Midterm review Flashcards

1
Q

Identify the substrates that PKA/G enzymes act on to influence cellular response patterns

A
  • Voltage-gated ion channels
  • Ligand-gated ion channels
  • Synaptic vesicle proteins
  • Enzymes involved in neurotransmitter synthesis
  • Proteins that regulate gene transcription
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2
Q

Describe the structure of the blood-brain barrier

A

The blood-brain barrier is the separation between brain capillaries and the brain/cerebrospinal fluid, and it is selectively permeable; it allows lipid soluble molecules

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3
Q

Give a step-by-step account of how the process of neurotransmission works.

A
  1. ) Neurotransmitter is synthesized and then stored in vesicles
  2. ) An action potential invades the presynaptic terminal
  3. ) Depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels
  4. ) Influx of Ca2+ ions through channels
  5. ) Ca2+ causes vesicles to fuse with presynaptic membrane
  6. ) Neurotransmitter is released into synaptic cleft via exocytosis
  7. ) Neurotransmitter binds to receptor molecules in postsynaptic membrane
  8. ) Opening or closing of postsynaptic channels
  9. ) Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell
  10. ) Retrieval of vesicular membrane from plasma membrane
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4
Q

What is number 2 on figure 3.16?

A

An action potential invades the presynaptic terminal

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5
Q

What is number 3 on figure 3.16?

A

Depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels

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6
Q

What is number 4 on figure 3.16?

A

Influx of Ca2+ ions through channels

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7
Q

What is number 5 on figure 3.16?

A

Ca2+ causes vesicles to fuse with presynaptic membrane

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8
Q

What is number 6 on figure 3.16?

A

Neurotransmitter is released into synaptic cleft via exocytosis

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9
Q

What is number 7 on figure 3.16?

A

Neurotransmitter binds to receptor molecules in postsynaptic membrane

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10
Q

What is number 8 on figure 3.16?

A

Opening or closing of postsynaptic channels

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11
Q

What is number 9 on figure 3.16?

A

Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell

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12
Q

What is number 10 on figure 3.16?

A

Retrieval of vesicular membrane from plasma membrane

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13
Q

What is number 10 on figure 3.16?

A

Retrieval of vesicular membrane from plasma membrane

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14
Q

For the 5 major divisions of the brain (-cephalons), identify a structure, substructure, and general function for that substructure.

A
  • Myelencephalon (structure: medulla; substructure: area postrema); the area postrema initiates vomiting in response to toxins in the blood
  • Metencephalon (structure: pons; substructure: reticular formation); the reticular formation is involved in arousal, attention, sleep, and muscle tone
  • Mesencephalon (structure: tegmentum; substructure: periaqueductal gray); the periaqueductal grey is responsible for pain modulation
  • Diencephalon (structure: thalamus; substructure: lateral geniculate nucleus); the lateral geniculate nucleus is responsible for receiving visual info from the eyes and projecting it to the primary visual cortex
  • Telencephalon (structure: limbic system; substructure: amygdala); the amygdala is involved in emotional responses
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15
Q

What are the 5 major divisions of the brain?

A
  • Myelencephalon
  • Metencephalon
  • Mesencephalon
  • Diencephalon
  • Telencephalon
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16
Q

What is a structure of the myelencephalon?

A

Medulla

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17
Q

What is a substructure of the medulla?

A

Area postrema

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18
Q

What is a function of the area postrema?

A

Initiating vomiting as a response to toxins in the blood

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19
Q

The area postrema is located in what division of the brain?

A

Myelencephalon

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20
Q

What is a structure of the metencephalon?

A

Pons

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21
Q

What is a substructure of the pons?

A

Reticular formation

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22
Q

What is a function of the reticular formation?

A

Sleep, arousal, attention, muscle tone

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23
Q

The reticular formation is located in what division of the brain?

A

Metencephalon

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24
Q

What is a structure of the mesencephalon?

A

Tegmentum

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25
Q

What is a substructure of the tegmentum?

A

Periaqueductal grey

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26
Q

What is a function of the periaqueductal grey?

A

Pain modulation

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27
Q

The periaqueductal grey is located in what division of the brain?

A

Mesencephalon

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28
Q

What is a structure of the diencephalon?

A

Thalamus

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29
Q

What is a substructure of the thalamus?

A

Lateral geniculate nucleus

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30
Q

What is a function of the lateral geniculate nucleus?

A

Receiving visual info from the eyes and projecting it to the primary visual cortex

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31
Q

The lateral geniculate nucleus is located in what division of the brain?

A

Diencephalon

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32
Q

What is a structure of the telencephalon?

A

Limbic system

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33
Q

What is a substructure of the limbic system?

A

Amygdala

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34
Q

What is a function of the amygdala?

A

Emotion

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35
Q

The amygdala is located in what division of the brain?

A

Telencephalon

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36
Q

The amygdala is located in what division of the brain?

A

Telencephalon

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37
Q

Explain what the resting membrane potential is and how it is generated.

A
  • The resting membrane potential is the difference in electrical charge inside the cell compared with outside the cell
  • Equal to -70mV
  • It is generated because of selective permeability of the membrane and uneven distribution of ions inside and outside the cell
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38
Q

What is the resting membrane potential?

A

The resting membrane potential is the difference in electrical charge inside the cell compared with outside the cell

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39
Q

How is the resting membrane potential generated?

A

It is generated because of selective permeability of the membrane and uneven distribution of ions inside and outside the cell

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40
Q

Explain what reliability and validity are in scientific research

A
  • Validity is the extent to which the research is consistent with human subjects
  • Reliability refers to the extent to which the tests can be replicated and have the same result
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41
Q

What is reliability?

A

The same results will be recorded each time the test is used

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42
Q

What is validity?

A

The expectation that the variable that is being measured reflects the variable that is meant to be measured

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43
Q

What is long-term potentiation and how does it work?

A
  • Long-term potentiation is a persistent increase in synaptic strength produced by a burst of activity in the presynaptic neuron
  • The burst of firing is produced experimentally by a single brief train of electrical stimuli
  • Two types: early and late
  • Late LTP requires early LTP to be initiated first
  • Early LTP lasts a few hours at most
  • LTP occurs throughout the brain but is most studied in hippocampal pyramidal cells
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44
Q

What is long-term potentiation?

A

A persistent increase in synaptic strength produced by a burst of activity in the presynaptic neuron

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45
Q

How does long-term potentiation work?

A

A burst of firing is produced experimentally by a single brief train of electrical stimuli which strengthens the synaptic strength

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46
Q

Outline the roles of glutamate and GABA in epileptic seizures

A
  • Associations between mutations in the GABA(A) receptor subunits and various types of seizure disorders confirm that normal GABA(A) receptor functioning is required to prevent abnormal increases in brain excitability
  • The cause of some epileptic seizures involves a defective GABAergic process of hyperpolarization of neurons after prolonged depolarization
  • In cases without GABA(A) receptor mutations, dysregulation of the GABAergic systems may still be involved
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47
Q

Mutations in what type of receptor subunits are linked to various types of seizure disorders?

A

GABA(A)

48
Q

Normal GABA(A) receptor functioning is require to prevent what?

A

Abnormal increases in brain excitability

49
Q

In cases of seizure disorders without GABA(A) receptor mutations, what else could be involved?

A

Dysregulation of the GABAergic systems

50
Q

Explain the rat park experiments and their importance in our understanding of drug addiction and research

A
  • An experiment that involved separating rats into isolated or socialized groups
  • They were given an initial choice of morphine laced water, and then only morphine water, and then alternating
  • No gender differences, but some difference between groups (isolated rats chose morphine water more often)
  • This is important because many human addicts experienced neglect, isolation, etc. prior to drug abuse
51
Q

What was the order of choices given to subjects in the rat park experiments?

A

They were given an initial choice of morphine laced water, and then only morphine water, and then alternating

52
Q

Was there any gender differences in the rat park experiments?

A

No significant differences

53
Q

Was there between group differences in the rat park experiments?

A

Yes, isolated rats chose morphine water more often

54
Q

Why are the rat park experiments important in our understanding of drug addiction and research?

A

This is important because many human addicts experienced neglect, isolation, etc. prior to drug abuse

55
Q

Explain serotonin’s role in pain modulation, including the roles of specific 5-HT receptor subtypes

A
  • Descending serotonergic fibres receive input from the periaqueductal grey and synapse to the dorsal horn neurons of the spinal cord
  • Serotonin along this pathway tends to inhibit pain signals from periphery through 5HT(1b) and 5HT(3) receptors
56
Q

Serotonin activity along the pathway between the periaqueductal grey and spinal cord tends to inhibit pain signals from periphery through what receptors?

A

5HT(1b) and 5HT(3)

57
Q

Summarize norepinephrine’s role in arousal and cognition

A
  • Prefrontal cortex expresses abundance of α1 and α2 receptors; α2 agonists produce an increase in working memory and α1 agonists decreases cognitive performance, indicating a homeostatic balance between these two receptors
  • LC neurons fire more rapidly during waking than during sleep; projetions to medial septal nuclei and medial preoptic area (hypothalamus) initiate this arousal
58
Q

The prefrontal cortex expresses an abundance of what receptors?

A

α1 and α2

59
Q

What do α2 agonists do?

A

Produce an increase in working memory

60
Q

What do α1 agonists do?

A

Decrease cognitive performance

61
Q

All drug experiences are a function of dose, set, and setting. Give a brief historical account of drug prohibition and briefly speculate about how these events have influence the set and setting parameters today

A
  • Prior to 1914, ALL drugs were legal, and then in 1914 they could only be prescribed
  • Alcohol prohibition came in 1919 and was appealed in 1933 (this is in the US)
  • 1937 marihuana tax act passed
  • 1969 Leary vs US - supreme court case that overturned the marihuana tax act
  • Modern war on drugs began in 1970
  • This history helped develop a system for determining drug parameters based on abuse potential and risk potential (for example, some drugs like heroin have a high abuse potential and a high risk potential, with no medical use)
62
Q

Prior to what year were all drugs legal?

A

1914

63
Q

When was the alcohol prohibition introduced?

A

1919

64
Q

When was the alcohol prohibition appealed?

A

1933

65
Q

When did the modern war on drugs begin?

A

1970

66
Q

Delineate the three dopamine pathways that originate in the midbrain and identify each of their primary functions

A
  • The nigrostriatal pathway originates in the substantial nivea and innervates the caudate-putamen
  • The mesolimbic pathway originates in the VTA and innervates various limbic system structures
  • The mesocortical pathway originates in the VTA and innervates the cerebral cortex
  • The nigrostriatal pathway is linked to voluntary movement
  • The mesolimbic and mesocortical pathways have been implicated in the neural mechanisms underlying drug abuse and schizophrenia
67
Q

What are the three dopamine pathways that originate in the midbrain?

A
  • Nigrostriatal
  • Mesolimbic
  • Mesocortical
68
Q

Delineate the nigrostriatal pathway

A

The nigrostriatal pathway originates in the substantial nivea and innervates the caudate-putamen

69
Q

Delineate the mesolimbic pathway

A

The mesolimbic pathway originates in the VTA and innervates various limbic system structures

70
Q

Delineate the mesocortical pathway

A

The mesocortical pathway originates in the VTA and innervates the cerebral cortex

71
Q

How is ethanol metabolized in humans? Outline some of the ethnic and sex differences in this process.

A
  • Once consumed, it is diffused passively into the blood
  • 10% absorbed in the stomach, 90% absorbed in the small intestine
  • Once in circulation it moves to all tissue, not just the brain
  • Liver enzymes break it down at a constant rate
  • Majority of it is broken down by enzymes cytochrome P450 and alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH)
  • Alcohol has a proportionally greater effect on women (due to body size)
  • Some enzymes are more active in men
  • B1 deficiency is greater in alcoholic women
72
Q

The majority of ethanol is broken down by what enzymes?

A

Cytochrome P450 and alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH)

73
Q

Outline the neurochemical targets of ethanol. How does it affect various neurotransmitter receptor subtypes?

A
  • Glutamate: has a high affinity for NMDA glutamate receptors; ethanol acts as an antagonist inhibits glutamate neurotransmission by reducing the effects of glutamate at NMDA receptor; induces memory loss, hyper excitability, excitotoxicity
  • GABA: ethanol acts as an agonist and enhances GABA induced chloride entry and hyper polarization by modulating extra synaptic GABA(A) receptors and stimulating GABA release; chronic alcohol consumption causes down-regulation of GABA(A) receptors which increases the likelihood of seizures and lowers the effects of benzodiazepine
  • Dopamine: ethanol increases firing rate of mesolimbic neurons; activates dopaminergic cells in VTA; positive reinforcement which leads to repeated drug use
74
Q

Identify the five factors that influence drug action and give an example influence for each of them

A
  • Routes of administration
  • Absorption and distribution
  • Binding
  • Inactivation
  • Excretion
75
Q

Identify all of the ways in which drugs can affect synaptic transmission

A
  • Drug serves as neurotransmitter precursor
  • Drug inhibits neurotransmitter synthesis
  • Drug prevents storage of neurotransmitter in vesicles
  • Drug stimulates release of neurotransmitter
  • Drug inhibits release of neurotransmitter
  • Drug stimulates postsynaptic receptors
  • Drug blocks postsynaptic receptors
  • Drug stimulates autoreceptors; inhibits release of neurotransmitter
  • Drug blocks autoreceptors; increases release of neurotransmitter
  • Drug inhibits neurotransmitter degradation
  • Drug blocks reuptake
76
Q

List all of the receptor subtypes (both ionotropic and metabotropic) for acetylcholine

A

α, β, γ, δ, ε

77
Q

Explain the structure and function of the glutamate NMDA receptor

A
  • Ca2+ can act as a second messenger, which makes NMDA both ionotropic and metabotropic
  • In order to stimulate the NMDA receptor and open its ion channel, both glutamate and glycine are required
  • Mg2+ binding site blocks the channel even in presence of glutamate and co-agonist until membrane is depolarized
78
Q

Describe the neurobiology of drug reinforcement

A
  • Reward circuit: VTA mesolimbic dopaminergic neurons code for reward prediction error; Fibers terminate in NAcc, amygdala, and prefrontal cortex; Amygdala has reciprocal connections with NAcc and BNST; NAcc has subsequent output to the ventral pallidum VP
  • Once a reward is paired with a conditioned stimulus, these neurons will fire in response to the conditioned stimulus even before the reward is signalled (reward prediction); Failure of reward after conditioned stimulus leads to decreased activity (prediction error)
79
Q

What are the 3 types of validity?

A
  • Face validity
  • Construct validity
  • Predictive validity
80
Q

What are the five gross categories of drugs?

A
  • CNS stimulants
  • CNS depressants
  • Analgesics
  • Hallucinogens
  • Psychotherapeutics
81
Q

What is an example of a CNS stimulant?

A
  • Amphetamine
  • Cocaine
  • Nicotine
82
Q

What is an example of a CNS depressant?

A
  • Barbiturates

- Alcohol

83
Q

What is an example of an analgesic?

A
  • Morphine

- Codeine

84
Q

What is an example of a hallucinogen?

A
  • Mescaline
  • LSD
  • Psilocybin
85
Q

What is an example of a psychotherapeutic?

A
  • Prozac

- Thorazine

86
Q

Describe a psychological effect of a CNS stimulant at a typical dose

A

Increased electrical activity in the brain and behavioural arousal, alertness, and a sense of well-being in the individual

87
Q

Describe a psychological effect of a CNS depressant at a typical dose

A

Depress CNS function and behaviour to cause a sense of relaxation and drowsiness

88
Q

Describe a psychological effect of an analgesic at a typical dose

A

Reduce the perception of pain

89
Q

Describe a psychological effect of a hallucinogen at a typical dose

A

Alter one’s perceptions, leading to vivid visual illusions of distortions of objects and body image

90
Q

Describe a psychological effect of a psychotherapeutic at a typical dose

A

Treat clinical disorders of mood or behaviour

91
Q

List the cranial nerves, what they involve, and whether they are sensory or motor

A
  • Olfactory - smell (S)
  • Optic - vision (S)
  • Oculomotor - moves the eyes (M)
  • Trochlear - moves the eyes (M)
  • Trigeminal - face, sinuses, teeth, jaw muscles (S/M)
  • Abducens - moves the eyes (M)
  • Facial - tongue, soft palate, facial muscles, salivary glands, tear glands (S/M)
  • Vestibulocochlear - inner ear, hearing and balance (S)
  • Glossopharyngeal - throat muscles, taste, and mouth sensations (S/M)
  • Vagus - info from internal organs (S/M)
  • Spinal accessory - neck muscles (M)
  • Hypoglossal - tongue muscles (M)
92
Q

Is the Olfactory cranial nerve sensory or motor?

A

Sensory

93
Q

Is the optic cranial nerve sensory or motor?

A

Sensory

94
Q

Is the oculomotor cranial nerve sensory or motor?

A

Motor

95
Q

Is the trochlear cranial nerve sensory or motor?

A

Motor

96
Q

Is the trigeminal cranial nerve sensory or motor?

A

Both

97
Q

Is the abducens cranial nerve sensory or motor?

A

Motor

98
Q

Is the facial cranial nerve sensory or motor?

A

Both

99
Q

Is the vestibulocochlear cranial nerve sensory or motor?

A

Sensory

100
Q

Is the glossopharyngeal cranial nerve sensory or motor?

A

Both

101
Q

Is the vagus cranial nerve sensory or motor?

A

Both

102
Q

Is the spinal accessory cranial nerve sensory or motor?

A

Motor

103
Q

Is the hypoglossal cranial nerve sensory or motor?

A

Motor

104
Q

What does the optic cranial nerve involve?

A

Vision

105
Q

What does the oculomotor cranial nerve involve?

A

Muscles that move the eyes

106
Q

What does the trochlear cranial nerve involve?

A

Muscles that move the eyes

107
Q

What does the abducens cranial nerve involve?

A

Muscles that move the eyes

108
Q

What does the trigeminal cranial nerve involve?

A

Face, sinuses, teeth, jaw muscles

109
Q

What does the facial cranial nerve involve?

A

Tongue, soft palate, facial muscles, salivary glands, tear glands

110
Q

What does the vestibulocochlear cranial nerve involve?

A

Inner ear, hearing and balance

111
Q

What does the glossopharyngeal cranial nerve involve?

A

Throat muscles, taste and other mouth sensations

112
Q

What does the vagus cranial nerve involve?

A

Internal organs, info from internal organs

113
Q

What does the spinal accessory cranial nerve involve?

A

Neck muscles

114
Q

What does the hypoglossal cranial nerve involve?

A

Tongue muscles

115
Q

Delineate the Gq second messenger signalling pathway.

A
  • Gq-protein binds to PLC, PLD, PLA2
  • PLA2 hydrolyzes PI, releasing arachidonic acid
  • PLD hydrolyzes other membrane lipids, producing anandamide
  • PLC hydrolyzes PIP2 into inositol IP3 and DAG
  • DAG remains in membrane and activates PKC
  • IP3 binds to Ca2+ channel receptors on endoplasmic reticulum