Exam 2 Flashcards

1
Q

What are receptors?

A

Chemical messengers bind to specific target-cell proteins

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2
Q

Where do most chemical messengers that are water-soluble bind to?

A

receptors located at the plasma membrane

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3
Q

Where do other chemical messengers, like steroids, that are lipid-soluble bind to?

A

An intracellular receptor

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4
Q

What does the N-terminal domain participate in?

A

gene activation

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5
Q

What does the DNA-binding domain determine?

A

which segments of DNA are bound by different receptors

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6
Q

What is the hinge domain required for?

A

Nuclear receptors to localize in the cell nucleus

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7
Q

What does the ligand-binding domain determine?

A

Which messenger binds to a given receptor

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8
Q

Specificity

A

The ability of a receptor to bind only one type or a limited number of structurally related types of chemical messengers. Only cells that express the correct receptor can bind a particular messenger.

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9
Q

Saturation

A

The degree to which receptors are occupied by messengers. If all are occupied, the receptors are fully saturated; if half are occupied, the saturation is 50%, and so on.

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10
Q

Affinity

A

The strength with which a chemical messenger binds to its receptor.

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11
Q

Competition

A

The ability of different molecules to compete with a ligand for binding to its receptor. Competitors generally are similar in structure to the natural ligand.

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12
Q

Antagonist

A

A molecule that competes with a ligand for binding to its receptor but does not activate signaling normally associated with the natural ligand. Therefore, an antagonist prevents the actions of the natural ligand. Certain types of antihistamines are examples of antagonists.

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13
Q

Agonist

A

A chemical messenger that binds to a receptor and triggers the cell’s response; often refers to a drug that mimics a normal messenger’s action. Some decongestants are examples of agonists.

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14
Q

Down-regulation

A

A decrease in the total number of target-cell receptors for a given messenger; may occur in response to chronic high extracellular concentration of the messenger.

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15
Q

Up-regulation

A

An increase in the total number of target-cell receptors for a given messenger; may occur in response to a chronic low extracellular concentration of the messenger.

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16
Q

Increased sensitivity

A

The increased responsiveness of a target cell to a given messenger; may result from up-regulation of receptors.

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17
Q

Can lipid messengers diffuse through the plasma membrane?

A

yes

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18
Q

Where do the signal receptor complexes in lipid soluble messengers bind?

A

directly to recognized sequences in the DNA and alter gene transcription

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19
Q

What does activation of the receptor by a first messenger (ligand) result in?

A

a conformational change of the receptor so it forms an open channel through the plasma membrane.

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20
Q

What does the opening of ligand-gated ion channels in response to binding of a first messenger result in?

A

an increase in the net diffusion across the plasma membrane of one or more types of ions specific to that channel.

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21
Q

What is the sequence of protein kinases?

A
  • messenger binds to the receptor
  • changes the conformation of the receptor
  • enzymatic portion on the cytoplasmic side of the plasma membrane becomes activated.
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22
Q

autophosphorylation of the receptor

A

the receptor phosphorylates some of its own tyrosine residues

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23
Q

what does the cytoplasmic portion of the receptor serve as?

A

docking sites for cytoplasmic proteins

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24
Q

What do docking proteins do?

A

bind and activate other proteins which in turn activates one or more signaling pathways within the cell.

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25
Q

What is the common denominator for enzyme pathways?

A

they all involve activation of cytoplasmic proteins by phosphorylation.

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26
Q

What does a guanylyl cyclase catalyze the formation of?

A

a molecule known as cyclic GMP (cGMP) in the cytoplasm

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27
Q

What does cyclic GMP (cGMP) function as

A

a second messenger to activate a protein kinase called cGMP-dependent protein kinase.

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28
Q

what does cGMP-dependent protein kinase do?

A

phosphorylates specific proteins that then mediate the cell’s response to the original messenger.

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29
Q

Where are Receptors that function both as ligand-binding molecules and as guanylyl cyclases abundantly expressed?

A

in the retina of the eye where they are important for processing visual inputs

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30
Q

what are janus kinases (JAKs) associated with?

A

the receptor

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31
Q

G proteins

A

Bound to the inactive receptor; located on the cytosolic surface of the plasma membrane

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32
Q

What are the the three subunits of g proteins?

A

alpha, beta, and gamma

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33
Q

What does the alpha subunit of g proteins bind?

A

GDP and GTP

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34
Q

What do the beta and gamma subunits of g proteins do?

A

help anchor the alpha subunit in the membrane

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35
Q

What does the binding of a first messenger to the receptor do?

A

changes the conformation of the receptor

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36
Q

What does the activated receptor do for GTP?

A

increases the affinity of the alpha subunit of the G protein for GTP

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37
Q

What happens to the alpha subunit of g proteins when it is bound to GTP?

A

it dissociates from the beta and gamma subunits of the trimeric G protein

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38
Q

What does the dissociation of the alpha subunit from the beta and gamma subunits allow?

A

the activated alpha subunit to link up with still another plasma membrane protein, either an ion channel or an enzyme.

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39
Q

What does a G protein serve as?

A

a switch to couple a G-protein-coupled receptor to an ion channel or to an enzyme in the plasma membrane

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40
Q

What two functions can G proteins have?

A

either stimulate (Gs) or inhibit (Gi) some aspect of cell function.

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41
Q

What does activation of the receptor by the binding of the first messenger allow?

A

the receptor to activate its associated G protein

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42
Q

What is the Gs effector protein?

A

adenylyn cyclase

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43
Q

What does activated adenylyl cyclase catalyze?

A

the conversion of cytosolic ATP molecules to cyclic AMP (cAMP)

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44
Q

What does cyclic AMP (cAMP) act as?

A

a second messenger

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45
Q

what does cAMP phosphodiesterase catalyze?

A

The action of cAMP eventually terminates when it is broken down to AMP

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46
Q

What does the activation of Gi cause?

A

the inhibition of adenylyl cyclase

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47
Q

What does the inhibition of adenylyl cyclase cause?

A

decrease the concentration of cAMP in the cell and thereby the phosphorylation of key proteins inside the cell

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48
Q

what does phospholipase C (PLC) catalyze?

A

the breakdown of a plasma membrane phospholipid

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49
Q

What does DAG activate?

A

protein kinase C, which then phosphorylate a large number of other proteins, leading to the cell’s response.

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50
Q

where does Cytosolic IP3 bind?

A

ligand-gated Ca^(2+) channel receptors on the endoplasmic reticulum that open when bound to IP3 resulting in increased cytosolic Ca^(2+) concentration

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51
Q

What is an action of Ca2+?

A

to help activate some forms of protein kinase C

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52
Q

What are the two ways Ca2+ can be used in the cytosol?

A

can be either increased or decreased in the cytosol to elicit a cellular response (change in membrane potential)

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53
Q

How is Ca2+ maintained at an extremely low level in the cytosol?

A

By means of active-transport systems in the plasma membrane and cell organelles

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54
Q

eicosanoids

A

present in plasma membrane phospholipids.

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55
Q

when does the synthesis of eicosanoids begin?

A

when an appropriate stimulus binds to its receptor and activates phospholipase 𝐀_𝟐 (PLA_2 )

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56
Q

Afferent neurons

A
  • sensory
  • Transmit information into the CNS from receptors at their peripheral endings
  • Single process from the cell body splits into a long peripheral process (axon) that is in the PNS and a short central process (axon) the enters the CNS
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57
Q

Efferent neurons

A
  • motor
  • Transmit information out of the CNS to effector cells, particularly muscles, glands, neurons, and other cells
  • Cell body with multiple dendrites and a small segment of the axon are in the CNS; most of the axon is in the PNS
58
Q

Interneurons

A
  • Function as integrators and signal changers
  • Integrate groups of afferent and efferent neurons into reflex circuits
  • Lie entirely within the CNS
  • Account for > 99% of all neurons
59
Q

What causes changed in membrane potential?

A

movement of ions

60
Q

The Changes in Membrane Potential and Relative Membrane Permeability to 〖𝐍𝐚〗^+ and 𝐊^+ During an Action Potential

A
  1. Steady resting membrane potential is near E_K, P_K>P_(Na^+ ), due to leak K^+ channels.
  2. Local membrane is brought to threshold voltage by a depolarizing stimulus.
  3. Current through opening voltage-gated Na^+ channels rapidly depolarizes the membrane, causing more Na^+ channels to open.
  4. Inactivation of Na^+ channels and delayed opening of voltage-gated K^+ channels halt membrane depolarization.
  5. Outward current through open voltage-gated K^+ channels repolarizes the membrane back to a negative potential.
  6. Persistent current through slowly closing voltage-gated K^+ channels hyperpolarizes membrane toward E_K: Na^+ channels return from inactivated state to closed state (without opening).
  7. Closure of voltage-gated K^+ channels returns the membrane potential to its resting value.
61
Q

What maintains concentration gradients?

A

Na+/K+ pump

62
Q

What does K+ do in the Na+/K+ pump?

A
  • K+ leaks out of the cell down its concentration gradient based on increased membrane permeability (more K+ channels)
  • This results in an increasingly negative charge inside the cell
63
Q

Why is the plasma membrane more permeable to K+?

A

because there are more K+ channels than there are Na+ channels

64
Q

What does Na+ do in the Na+/K+ pump?

A

Na+ leaks into the cell down its concentration gradient based on the magnitude of the electrochemical gradient

65
Q

K+ has a…

A

high permeability and a low electrochemical gradient

66
Q

Na+ has a…

A

low permeability and a high electrochemical gradient

67
Q

Graded potential

A

A potential change of variable amplitude and duration that is conducted decrementally; has no threshold or refractory period

68
Q

Action potential

A

A brief all-or-none depolarization of the membrane, which reverses polarity in neurons; has a threshold and refractory period and is conducted without decrement

69
Q

What are Adrenergic receptors used by?

A

the neurotransmitters norepinephrine (NE) and epinephrine (Epi)

70
Q

What does it mean that all adrenergic receptors are metabotropic?

A

thus use second messengers to transfer a signal from the surface of the cell to the cytoplasm

71
Q

Alpha-adrenergic receptors

A

Alpha_1 (α_1 ) and Alpha_2 (α_2 )

72
Q

What do the cells of the adrenal medulla release?

A

a mixture of about 80% epinephrine and 20% norepinephrine into the blood

73
Q

excitability

A

The ability to generate action potentials

74
Q

what do Voltage-gated ion channels do?

A

give a membrane the ability to undergo action potentials.

75
Q

What do graded potential produced from ligand-gated ion channels and mechanically gated ion channels do?

A

serve as the initiating stimulus for an action potential.

76
Q

Modality

A

specific is information is carried by specific receptors

77
Q

Sensory Coding

A

conversion of stimulus energy into a signal that conveys the relevant sensory information to the central nervous system.

78
Q

What are the three components of sensory coding?

A

Modality
Intensity
Location

79
Q

Lateral inhibition

A

enables the localization of a stimulus site for some sensory systems.
a neuron’s response to a stimulus is inhibited by the excitation of a neighboring neuron.

80
Q

Why is exact localization possible?

A

because lateral inhibition removes the information from the peripheral regions.

81
Q

What are Afferent sensory pathways formed by?

A

chains of three or more neurons connected by synapses that form ascending pathways to the central nervous system.

82
Q

somatic sensation

A

Sensation from the skin, skeletal muscles, bones, tendons, and joints

83
Q

Activation of somatic receptors gives rise to the sensations of

A
  • Touch and pressure
  • Awareness of the position of the body parts and their movement
  • Temperature
  • Pain
  • Itch
84
Q

Meissner’s corpuscle

A

rapidly adapting mechanoreceptor, touch and pressure

85
Q

Merkel’s corpuscle

A

slowly adapting mechanoreceptor, touch and pressure

86
Q

Free neuron ending

A

slowly adapting, including nociceptors, itch receptors, thermoreceptors, and mechanoreceptors

87
Q

Pacinian corpuscles

A

rapidly adapting mechanoreceptor, vibration and deep pressure

88
Q

Ruffini corpuscle

A

slowly adapting mechanoreceptor, skin stretch

89
Q

Referred pain

A

the sensation of pain that is experienced at a site other than the injured or diseased tissue.

90
Q

Hyperalgesia

A

an increased sensitivity to painful stimuli. The pain can last for hours after the original stimulus is gone. This type of pain response is common with severe burn injuries.

91
Q

Analgesia

A

the selective suppression of pain without effects on consciousness or other sensations.

92
Q

basal cells

A

divide and differentiate to continually replace taste receptor cells damaged in the occasionally harsh environment of the mouth.

93
Q

adequate stimulus

A

the amount and type of energy required to stimulate a specific sensory organ

94
Q

Sensory receptors

A
  • at the peripheral ends of afferent neurons.

- generate receptor potentials (a graded potential)

95
Q

Sensory Coding

A

conversion of stimulus energy into a signal that conveys the relevant sensory information to the central nervous system.

96
Q

Where do the olfactory receptors lie?

A

in the olfactory epithelium in the upper part of the nasal cavity

97
Q

States of consciousness

A

levels of alertness such as being awake, drowsy, or asleep.

98
Q

A person’s state of consciousness is defined clinically?

A

by behavior, covering the spectrum from maximum attentiveness to comatose

99
Q

A person’s state of consciousness is defined diagnostically?

A

by the pattern of brain activity that can be recorded electrically

100
Q

What is EEG useful for?

A

to monitor cerebral activity of surgical patients under anesthesia, in the diagnosis of neurological diseases, and in the diagnosis of coma and brain death.

101
Q

Epilepsy

A

a common neurological disease, occurring in about 1% of the population. It manifests in mild, intermediate, and severe forms and is associated with abnormally synchronized discharges of cerebral neurons.

102
Q

alpha rhythm

A

The most prominent EEG wave pattern of an awake, relaxed adult whose eyes are closed, is an oscillation of 8 to 12 hertz

103
Q

Where is the alpha rhythm best recorded>

A

over the parietal and occipital lobes and is associated with decreased levels of attention

104
Q

beta rhythm

A

people are attentive to an external stimulus or are thinking hard about something, the alpha rhythm is replaced by smaller-amplitude, higher-frequency (>12 hertz) oscillations

105
Q

When someone becomes increasingly drowsy, what happens to their beta rhythm?

A

It transitions into a predominately alpha rhythm.

106
Q

What rhythm appears when sleep actually occurs?

A

the theta rhythm (4 to 8 hertz) and the delta rhythm (slower than 4 hertz)

107
Q

What is NREM Sleep

A

The initial phase of sleep

108
Q

What is stage N1 of NREM sleep?

A

theta waves begin to be interspersed among the

alpha pattern.

109
Q

What is stage N2 of NREM sleep?

A

high-frequency bursts called sleep spindles and

large-amplitude K complexes occasionally interrupt the theta rhythm.

110
Q

What happens in stage N3 of NREM sleep?

A

delta waves first appear along with the theta rhythm;
as this stage continues, the dominant pattern becomes a delta rhythm,
sometimes referred to as slow-wave sleep.

111
Q

How long does NREM sleep take?

A

30 to 45 minutes

112
Q

REM (paradoxical) sleep

A

Greatest muscle relaxation and difficulty of arousal; begins 50 to 90 minute after sleep onset, episodes repeated every 60 to 90 minute, each episode lasting about 10 minute; dreaming frequently occurs, rapid eye movements behind closed eyelids; marked increase in brain O2 consumption.

113
Q

Schizophrenia

A

disease in which information is not properly regulated in the brain.

114
Q

catatonia

A

total immobilization

115
Q

What is a widely accepted explanation for schizophrenia?

A

certain mesocortical dopamine pathways are overactive

116
Q

What kind of drugs would make schizophrenia worse?

A

amphetamine-like drugs, which enhance dopamine signaling

117
Q

What do most drugs used to treat schizophrenia do?

A

block dopamine receptors

118
Q

What are some implicated causes of mood disorders?

A

biogenic amine neurotransmitters (norepinephrine, dopamine, and serotonin) and acetylcholine

119
Q

Bipolar disorder

A

characterized by swings between depression and mania.

120
Q

Mania

A

abnormally and persistently elevated mood.

121
Q

What do tricyclic antidepressant drugs do?

A

interfere with serotonin and/or norepinephrine reuptake by presynaptic endings.

122
Q

What do monoamine oxidase (MAO) inhibitor drugs do?

A

interfere with the enzyme responsible for the breakdown of these same two neurotransmitters.

123
Q

What do serotonin-specific reuptake inhibitors (SSRIs) do?

A

these drugs selectively inhibit serotonin reuptake by presynaptic terminals

124
Q

What is the most commonly used antidepressant drugs?

A

serotonin-specific reuptake inhibitors (SSRIs)

125
Q

What is the major drug used in treating bipolar disorder?

A

the chemical element lithium, sometimes given in combination with anticonvulsant drugs.

126
Q

What do most psychoactive drugs interfere with?

A

dopamine and seratonin (biogenic amine) pathways

127
Q

What is the primary effect of cocaine?

A

block the reuptake of dopamine into the presynaptic axon terminal.

128
Q

What is tolerance?

A

when increasing doses of the substance are required to achieve effects that initially occurred in response to a smaller dose.

129
Q

What can cause tolerance?

A
  • changes in the number or sensitivity of receptors that respond to the substance
  • how many or the activity of the enzymes involved in the neurotransmitter release and degradation
  • the activity of reuptake molecules
  • signal transduction pathways in postsynaptic cells
130
Q

What is the MAIN neurotransmitters used in psychoactive substances?

A

dopamine

131
Q

Declarative memory

A

(explicit memory): the retention and recall of conscious experiences that can be put into words (declared)

132
Q

What parts of the brain are used in the formation of declarative memories?

A

The hippocampus, amygdala, and other parts of the limbic system

133
Q

Procedural memory

A

the memory of how to do things

134
Q

What parts of the brain are used in the formation of procedural memories?

A

regions of sensorimotor cortex, the basal nuclei, and the cerebellum.

135
Q

Short term memory

A

Working memory; registers and retains incoming information for a short time—a matter of seconds to minutes—after its input

136
Q

Long term memory

A

may be stored for days to years and recalled at a later time.

137
Q

Consolidation

A

The process by which short-term memories become long-term memories

138
Q

anterograde amnesia

A

damage to the limbic system and associated structures, including the hippocampus, thalamus, and hypothalamus

139
Q

retrograde amnesia

A

memories are abolished for all that happened for a variable period of time before a blow to the head

140
Q

Adrenergic Alpha 1

A

vasoconstriction

141
Q

Adrenergic Beta 1

A

regulate heart rate and myocardial contractility

142
Q

Adrenergic Beta 2

A

lungs/bronchi