Exam2 Flashcards

(77 cards)

1
Q

release of neurotransmitters from the terminal button into the synapse

A

Exocytosis

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2
Q

Neurotransmitter rules

A

A given neuron can produce only one neurotransmitter.
A given neurotransmitter only binds to specific neurotransmitter receptors (e.g., dopamine only binds to dopamine receptors and not serotonin receptors).
The smallest unit of neurotransmitter release is one vesicle of neurotransmitters.

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3
Q

the space between two neurons where neurotransmission takes place

A

Synapse

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4
Q

A protein found on a neuron that, when bound by a NT, alters the membrane potential or metabolism of a neuron.

A

Signaling proteins (NT RECEPTORS)

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5
Q

are chemical messengers
released by exocytosis from one neuron
bind to signaling proteins on another neuron.

A

Neurotransmitters

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6
Q

In the 6 steps for neurotransmission _____ is needed to enter terminal buttons (for neurotransmitter release)

A

calcium

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7
Q

When neurotransmitters bind to “metabotropic” receptors, which is the following happens upon the neurotransmitter binding to the receptor?

A

The rate of gene expression can be altered
The activity of second messengers within the cell can be altered.
The activity of ionotropic receptors near the metabotropic receptor can be altered.

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8
Q

The drug reserpine is used to reduce high blood pressure. It works by making vesicles within the terminal button 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.

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9
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.

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10
Q

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

A

metabolism or enzymatic breakdown
reuptake
autoreceptors

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11
Q

The immediate precursor molecule for GABA is:

A

glutamate.

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12
Q

How does our auditory system distinguish differences in tone or pitch?

A

Most tones are detected based on the location or place of the activated hair cell within the cochlea.
and
Very low tones (below 200 Hz) are detected by the rate at which cochlear hair cells depolarize.

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13
Q

Which of the following sequences best represents how signals related to the detection of light are transmitted in the retina?

A

Light strikes the photoreceptor. Opsin and retinal break apart. Sodium channels close. The photoreceptor becomes inhibited. The bipolar cell is excited. The retinal ganglion cell fires more often.

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14
Q

Antagonist or Agonist: Drug X stimulates dopamine autoreceptors on terminal buttons.

A

Antagonist

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15
Q

Antagonist or Agonist: Riluzole causes glutamate transporters to work faster and usher more glutamate out of synapses.

A

Antagonist

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16
Q

Antagonist or Agonist: Nardil is an antidepressant drug that inhibits the enzyme, monoamine oxidase or MAO.

A

Agonist

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17
Q

Antagonist or Agonist: Antidepressants known as selective serotonin reuptake inhibitors or SSRIs block transporters for serotonin on terminal buttons.

A

Agonist

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18
Q

The opponent-process theory of color vision proposes that:

A

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.

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19
Q

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.

A

Ionotropic neurotransmitter receptor

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20
Q

Receptors that, when bound with a NT, activate other molecules and proteins within neurons.
The other proteins and molecules include G proteins and second messengers (some known as kinases

A

Metabotropic neurotransmitter receptor

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21
Q

Examples of what a “second messenger” metabotropic neurotransmitter can do (AKA processes they regulate):

A

Increase or decrease cell metabolism.
Increase the likelihood that an ionotropic receptor will open (see slide before the last one).
Increase or decrease gene expression.

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22
Q

directly stimulates receptors (e.g., nicotine binds to acetylcholine receptors)

A

Direct Agonist

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23
Q

drugs that enhance NT effects at their receptors

A

Agonist

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24
Q

increases NT levels in synapse (e.g., Aricept inhibits acetylcholine breakdown)

A

Indirect Agonist

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25
drugs that decrease NT effects at their receptor | typically by blocking a specific NT receptor
Antagonist
26
drug that stimulates a receptor but not as well as the actual NT Buprenorphine weakly stimulates opioid receptors in the brain
Partial Agonist
27
3 ways to terminate neurotransmitter action
1. Metabolism: enzyme breaks down Neurotransmitter 2. (Re)uptake or transport: Protein on terminal or glial cell removes NT from synapse 3. Autoreceptors: NT receptor on terminal shuts off NT release or synthesis
28
``` Glutamate main effect on neurons, precursor, types of receptors, where it is found in the brain, how do we get rid of it? ```
The principal excitatory neurotransmitter in the mammalian brain Is made from the amino acid, glutamine, in terminal buttons. Binds to three receptors NMDA (N-methyl-D-aspartate): gates Na+ and Ca2+ AMPA: gate Na+ Metabotropic glutamate receptors (mGluRs) Released mainly by neurons in the cortex, limbic system, and thalamus Removed from synapse through reuptake into glial cells and terminal buttons.
29
``` GABA main effect on neurons, precursor, types of receptors, where it is found in the brain, how do we get rid of it? ```
Major inhibitory neurotransmitter in brain Made from glutamate by an enzyme called glutamic acid decarboxylase (GAD). Binds to two receptors: GABAA gates a Cl- channel. GABAB is a metabotropic receptor. Released throughout the brain by inhibitory interneurons. Removed from synapse by reuptake.
30
Acetylcholine types of receptors, where it is found in the brain, how do we get rid of it?
Binds to two receptors. Nicotinic receptor is ionotropic and tends to excite neurons. Muscarinic receptor is metabotropic. Released by neurons in reticular formation and basal forebrain. Broken down by the enzyme, acetylcholinesterase (AChE), in synapse.
31
Dopamine precursor, types of receptors, where it is found in the brain?
Made from an amino acid, tyrosine, by an enzyme known as tyrosine hydroxylase (TH). Binds to D1 and D2 receptors – both metabotropic. released from neurons in the substantia nigra and ventral tegmental area into caudate nucleus and nucleus accumbens respectively.
32
Norepinephrine precursor brain regions
Norepinephrine made from dopamine. Released by neurons in the locus coeruleus. Located in the midbrain.
33
Serotonin precursor brain regions
Is made from the amino acid, tryptophan. Released by neurons in the dorsal and median raphe (region of the midbrain).
34
What is monoamine oxidase?
Monoamine oxidase (MAO) is an enzyme that breaks down Dopamine
35
Endocannabinoids what are they made of? cb1 receptors how they inhibit neurotransmitter release
Best known ECs are ananamide and 2-AG (2-arachidonoyl glycerol). Lipids produced in dendrites during depolarization. ECs bind to cannabinoid (CB) 1 & 2 receptors. They are metabotropic. CB1 found in high levels in cortex, hippocampus, basal ganglia, parabrachial nucleus (feeding). CB2 receptors exist outside of the brain. 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.
36
Dimensions of Light
Hue or color depends on the wavelength. Brightness or intensity depends on how tall the waves are
37
Functions of different parts of the eye
RETINA - contains light-sensitive, photoreceptor cells that send signals to brain VITREOUS HUMOR - fluid that fills the eye LENS - focuses images onto retina PUPIL - regulates amount of light entering eye
38
compare and contrast cones and rods
Cones (6 million) Detect contrast Detect colors different cones for red, green, and blue depending on presence of red, green, or blue opsin protein present in cone Found mainly in center of retina – the fovea Rods (120 million) Detect gross changes in light Dark vision Found mainly in periphery of retina
39
How visual information is processed in the retina **
1. Light breaks bond between opsin and retinal in photoreceptor. 2. Sodium channel closes. 3. Photoreceptor is inhibited. 4. Bipolar cell is excited. 5. Firing rate of retinal ganglion cell increases
40
An area of the retina or group of photoreceptors that provide input to a given retinal ganglion cell
RECEPTIVE FIELDS
41
Trichromatic theory of color vision: **
three different opsin proteins (red, green, and blue opsin) in the cones allow us to detect color.
42
Opponent-process theory of color vision:
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 (see next slide) gives rise to color.
43
Role of V4 and v5, and superior temporal sulcus in vision: **
V4: Contains neurons that are sensitive to color contrast V5: Neurons sensitive to motion (and not head movement). The right superior temporal sulcus (STS) is a brain region activated by perception of human motion. Located at junction of dorsal and ventral streams. P
44
__________ processes information about where an object is. *
Posterior parietal cortex
45
__________ process information about what an object is. | *
Inferior temporal cortex
46
3 regions involved in object identification within the inferior temporal cortex
Parahippo-campal Place Area (PPA) - places Medial fusiform - tools Lateral fusiform & fusiform facial area (FFA) - faces & animals
47
type of touch: pressure, vibration, hot, cold, pain
Cutaneous
48
type of touch: stretch in muscles, tendons
Kinesthetic
49
type of touch: stretch in gut
organic
50
Sensory nerve endings in the skin, 2 types
Sensory neurons that detect touch (pressure, vibration) have corpuscle-like coverings on their endings. Sensory neurons that detect pain have free nerve endings or no covering. They are called nociceptors.
51
Touch to action potentials
1. Mechanical force pulls an ion channel open on nerve ending of sensory neuron. 2. Cations enter and depolarize nerve ending. 3. If enough nerve endings are depolarized, firing rate of sensory neuron increases. 4. Sensory neuron releases glutamate into the spinal cord and stimulates ascending neurons.
52
Are there different receptors for pain and temperature? How about hot and cold? Warm and hot?
yes, There are receptors on free nerve endings that selectively detect hot, warm, and cold. Yes, TRPM8 receptor detects cold (also sensitive to menthol). Yes, TRPV1 (transient receptor potential) receptor detects warm and TRPV2 receptor detects hot.
53
Causes of inflammatory pain
Due to non-nervous tissue damage at site of injury. | Usually ends when tissue damage resolves
54
Causes of neuropathic pain
Due to damage to sensory nerves | Does not end because pain is due to a pathologically “rewired” nervous system
55
How inflammatory pain works
Tissue damage results in prostaglandin (PG) synthesis. PGs sensitize nerve endings to histamine or bradykinin (BK). Latter two chemicals released by injured tissue or immune system cells. Pain ends when tissue damage resolves.
56
Symptoms of neuropathic pain *
Allodynia painful responses to stimuli that should not cause pain Hyperalgesia greater and more prolonged responses to a painful stimulus
57
How neurons rewire themselves in neuropathic pain **
Injured sensory neuron responds to injury-induced decrease in function by: Placing more pain receptors on the free nerve endings. Creating more branches of the free nerve endings Results in the sensory neuron now becoming hypersensitive to stimulation Remains hypersensitive to a long time – becomes the sensory neuron’s “new” normal state.
58
one of Two main types of endogenous opioids in the brain, play primary role in analgesia (pain relief). *
enkephalins
59
one of Two main types of endogenous opioids | in the spinal cord, primary role in analgesia (pain relief). *
dynorphins
60
How do opioids work in the brain to stop incoming pain signals to the spinal cord?
When pain is perceived, enkephalins inhibit inhibitory interneurons into the periaquaductial gray (PAG) matter. This action disinhibits large projection neurons in the PAG, that then activate neurons in the medulla. Activated medulla neurons then activate interneurons in the spinal cord that release dynorphins. Dynorphins act to block neurotransmission in pain-sensitive sensory neurons.
61
Brain changes that accompany chronic opioid use *
Brain responds by decreasing opioid receptors, decreasing dopamine production, and decreasing dopamine receptors. Decreases in receptors due to excess stimulation known as receptor down-regulation. Brain response leads to negative mood and craving for drug when user is abstinent. Explains tolerance and need for higher doses and more frequent dosing to counter cravings.
62
Role of different cortical regions in pain recognition
Somatosensory cortex - stimulus location, intensity, and quality Insular cortex - how unpleasant is the stimulus? Anterior cingulate cortex - how should we react to an unpleasant stimulus? Prefrontal cortex - when will we experience the stimulus again (secondary pain affect)?
63
Empathy for pain
Insula or insular cortex is activated by empathy for others in pain as well as experiencing actual pain. Higher rating on empathy leads to greater activity in insula during observation of pain.
64
What are two main theories for pitch detection?*
Place theory: The location of the stimulated hair cell determines the pitch. backwards piano Rate theory: The rate of the hair cell stimulation determines the pitch; applies to low tones below 200 Hz.
65
Role of olivary complex*
Receives direct input from auditory nerve. Detects interaural temporal differences Difference in timing of sound arrival at each ear Used to detect sounds below 3000 Hz Detects interaural intensity differences Differences in sound loudness at each ear Used to detect sounds above 3000 Hz
66
Role of inferior colliculus*
Receives input from olivary complex | Controls reflexive responses (e.g., startle) to auditory stimuli.
67
role of auditory cortex *
The primary auditory cortex is arranged in a tonotopic manner. Tonotopic - neurons spatially organized according to pitch. like basilar membrane of cochlea However, neurons can “change their tune” or learn to respond to a different pitch. Usually occurs when a specific tone is heard more frequently or is associated with more important outcomes than other tones.
68
Flexes in response to sound waves.
Tympanic membrane (or ear drum
69
smallest bones in the body; respond to movement in tympanic membrane.
Ossicles
70
connected to ossicles by oval window; contains hair cells that convert sound waves into membrane potentials.
Cochlea
71
connects cochlea to the brain.
Auditory nerve
72
How do hair cells and the auditory nerve respond to sounds?
Bend in response to changes in cochlear fluid pressure produced by sound waves. When hairs are bent, cells act to stimulate auditory nerve.
73
the relative width of the bands in a sine-wave grating, measured in cycles per degree of visual angle
spatial frequency
74
an orientation-sensitive neuron in the striate cortex whose receptive field is organized in an opponent fashion
simple cell
75
a neuron in the visual cortex that responds to the presence of a line segment with a particular orientation located within its receptive field, especially when the line moves perpendicularly to its orientation
complex cell
76
a neuron in the visual cortex that responds to the presence of a line segment with a particular orientation that ends at a particular point within the cell's receptive field
hypercomplex cell
77
odorants and the perception of specific odors
- some odors can mask others, | - humans can recognize up to 10,000 odorants