight gain
  • Increased abdominal fat releases chemicals that increase risk of cardiovascular disease and insulin-resistant diabetes
  • Glucose intolerance
  • Increased risk of insulin-resistant diabetes (NIDDM)
  • Marker for depression
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25
Q

Corticotropin-releasing hormone (CRF or CRH)

A
  • Released by hypothalamus (and other structures) in response to stress
  • Leads to increased ACTH, which increases cortisol
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26
Q

Hypothalamo-pituitary adrenal axis

A

central place for stress

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27
Q

Cortisol and the hippocampus

A

Chronic stress results in continued high level of cortisol, which destroys hippocampal cells.

Impairs ability to provide negative feedback
May impair memory

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28
Q

Cortisol and ptsd

A
  • May decrease glucocorticoid-receptor density in hippocampus
  • Impairs ability of hippocampus to control cortisol.
  • Even short term stress can result in memory problems
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29
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

Chronic primary insomnia is the most common sleep disorder; over 30% of primary care patients

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30
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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31
Q

Factors affecting chronic insomnia

A

Most important are behavioral and psychological factors, not addressed by over the counter drugs

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32
Q

Insomnia and psychiatric conditions

A

35% of patients seen in sleep disorder centers have an identifiable psychiatric or psychological cause.

  • Major depression, dysthymia
  • Bipolar disorder, mania
  • Anxiety disorders
  • Schizophrenia: Voices are often more prominent at night when it is quieter.
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33
Q

Insomnia and medical conditions

A
  • Chronic pain (rheumatoid arthritis, peptic ulcer disease, GERD, fibromyalgia, neuropathies, lower-back pain)
  • Hypertension
  • Congestive heart failure (CHF)
  • Chronic obstructive pulmonary disease (COPD)
  • Benign prostatic hypertrophy (BPH)
  • Incontinence
  • Urinary tract infection (UTI)
  • Hyperthyroidism
  • Diabetes
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34
Q

Sleep-wake switch

A

Hypothalamus has switch:

  • Throughout day, various chemicals gradually increase, making a person feel increasingly tired.
  • At bedtime, chemicals combine w/ the “sleep” component of the “sleep-wake switch,” which releases GABA (inhibitory)
  • Brain is inhibited and put to sleep.
  • In AM, the “wake” component of the “sleep-wake switch” releases histamine (excitatory), which “wakes up” the brain.
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35
Q

Factors that 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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36
Q

Drugs that interfere with slow wave sleep

A

Most sedatives/hypnotics:

  • All benzodiazepines (BZDs), including ones used for sleep
  • Alcohol
  • Many antihistamines (Benadryl, Nytol, Simply Sleep, Sominex)

Caffeine:

  • Even if don’t drink after noon, enough stays in system to interfere.
  • At risk, if 250 mg/day (2 cups)
  • Very likely to have problem if > 550 mg/day
  • Certain drugs may cause caffeine to stay in system for up to 31 hrs (by interfering w/ metabolism).
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37
Q

Drug exceptions to sleep interference

A

“Z” drugs.
zolpidem (Ambien), zaleplon (Sonata), eszopliclone (Lunesta)
ramelteon (Rozerem)
melatonin supplement

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38
Q

Neurons

A

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

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39
Q

Glial cells

A

the support cells (structural and functional support)

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40
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)

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41
Q

Resting potential

A

Semipermeability of membrane

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

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42
Q

Synapse

A

Site of functional contact

  • Presynaptic membrane w/ active zone (where vesicles are located waiting to release NT’s)
  • Synaptic cleft – Space between neurons (not truly empty; scaffolding proteins connect two neurons)
  • Postsynaptic membrane w/ receptors
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43
Q

excitatory post-synaptic potential (EPSP)

A

If Na+ or Ca++ channels open, Na+ or Ca++ can enter.

  • If that happens, charge on membrane becomes less negative, or depolarized (excited).
  • It is now closer to its firing threshold of -50 mV.
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44
Q

inhibitory post-synaptic potential (IPSP)

A

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.
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45
Q

Action potential

A
  • Neuron sums up various excitatory and inhibitory receptors

- When summation reaches -50mV at axon hillock (where axon begins), neuron fires

46
Q

Amplitude of action potential

A

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

Occurs quickly and lasts for seconds

47
Q

Saltatory conduction

A

Action potential “jumps” from node to node- means it can go faster because fewer gates need to open and shut

  • Made possible by myelin (prevents ions from crossing membrane - so no action potential)
48
Q

Nodes of ranvier

A

There is no myelin but rich in voltage-sensitive channels

Where action potential is re-generated

49
Q

Intensity of action potential

A

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

Brain processes patterns of these action potentials.

50
Q

Pathology and action potential

A

Nay cause neurological diseases.

51
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
52
Q

Two types of MS

A
  1. Relapsing-remitting (RRMS)
    Accounts for 80-85% of new cases of MS
    After 15 yrs, most evolve into secondary
  2. Progressive MS (SPMS)
    Most will require assistance w/ ambulation; some will become totally dependent for ADL’s
    Primary progressive MS – 15-20% of new cases
  • Most have mood & affective instability, alterations in behavior or personality, which usually occur throughout illness.
  • mild-moderate cognitive deficits
53
Q

Glutamate

A

Excites neurons.

Most common excitatory NT (Experiences an EPSP)

54
Q

Gamma-aminobutyric acid (GABA)

A

Generally inhibits neurons.

Most common inhibitory NT (experiences IPSP)

55
Q

Acetylcholine (ACh)

A

NT used for neuromuscular transmission.

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

56
Q

Histamine (H)

A

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

57
Q

Dopamine (DA) in substantia nigra

A

Project to: striatum of BG (nigrostriatal pathway)

When 90% of DA neurons die, you end up with Parkinson’s

58
Q

DA in ventral tegmental area (VTA)

A

Project to:

  • Limbic system including nucleus accumbens (mesolimbic pathway)
  • Reward system
  • Cortex (mesocortical pathway)

Helps to promote optimal attention, cognition, positive mood

59
Q

Norepinephrine (NE)

A

In the locus coeruleus project to entire cortex:

  • 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
60
Q

5-HT (Seratonin)

A

In raphe nuclei project to: hippocampus, hypothalamus, limbic system, cortex

  • Mood
  • Anxiety
  • Modulate reflexes through spinal cord (including sexual) and pain (although less than NE)
61
Q

Synthesis and storage

A

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

62
Q

Activation

A

Occurs when neurotransmitter binds to specific binding site on specific receptor

Results in:

  • Excitation
  • Inhibition
  • Other chemical reactions
63
Q

Deactivation: reuptake

A

Neurotransmitter or its degraded end-product taken up by presynaptic membrane via transporter proteins (“reuptake pumps”)

Most common type of deactivation

64
Q

Enzymatic degradation

A

(e.g., monoamine oxidase- deactivates monoamines)

  • Simple diffusion
  • Taken up by glia, which may degrade or store neurotransmitter for re-export to axon terminal
65
Q

ionotropic receptors (ligand-gated channels)

A

Allow movement of ions across membrane through a gate that opens when neurotransmitter binds

Mediate fast bx

66
Q

metabotropic receptors

A

Alter internal chemistry, including altering ion channels and activating enzyme

Can activate a “second messenger” (cascade) which in turn can activate other enzymes that can affect many chemical reactions

Modulate synaptic actions & behavior by altering excitability of neurons, strength of synapses and efficiency of neurocommunication.–> reinforcement during learning and neuroplasticity

67
Q

Second messenger

A

Can travel to nucleus and affect DNA resulting in change in production of proteins (gene transcription)- turn a gene on or off

68
Q

Up-regulation

A

Increase in number or sensitivity of receptors

(more proteins being made or they become more sensitive and respond more readily; tends to happen when not enough of NT is there that is supposed to be there)

69
Q

Down-regulation

A

Decrease in number or sensitivity of receptors

70
Q

NT’s the alter internal chemistry of a neuron

A

ACh, DA, NE, E, 5-HT, Glu

71
Q

Hormones

A

bind to metabotropic receptors

72
Q

Characteristics of metabotropic receptors:

A
  1. Flexibility & diversity of responses
  2. Diversity of receptor subtypes
  3. Amplification of signal
73
Q

Protein synthesis

A
  • Onset of action will be delayed 30 minutes to hours.
  • Effects will persist hours to days (or longer)

** Learning is best through repetition and distribution over time because the synapses take time (protein synthesis/consolidation)

74
Q

Sample question: Neurotransmitters may:

A

A. Inhibit neurons
B. Excite neurons
C. Alter DNA function
D. All of the above***

75
Q

Sample question:

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

True

76
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
77
Q

Neurodevelopment

A

Starts on day 18 of gestation.

- Particularly critical to avoid stress, most drugs and toxins during 1st trimester

78
Q

Neurogenesis

A

Growth of new neurons
Mostly complete by end of 2nd trimester

  • Occurs when animals learn, especially in hippocampus, throughout lifetime
  • Enhances latter learning
79
Q

Neuronal selection

A

Selection of best neurons

Mostly complete by end of 2nd trimester

80
Q

Migration

A

Move to destinations

Starts by 8 wks and mostly complete by birth

81
Q

Differentiation

A

specialization, mostly before birth

82
Q

Myelination

A

Formation of myelin; Most myelination of prefrontal cortex is not complete until early adulthood….Impulsivity, emotional lability, difficulty planning etc

83
Q

Competitive elimination

A

(reorganization, restructuring, pruning): weak synapses or rarely used

  • Intense during late childhood & adolescence but continue somewhat throughout lifetime
84
Q

Long-term potentiation (LTP)

A

A change in amplitude of EPSP (NT released from presynaptic neuron and attached to receptor on post-synaptic neuron and changes the potential), which lasts from hours to days or longer, in response to stimulation of a synapse

Occurs especially in hippocampus

85
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

86
Q

NMDA-Glu receptor

A

“coincidence detector” in that it opens its channel for Ca2+ influx if 3 events occur: (3 things have to happen simultaneously so that Ca can enter the cell)

  1. Membrane has depolarized sufficiently to remove Mg2+ from blocking the pore.
  2. Glutamate has bound to NMDA receptor.
  3. Glycine (or serine/NT) has bound to NMDA receptor (at a different site than Glu)
87
Q

Ca2+

A
  • 2nd messenger changes internal chemistry of neuron
  • Strengthens the synapse
  • Allows for cellular learning, neuroplasticity
88
Q

Associative learning

A

A form of learning in which unrelated stimuli become associated to produce a behavioral response

  • May use coincidence detector and thereby causing neuron to form association
89
Q

Neurons the fire together wire together

A

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.

90
Q

Repetition

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).

91
Q

Complex communication

A

Increased dendritic connections increase the number of synapses, thereby allowing more complex communication among a network of neurons

92
Q

Dendritic branching/arborization

A

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

93
Q

Neurotrophic factors

A

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

Conversely, child who is deprived may not have neurotrophic factors being made. Also possible in mood disorders and schizophrenia.

94
Q

Explicit Memory

A

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

  • Declarative
  • Conscious
  • “Knowing that”
  • Depends on working memory
95
Q

Encoding

A

Short-term storage, initial processing, working memory (short-term memory)

Consciously maintaining limited amount of information in temporary state for further processing

96
Q

4 components of working memory

A
  1. “Phonological loop” for auditory
  2. “Visuospatial sketchpad” for visuospatial
  3. “Central executive”
  4. “Episodic buffer” for interaction of semantic memory on working memory (for gist)
97
Q

Consolidation/storage

A

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

98
Q

Retrieval

A

from long-term memory

99
Q

Hippocampal formation

A

associate data from cortical association areas

  • Involved in forming, maintaining, & retrieving new and fairly recent memories
100
Q

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)

**Medial temporal pathway is reciprocal, which allows memories to be conscious, explicit

101
Q

Memory storage

A

Memories are stored in specific association cortices

Semantic knowledge is distributed throughout neocortex.

102
Q

Deficits in explicit memory:

A
  1. Anterograde amnesia- confabulation, especially w/ lesions in hippocampal formation
  2. Anoxia/hypoxia - oxygen deprivation
  3. Alzheimer’s disease (initial dysfunction of hippocampus, followed by more extensive cortical damage)
103
Q

Anterograde amnesia

A

Impaired ability to learn new information after a lesion

104
Q

Retrograde amnesia

A

Impaired ability to recall memories prior to lesion

105
Q

Implicit memory

A

Individual can demonstrate knowledge (memory) but cannot explicitly retrieve the information:

  • “Knowing how”
  • “Procedural memory”
106
Q

Examples of implicit memory

A

classical and operant conditioning

107
Q

Neural circuits for implicit memory

A

Connections from cortex to basal ganglia are unidirectional, so cortex oesn’t get feedback that information is being stored; May account for subconscious nature of implicit memory

108
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.”*
“Prenatal events can influence plasticity throughout life.”*
“Plastic changes are brain-region dependent.”*
“Experience-dependent changes interact.”*
“Plasticity has pros and cons.”*

109
Q

Review question: Neuroplasticity:

A

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***

110
Q

Which form of memory is most improved by “top-down” organizing of information?

A

Declarative memory

Bio Bases Of Bx (3 decks)

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