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Biopsychology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What does an EEG electrode measure?

A

An EEG measures the summation of action potentials within a given area of the cortex over time.

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2
Q

• What do alpha waves look like? What states of consciousness is it associated with? *

A

moderate frequency, moderate amplitude

Associated with wakeful rest with eyes closed

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3
Q

• What do beta waves look like? What states of consciousness is it associated with? *

A

high frequency, low amplitude

associated with normal wakeful consciousness and concentration

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4
Q

• What do delta waves look like? What states of consciousness is it associated with? *

A

low frequency, high amplitude (hence – slow-wave sleep)

associated with deep often dreamless sleep, slowest brain waves

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5
Q

• Characteristics of REM sleep

A
  • has an awake EEG pattern
  • rapid eye movement during this period
  • associated with narrative dreams
  • no muscle tone during REM sleep
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6
Q

• Activity in the reticular activating system during arousal, sleep, and REM *

A

Reticular activating system (RAS) is active during arousal.
RAS is inactive during slow wave sleep.
RAS becomes active again in REM sleep

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7
Q

• Can dreams occur during non-REM sleep? How does dream content map onto brain anatomy?

A
  • Nightmares with static images tend to occur in slow wave sleep not REM
  • dreams can occur in non-REM sleep.
  • perception of movement activates the superior temporal sulcus (what we dream about can activate the area of the brain associated with that action)
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8
Q

• Effects of ventral lateral preoptic area activity and damage on sleep *

A

The ventral lateral prep-tic area becomes active at night and inhibits activity in the RAS.

  • it promotes sleep
  • if damaged, leads to insomnia and death.
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9
Q

• Role of orexin in sleep

A
  • Stimulant neurotransmitter
  • Damage to these neurons results in narcolepsy.
  • Contributes to “effortful wakefulness”.
  • VLPA makes it inactive at night
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10
Q

• Role of histamine in sleep

A
  • Stimulant Neurotransmitter
  • Drugs that block histamine receptors cause drowsiness.
  • VLPO makes it inactive at night
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11
Q

• Role of adenosine in sleep

A
  • hypnotic neurotransmitter
  • Builds up in the basal forebrain during day and inhibits neurons.
  • Caffeine is an adenosine antagonist
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12
Q

• What is the role of sleep in learning and synapse size? *

A

Sleep is the time when we consolidate information gathered during the day.

-important information stored in large synapses.
-less important information being held in smaller synapses.
(Also if you smell something and smell it again during slow wave sleep you recall the information better)

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13
Q

• Brain activity in some cases of persistent vegetative states

A

Case study shows brain activity that suggests awareness of commands.
-awake but unaware of surroundings

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14
Q

• What are the changes in gene expression across daily circadian cycle

A

gene activity is increased during the day and decreased at night.

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15
Q

• Do circadian rhythms change in the absence of daily light/dark cycle?

A
  • Light does impact our circadian rhythm
  • However the blind still have circadian rhythms
  • If one lives in constant light conditions for weeks, the cycles become prolonged
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16
Q

• Role of the suprachiasmatic nucleus in circadian rhythms.

A
  • Circadian rhythms are dependent on SCN
  • Removal of SCN leads to lack of circadian rhythm
  • SCN receives direct input from the eye
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17
Q

• Organizational vs. activational effects of hormones *

A

Organizational: (developmental) permanent change in brain and sex organs due to hormonal exposure during development
Activational: temporary change (e.g. functional) in sexual behavior due to hormonal exposure during adulthood

18
Q

• Development of primary sex organs and gender-specific brain *

A

Males XY Females XX

  • Testes are the Determining Factor (or SRY) gene on Y chromosome causes testicular development in males
  • Nature produces a female by default unless two hormones are released by testes: Mullerian-inhibiting hormone (prevents ovaries/defeminization), and Testosterone (stimulates male development, masculinization.)
19
Q

• Hormonal cascade during puberty

A
  1. release of gonadotropin-releasing hormone (GnRH) from hypothalamus
  2. Stimulates release of follicle-stimulating hormone (FSH) and lutenizing hormone (LH) from pituitary.
  3. Stimulates estrogen (E) and progesterone (P) from ovaries or testosterone (T) from testes.
    = secondary sex characteristics
20
Q

• Activational effects of hormones on female and male sexual behavior

A

In human females, initiation of sexual activity is greater during ovulation (when Estrogen levels are high).
More testosterone in males = more sexual drive

21
Q

• Evidence for specific brain regions in male and female sexual behavior *

A

Males have a larger olfactory bulb and medial amygdala.
(Lesions on medial amygdala decrease Male sex drive)
-When viewing porn, males have greater amygdala activation
-High amygdala activity predicts more sexual partners in women but fewer partners in men. Low amygdala activity predicts more sexual partners in men but fewer partners in women.
- The medial preoptic area (MPA) of hypothalamus is larger in males. (Lesions abolish sexual behavior in males)
-Ventromedial nucleus of hypothalamus is larger in females (Lesions reduce sexual receptivity.)

22
Q

• Biological determinants of sexual orientation

  1. Activational effects
  2. Genetics
  3. Developmental effects
  4. Brain activation as a function of orientation
A
  1. T levels in lesbians are slightly higher than in straight women. (T levels in gay and straight human males do not differ.)
  2. Altering the function of specific genes in flies elicits change in orientation. (If sexual orientation in humans is genetic, it likely involves many genes.)
  3. Females with congenital adrenal hyperplasia (CAH) are overexposed to testosterone-like hormones in utero, 1/3 are gay. Individuals who are XY but have Androgen Insensitivity Syndrome (AIS) do not masculinize in utero and develop female appearance, most are interested in men. The greater the # of older biological brothers, the greater the likelihood of homosexuality in males (related to a mother’s antibodies against testosterone.)
  4. Smelling androstendione activates anterior hypothalamus in gay men and women. Estrogen smell activates anterior HT in gay males but posterior HT in straight males.
23
Q

pair bonding, oxytocin, and vasopressin in voles and people. *

A

Monogamous Prairie voles have a high level of oxytocin, vasporessin compared to other non monogamous montane voles.

  • an oxytocin antagonist administered to a female prairie vole and a vasopressin antagonist given to a male prairie vole decreased partner preference.
  • there is a SNP “334” identified that shows nonmongamous pair-bonding behavior in some men
  • Intranasal oxytocin increases positive behavior and decrease stress in marital fights
24
Q

• Advantages to studying simpler organisms (Aplysia)

A
  • Mammalian brains are too big.
  • Most higher order forms of learning and memory are too complicated.
  • Study the simplest forms of learning and memory in the simplest nervous systems
25
Q

• What is habituation and how it is produced in Aplysia? *

A

Habituation: a decline in an unconditioned response after repeated presentations of an unconditioned stimulus.
Touch the siphon, the gill withdraws.
Keep touching the siphon, the gill withdrawal response habituates.

26
Q

• Physiological responses in sensory and motor neurons of control and Habituated Aplysia

A
  • Touch increases firing rate of siphon sensory neurons.

- Sensory neuron firing activates gill motor neurons.

27
Q

• Biochemical basis of habituation *

A

Every tap on the siphon and action potential in the sensory neuron leads to less calcium entering the terminal. (And less neurotransmitter is released into the sensory-motor synapse.)

28
Q

• “Lessons” regarding habituation and learning in Aplysia

A
  • Transient learning is based on short-term chemical changes (e.g. changes in Ca+) in terminal buttons.
  • Memory is located in the terminal button of sensory neuron.
  • Memories are not housed in a separate set of “memory” neurons. (housed within the neurons that are directly involved in the behavior or thought process.)
29
Q

• What is sensitization and how it is produced in Aplysia?*

A

A generalization of an unconditioned response to previously neutral stimuli OR an enhancement of unconditioned response to an unconditioned stimulus.
Tap the siphon and gill withdraws.
Shock the tail.
Wait and tap the siphon - gill will withdraw for a longer time.

30
Q

• Physiological responses in sensory and motor neurons of control and Sensitized Aplysia

A
  • Touch increases firing rate of siphon sensory neurons.
  • Sensory neuron firing activates gill motor neurons.
  • addition of sensory neurons from the tail
  • facilitating interneurons that connect the tail’s sensory neurons to the terminal button of the siphon sensory neurons.
31
Q

• Biochemical steps involved in short-term sensitization*

A
  1. Initial tail shock causes interneuron to release serotonin.
  2. Serotonin binds to receptors on sensory neuron terminal.
  3. Receptor activates second messengers known as kinases.
    -Kinases add phosphates to calcium channels.
    -Calcium channel becomes more sensitive to incoming action potentials.
  4. Few minutes later, tap to siphon produces action potential in sensory neuron.
    When action potential arrives at terminal, more calcium enters the terminal because the kinases hold channels open longer.

More calcium = more neurotransmitter released

32
Q

• How is longer-term sensitization produced in Aplysia? *

A

-Stronger tail shock causes even greater kinase levels in the siphon sensory neuron terminal.
-Kinases interact with DNA to promote gene transcription and synthesis of proteins, such as:
>growth factors (promote new membranes for more or bigger terminals)
>more kinases (keep calcium channels open even longer or perpetually keep kinase genes active).

33
Q

• What is classical conditioning and operant conditioning?

A

Classical or Pavlovian conditioning: learning associations between stimuli
Operant conditioning: learning associations between behaviors and outcomes

34
Q

• What is the Hebb rule

A

Neurons that fire together wire together.

35
Q

• What is long-term potentiation (LTP) and how is it produced?

A

Long-term potentiation (LTP): High-frequency activation of a specific synaptic input will causes the post-synaptic neuron to become more responsive to that input.

36
Q

• Evidence that LTP is related to learning

A
  • it’s long lasting
  • the more trials the more permanent it becomes
  • The increased response of the post-synaptic cell is like a memory - adaptive change to altered input (increased reactivity)
  • can be classically conditioned
37
Q

• Effects of LTP on dendritic spine size

A

Following the induction of LTP, dendritic spines are larger on stimulated postsynaptic neurons.

38
Q

• Characteristics of NMDA receptors *

A
  • Use glutamate as a neurotransmitter.
  • Ionotropic receptor that gates a calcium channel
  • To open, two conditions must be met: 1. Glutamate must be bound to the NMDA receptor. 2. The inside of the dendrite must be depolarized.
  • Critical to LTP and to new learning
39
Q

• How does activity at strong synapses cause weakly active synapses to become better connected? *

A

> At the strong synapse, a lot of glutamate is released.This glutamate causes dendrites around the strong synapse to be depolarized.
At the weak synapse, a little bit of glutamate is released
Little bit of glutamate binds to NMDA-type glutamate receptors that are voltage-dependent.
Little bit of glutamate and slight depolarization opens the NMDA receptor.
Calcium flows into dendrite adjacent to weak synapse.

40
Q

• How does calcium influx through NMDA receptors establish long-term connections between neurons? *

A

> NMDA receptors gate calcium.
Influx of calcium increases kinase activity in dendrite.
Kinases can activate other non-NMDA type glutamate receptors. (Makes the dendrite more sensitive to input.)
Kinases can enhance gene expression to change receptor number or dendritic shape.

41
Q

• Comparison of short-term vs. long-term memory *

A

Short-term memories appear to involve changes in neurotransmitter release or the sensitivity of neurotransmitter receptors (local changes).
Long-term memories may involve changes in gene expression (distributed changes) that create structural changes in neurons.

42
Q

Causes of narcolepsy

A
  • hereditary, autoimmune disorder, during adolescence the immune system attacks orexinergic neurons
  • damage to the orexin system seems to cause narcolepsy

Biopsychology (5 decks)

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