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Biopsychology > Exam 2 > Flashcards

Exam 2 Flashcards

0
Q

What are the “rules” regarding neurotransmitters and receptors?

A

A given neuron only produces one neurotransmitter for release, but the same neuron can have receptors for many neurotransmitters?

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1
Q

What is the role of calcium in neurotransmission?

A

.

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2
Q

What are Ionotropic receptors?

A

Chemically-gated ion channel which opens when bound by a NT:

  • When open, it directly alters the membrane potential in a neuron
  • The NT only remains bound to the receptor for a short time and then returns to the synapse
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4
Q

What are metabotropic receptors and what types of processes can they regulate?

A

Receptors that, when bound with a NT, activate other proteins within neurons (The “other proteins” are G Proteins or second messengers)

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5
Q

What are agonists (direct vs. indirect) and antagonists?

*look at fig.4.4

A

Agonists: Drugs that enhance NT effects at their receptors.
Direct agonist: directly stimulates receptors (ex. nicotine)
Indirect agonist: increases NT levels in synapse by inhibiting NT breakdown (ex. Aricept)

Antagonists: drugs that decrease NT effects at their receptor, typically by blocking a specific NT receptor.

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6
Q

Describe three ways to terminate neurotransmitter action.

A
  1. ) Metabolism: an enzyme breaks down the neurotransmitter
  2. ) Reuptake or transport: a protein on the terminal or glial cell removes the neurotransmitter from the synapse
  3. ) Autoreceptors: A Neurotransmitter receptor on the terminal shuts off neurotransmitter release or synthesis
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7
Q

Describe the effects of neurotransmitters in the peripheral nervous system.

A

Neurotransmitters in the peripheral nervous system are excitatory.
Acetylcholine excites skeletal muscle.
Norepinephrine excites smooth muscle

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8
Q

Provide the following information on Glutamate:

  1. Main effect on neurons (inhibitory or excitatory)
  2. How is it made? (what is its Precursor?, what enzyme is needed to make it?)
  3. Types of receptors that bind it
  4. Where it is found/made in the brain
  5. How we get rid of it (how it is removed from the synapse?)
A
  1. EXCITATORY: it is the principle excitatory NT in the mammalian brain
  2. It is made from the amino acid GLUTAMINE
  3. Binds to 3 receptors:
    - NMDA (N-methyl-D-aspartate): gates Na+ and Ca2+
    - AMPA: gate Na+
    - Metabotropic glutamate receptors (mGluRs)
  4. Released mainly by neurons in the CORTEX, LIMBIC SYSTEM, and THALAMUS
  5. Removed from synapse through reuptake into glial cells and terminal buttons
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9
Q

Provide the following information regarding GABA:

  1. Main effect on neurons (inhibitory or excitatory)
  2. How is it made? (what is its Precursor?, what enzyme is needed to make it?)
  3. Types of receptors that bind it
  4. Where it is found/made in the brain
  5. How we get rid of it (how it is removed from the synapse
A
  1. INHIBITORY
  2. Made from GLUTAMATE by an enzyme called GLUTAMIC ACID DECARBOXYLASE (GAD)
  3. Binds to 2 receptors:
    - GABA-A gates a Cl- channel
    - GABA-B is a metabotropic receptor
  4. Released THROUGHOUT THE BRAIN by inhibitory interneurons
  5. Removed from synapse by reuptake
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10
Q

Provide the following information regarding Acetylcholine:

  1. Main effect on neurons (inhibitory or excitatory)
  2. How is it made? (what is its Precursor?, what enzyme is needed to make it?)
  3. Types of receptors that bind it
  4. Where it is found/made in the brain
  5. How we get rid of it (how it is removed from the synapse
A
  1. It depends
  2. Made from the synthesis of ACETATE and CHOLINE by an enzyme called CHOLINE ACETYLTRANSFERASE (ChAT)
  3. Binds to 2 receptors:
    - Nicotinic receptor is ionotropic and tends to excite neurons
    - Muscarinic receptor is metabotropic
  4. Released by neurons in RETICULAR FORMATION and BASAL FOREBRAIN
  5. Broken down by the enzyme, acetylcholinesterase (AChE), in synapse
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10
Q

Provide the following information about norepinephrine:
Precursor-
MAO-
Brain regions-

A

.

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11
Q

Provide the following information about Dopamine:

  1. Main effect on neurons (inhibitory or excitatory)
  2. How is it made? (what is its Precursor?, what enzyme is needed to make it?)
  3. Types of receptors that bind it
  4. Where it is found/made in the brain
  5. How we get rid of it (how it is removed from the synapse
A
  2. Made from an amino acid, TYROSINE, by an enzyme known as TYROSINE HYDROXYLASE (TH)
  3. Binds to two receptors (both are metabotropic):
    - D1
    - D2
  4. Released from neurons in the SUBSTANTIA NIGRA and VENTRAL TEGMENTAL AREA (into the caudate nucleus and nucleus accumbens respectively)
  5. Removed from the synapse via:
    - reuptake
    - “autoreceptors”
    - enzymatic breakdown (Monoamine oxidase, “MAO”, is an enzyme that breaks down DA)
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13
Q

Provide the following information about serotonin:

  1. Main effect on neurons (inhibitory or excitatory)
  2. How is it made? (what is its Precursor?, what enzyme is needed to make it?)
  3. Types of receptors that bind it
  4. Where it is found/made in the brain
  5. How we get rid of it (how it is removed from the synapse
A
  2. Made from the amino acid, Tryptophan
  3. Binds to seven different subtypes (5HT1-5HT7) and various iterations of each subtype (ex. 5HT1A, 5HT1B, 5HT1C)
  4. Released by neurons in the dorsal and median raphe (region of the midbrain).
  5. Removed from the synapse via:
    - reuptake
    - “autoreceptors”
    - enzymatic breakdown (Monoamine oxidase, “MAO”, is an enzyme that breaks down DA)
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14
Q

Provide the following information about Cannabinoids:
Where they come from-
CB1 receptors-
How they inhibit neurotransmitter release

A

They are lipids produced in dendrites during depolarization?
CB1-found in high levels in the cortex, hippocampus, basal ganglia, and parabrachial nucleus (feeding)
How they inhibit neurons:
-calcium entry into dendrites causes ananamide to be produced–>ananamide travels from dendrite to terminal in order to activate the CB1 receptor–>CB1 receptor activation blocks calcium entry into terminal during action potentials and stops NT release

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14
Q

What are the dimensions of light?

A

Hue or color: depends on the wavelength

Brightness or intensity: depends on how tall the waves are

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15
Q

List the steps from light hitting receptive fields to activation of retinal ganglion cells.

A
  1. Light breaks the bond between opsin and retinal proteins in photoreceptor.
  2. Sodium channels in the photoreceptor close.
  3. Photoreceptor is inhibited (it becomes less active/hyperpolarized and stops releasing inhibitory NT’s onto the bipolar cell).
  4. Bipolar cell is excited (it is disinhibited and becomes more active/depolarized.)
  5. Retinal ganglion cell increases firing rate.
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16
Q

List the theories of color vision.

A
  1. Trichromatic theory

2. Opponent-process theory

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17
Q

Lines and colors in primary visual cortex.

A

.

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18
Q

What are the pathways from retina to visual cortex?

A

Axons from the right side of each eye

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20
Q

Role of V4 and V5 in vision

A

V4: contains neurons that are sensitive to color contrast; process information about contrasting colors detected in the visual field
V5: Contains neurons sensitive to motion; process information about movement in the visual field

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20
Q

List the three different brain regions in the inferior temporal cortex that house neurons that recognize specific types of objects by sight or name. What object(s) are associated

A
  1. Parahippocampal Place Area (PPA): places
  2. Medial Fusiform: tools
  3. Lateral Fusiform & Fusiform Face Area (FFA): faces and animals
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21
Q

What area is involved in detection of human motion?

A

The right superior temporal sulcus (STS) is a brain region activated by perception of human motion; it is Located at junction of dorsal and ventral streams.

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22
Q

Describe the anatomy of spatial location and object identification.

A

.

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23
Q

What are the steps involved in converting sounds to biological signals?p. 158-161

A

.

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24
Q

How do we detect differences in tones or pitches? P. 162-4

A

.

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25
Q

*What are the functions of the olivary complex and inferior colliculus?

A

.

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27
Q

What are the different types of touch?

A

Cutaneous: pressure, vibration, hot, cold, pain
Kinesthetic: stretch in muscles and tendons
Organic: stretch in gut

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28
Q

What are the different nerve endings for pain and pressure/vibration? (What are the two main types of somatosensory neurons?)

A
  1. sensory neurons that detect TOUCH (pressure, vibration) have corpuscle-like coverings on their endings
  2. sensory neurons that detect PAIN have free nerve endings or no covering. The are called nociceptors
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29
Q

How does touch create action potentials in sensory neurons?

A
  1. mechanical force pulls an ion channel open on nerve ending of sensory neuron –> 2. Cations enter and depolarize the nerve ending –> 3. If enough nerve endings are depolarized, firing rate of the sensory neuron increases –> 4. sensory neuron releases glutamate into the spinal cord and stimulates ascending neurons
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30
Q

Are there different receptors for pain and temperature? How about hot and cold? How about warm and hot?

A

-Heat is detected by sensory neurons dedicated to detecting painful stimuli.
-There are receptors on free nerve endings that selectively detect hot, warm, and cold
Hot: TRPV2
Warm: TRPV1
Cold: TRPV8 (also sensitive to menthol)

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31
Q

What are causes of inflammatory and neuropathic pain?

A

Inflammatory Pain: Due to non-nervous tissue damage at the site of injury
Neuropathic Pain: Due to damage of sensory nerves

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32
Q

How does inflammatory pain work?

A

Tissue Damage–>synthesis of prostaglandin (PG)–>PG sensitizes nerve endings to histamine or bradykinin (BK), which are released by injured tissue or immune system cells–>pain ends when tissue damage resolves

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32
Q

What are symptoms of neuropathic pain?

A

Two Main Symptoms

  1. Allodynia: painful responses to stimuli that should not cause pain
  2. Hyperalgesia: greater and more prolonged responses to a painful stimulus
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33
Q

What are Enkephalins and dynorphins?

A

Enkephalins and dynorphins are the two main types of endogenous opioids.
Both types play a primary role in analgesia (aka pain relief). Enkephalins work through the brain and dynorphins work through the spinal cord.

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35
Q

How do opioids work in the brain to stop incoming pain signals to the spinal cord?

A

When pain is perceived: 1.enkephalins are released into the periaquaductal gray (PAG) matter and inhibit inhibitory interneurons –> 2. this activates projection neurons in the PAG –which activate neurons in the medulla –> 3. Activated medulla neurons then work to activate small neurons in the spinal cord that release dynorphins –> dynorphins act to block neurotransmission in pain-sensitive sensory neurons

35
Q

Ch. 2: Axoaxonic synapses (p.44)

A

A type of synapse that alters the amount of neurotransmitter released by the terminal buttons of the postsynaptic axon. They can produce presynaptic modulation, presynaptic inhibition, or presynaptic facilitation.
*this type of synapse does NOT contribute directly to neural integration.

36
Q

Which part of the brain is activated by empathy for others in pain as well as experiencing actual pain?

A

The Insular Cortex

*Note: there is also slight activation of the prefrontal cortex

37
Q

Ch. 2: Hormones (p. 4-45)

A

.

38
Q

Ch. 4: Drug effectiveness, effects of repeated administration (& compensatory mechanisms), placebo effects (p.80-82) —-read page 81 for more information on two types of compensatory mechanisms

A

.

39
Q

Ch. 6: Perception of orientation and movement, spatial frequency, and depth (p. 139-140)

A

.simple cells: have receptive fields organized in an opponent fashion (might be excited by a line of a particular orientation if it is placed in the center of the receptive field but not if it is moved away from the center)
complex cells: serve as movement detectors
hypercomplex cells: detect the location of ends of lines of a particular orientation

40
Q

Ch. 7: Odorants and perception of specific odors (p. 184-186; Figure 7.29)

A

.

41
Q

The action of a presynaptic terminal button in an axoaxonic synapse; reduces the amount of neurotransmitter released by the postsynaptic terminal button.

A

Presynaptic Inhibition

42
Q

The action of a presynaptic terminal button in an axoaxonic synapse; increases the amount of neurotransmitter released by the postsynaptic terminal button.

A

Presynaptic Facilitation

43
Q

A chemical substance that is released by an endocrine gland and that has effects on target cells in other organs

A

Hormone

44
Q

List 3 examples of what a “second messenger” protein can do.

A
  1. Increase the likelihood that an ionotropic receptor will open
  2. Increase or Decrease the cell metabolism
  3. Increase or Decrease gene expression (therefore acting as a transcription factor)
45
Q

Provide examples of drugs that can act as agonists and antagonists.

A

The drug Aricept, which is used to treat the cognitive symptoms of Alzheimer’s disease, inhibits Acetylcholinesterase (AChE). AChE is an enzyme that breaks down acetylcholine, thus Aricept acts as an INDIRECT acetylcholine agonist.

Cocaine is an indirect dopamine agonist because it blocks the dopamine transporter, therefore leaving more dopamine in the synapse

46
Q

The part of the eye that focuses images onto the retina

A

Lens

47
Q

The part of the eye that regulates the amount of light entering the eye

A

Pupil

48
Q

Fluid that fills the eye

A

Vitreous Humor

49
Q

The part of the eye that contains light-sensitive, photoreceptor cells that send signals to the brain

A

Retina

50
Q

Photoreceptor cells (120 million in retina) that detects gross changes in light. They are responsible for dark vision and are found primarily in the periphery of the retina

A

Rods

51
Q

Photoreceptor cells (6 million in retina) that detect colors, have good acuity, and are found mainly in the center of the retina

A

Cones
Note: We have different cones for red, green, and blue depending on the presence of red, green, or blue opsin protein present in the cone.

52
Q

Nardil and Marplan are among the most widely prescribed MAO inhibitors used for depression. If these drugs inhibit MAO in the brain, what action will they have on neurotransmitter levels in the brain? Should an MAO inhibitor be considered a neurotransmitter agonist or antagonist?

A.) They should decrease norepinephrine, dopamine, and serotonin. They should be considered antagonists.

B.) They should increase norepinephrine, dopamine, and serotonin. They should be considered antagonists.

C.) They should increase norepinephrine, dopamine, and serotonin. They should be considered agonists.

D.) They should only increase norepinephrine. They should be considered an agonist.

A

C.) They should increase norepinephrine, dopamine, and serotonin. They should be considered agonists.

53
Q 
The immediate precursor molecule for GABA is:
A.) tyrosine.
B.) glutamate.
C.) lipids.
D.) tryptophan.
A

B.) glutamate

54
Q

The opponent-process theory of color vision proposes that:

A.) there are three types of cones that contain opsins for red, blue, and green.

B.) colors are detected by different groups of photoreceptors that are concentrically arranged in a given retinal ganglion cell’s receptive field.

C.) there are two main types of color sensitive retinal ganglion cells that signal one color when their activity increases and signal a different color when their activity decreases.

D.) colors are detected by opposing regions of region V4 in the occipital lobe that are dedicated to processing different colors.

A

C.) there are two main types of color sensitive retinal ganglion cells that signal one color when their activity increases and signal a different color when their activity decreases.

55
Q

If you were in a dark environment with your eyes open, which of the following would you NOT expect to occur in the retina?

A.) high activity in retinal ganglion cells.

B.) high levels of depolarization in photoreceptors.

C.) a lot of opsin and retinal bound together in photoreceptors.

D.) most sodium channels open in photoreceptors.

A

A.) high activity in retinal ganglion cells.

56
Q

Our ability to detect differences in the pitch or tone of auditory noises appears to be due to:

A.) differences in the location of hair cell stimulation along the length of the cochlea.

B.) differences in the firing rate of ALL hair cells.

C.) difference in types of auditory opsin proteins released as a function of each pitch.

D.) differences in the stimulation of hair cells as a function of the length of the cilia on each cell.

A

A.) differences in the location of hair cell stimulation along the length of the cochlea.

57
Q

Function of primary visual cortex

A

Individual neurons in the primary visual cortex (V1 and V2) process information about either:

  1. the orientation of lines detected in specific regions of the retina
  2. the color of stimuli detected in specific regions of the retina
59
Q

How is dopamine involved in Parkinson’s disease?

A

Dopamine Deficiency pg. 89-give better description

60
Q

How is dopamine involved in schizophrenia?

A

The positive symptoms of schizophrenia are caused by over-activity of Dopamine synapses.

60
Q

Theory of color vision which states that three different opsin proteins (red, green, and blue opsin) in the cones allow us to detect color

A

Trichromatic Theory

61
Q

What is hemispatial neglect and what part of the brain is typically damaged in people with this disorder?

A

Reduced awareness of stimuli on one side of space, even though there may be no sensory loss; results from damage to the parietal lobe.

62
Q

How do neurons “re-wire” themselves after damage?

A

-they place more pain receptors on the free nerve endings
-they create more branches of free nerve endings
The result: sensory neuron that is hypersensitive to stimulation

63
Q

Theory of color vision which states that the presence of retinal ganglion cells that respond in different ways to the input of cones that detect red vs. green light OR yellow vs blue light gives rise to color

A

Opponent-process Theory

64
Q

What is the first place in the brain that receives information from retinal ganglion cells?

A

The Thalamus

65
Q

Cortical region involved in pain perception, that identifies stimulus location, intensity, and type/quality

a. prefrontal cortex
b. insular cortex
c. somatosensory cortex
d. anterior cingulate cortex

A

c. somatosensory cortex

66
Q

Cortical region involved in pain perception, that makes us question how we should react to an unpleasant stimulus

a. prefrontal cortex
b. insular cortex
c. somatosensory cortex
d. anterior cingulate cortex

A

d. anterior cingulate cortex

67
Q

Cortical region involved in pain perception, that produces secondary pain affects, such as wondering when we will experience the stimulus again

a. prefrontal cortex
b. insular cortex
c. somatosensory cortex
d. anterior cingulate cortex

A

a. prefrontal cortex

68
Q

Cortical region involved in pain perception that allows us to recognize that the stimulus is unpleasant as well as its degree of unpleasantness

a. prefrontal cortex
b. insular cortex
c. somatosensory cortex
d. anterior cingulate cortex

A

b. insular cortex

69
Q

Pain-relieving, morphine-like peptides produced by the body; also affect temperature, respiration, and pleasure

A

Endogenous Opioids

70
Q

A graph that represents a drug’s effectiveness; it relates the amount administered to the resulting effect.

A

Dose-response curve

71
Q

The ratio between the dose that produces the desired effect in 50 percent of the animals and the dose that produces toxic effects in 50 percent of the animals

A

Therapeutic index

72
Q

The readiness with which two molecules join together

A

Affinity

73
Q

A decrease in the effectiveness of a drug that is administered repeatedly; the result of the body’s attempt to compensate for the effects of the drug; Seen in many drugs that are commonly abused.

A

Tolerance

74
Q

An increase in the effectiveness of a drug that is administered repeatedly; not very common

A

Sensitization

75
Q

The appearance of symptoms opposite to those produced by a drug when the drug is administered repeatedly and then suddenly no longer taken

A

Withdrawal symptoms

76
Q

An inert substance that is given to an organism in lieu of a physiologically active drug; used experimentally to control for the effects of mere administration of a drug

A

Placebo

78
Q

When an action potential arrives at the terminal button to cause the release of neurotransmitters, what intermediate step is required for neurotransmitter release?

A

Calcium must enter the terminal button.

79
Q

What process is primarly responsible for removing dopamine, norepinephrine, and serotonin from the synapse?

A

.

80
Q

True or False?
When neurotransmitters bind to “metabotropic” receptors, Ions can flow into the cell through a channel in the receptor protein.

.

A

False

81
Q

The drug reserpine is used to reduce high blood pressure. It works by making vesicles that contain the neurotransmitter, norepinephrine, leaky, and, as a consequence, less norepinephrine is released by exocytosis. The action of reserpine on norepinephrine can be characterized as:

A

an antagonist.

82
Q

True or False?

A given neuron only produces receptors for one neurotransmitter.

A

False

83
Q

What are the two reasons why drugs vary in their effectiveness?

A
  1. Different drugs–even those with the same behavioral effects–may have different sites of action
    ex. Morphine–>suppresses activity of neurons in brain and spinal chord vs. Aspirin–>reduces production of a chemical involved in transmitting information from damaged tissue to pain-sensitive neurons
  2. Drugs vary widely in their affinity for the molecules to which they attach (lower affinity requires a higher dose; higher affinity requires a smaller dose)
84
Q

Provide an example of a drug in which some of its effects show sensitization while others show tolerance.

A

Cocaine

sensitization: repeated injections become more and more likely to produce movement disorders and convulsions
tolerance: euphoric effects may decline after repeated injections

85
Q

When the effects of a drug alter systems in the body for long periods of time, ___________begin to produce the opposite reaction in order to, at least partially, make up for the disturbance from optimal value

A

Compensatory mechanisms

Biopsychology (6 decks)

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