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Biopsychology > Biopsych Exam 1 > Flashcards

Biopsych Exam 1 Flashcards

1
Q

Parts of a neuron

A
  • Presynaptic neuron
  • myelin sheath
  • nodes of ranvier
  • axon
  • axon hillock
  • cell nucleus
  • soma
  • dendrites
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2
Q

basic components of a synapse

A
  • composed of the axon terminal of one neuron, the synaptic cleft and dendrite of another neuron
  • axon terminal sends the message (releases the neurotransmitter), relays it across the synapse, and the dendrite receives it and sends through the neuron
  • synaptic cleft provides space for the chemical transmission of messages
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3
Q

what is the function of myelin sheath?

A
  • fatty white matter
  • coating along the axon
  • keeps signal intact inside neuron (protective layer)
  • increases speed of conduction by permitting flow of ionic current across the membrane
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4
Q

what cells produce myelin sheath?

A

CNS: oligodendrocyte
PNS: Schwann cell

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5
Q

What happens during resting (membrane) potential? What charge is inside of a neuron?

A
  • Resting potential: an electrical charge along the membrane during inactive state (-65mV)
  • Negative charge inside of a neuron during resting potential
    At resting potential:
  • Higher concentration of potassium ions INSIDE the cell
  • higher concentration of sodium ions OUTSIDE the cell
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6
Q

What is an ion distribution during resting potential?

A
  • sodium, chloride, and calcium are concentrated outside the cell
  • potassium and other anions are concentrated inside the cell
  • this leads to a negative resting membrane potential
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7
Q

what is action potential?

A

the change in membrane potential when a neuron sends the signal down the axon

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8
Q

explain action potential step by step

A

depolarization:
1. action potential begins when the neuron receives a stimulus (from sensory input or other neurons)
2. if stimulus is strong enough to reach the threshold of excitation, it triggers a change in the membrane potential (enough sodium floods the cell and it becomes positively charged)
3. voltage-gated sodium channels open, sodium rushes into the neuron from the extracellular fluid
- influx of positively charged sodium ions rapidly depolarize the membrane; potassium leaves the cell which leads to repolarization

repolarization:
1. after reaching peak voltage, the voltage gated-sodium channels and voltage-gated potassium channels open
2. potassium ions (K+) exit the neuron moving from inside to outside
- the efflux of positively charged potassium ions restores the negative charge inside the neuron
- brings the membrane potential back towards its resting state

hyperpolarization:
1. sometimes the efflux of potassium ions overshoots the resting membrane potential causing the inside of the neuron to become more negative than the resting state
2. this occurs because the potassium channels remain open for a brief period even after the resting membrane potential is reached

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9
Q

types of synapses

A
  • axo-dendritic
  • axo-somatic
  • axo-axonic
  • dendro-dendritic
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10
Q

What do glial cells do

A

help support, connect, and protect the neurons of the central and peripheral nervous systems

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11
Q

what are the glial cells of the central nervous system

A

astrocyte, oligodendrocyte, microglia, and ependymal cells

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12
Q

what are the glial cells of the peripheral nervous system

A

satellite and schwann cell

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13
Q

what do the astrocyte and satellite cells do, where are they located?

A
  • glial cells
  • astrocyte: CNS
  • satellite: PNS
  • they provide structure to the cell, remove excess neurotransmitters, direct neural growth
  • only astrocyte induced blood-brain barrier in the brain
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14
Q

what do oligodendrocyte and schwann cells do, where are they located?

A
  • glial cells
  • oligodendrocyte: CNS
  • Schwann: PNS
  • create myelin sheath
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15
Q

what does the microglia cell do and where is it located?

A
  • glial cell
  • CNS
  • immune surveillance and phagocytosis
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16
Q

what does the ependymal cell do and where is it located?

A
  • glial cell
  • CNS
  • create and circulate cerebrospinal fluid (CSF)
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17
Q

Types of nervous systems

A
  • Peripheral nervous system (PNS)
  • Central nervous system (CNS): spinal cord and brain
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18
Q

Which neurotransmitter is involved in schizophrenia?

A
  • too much dopamine
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19
Q

Which neurotransmitters are involved in addiction?

A
  • too much dopamine
  • norepinephrine
  • glutamate
  • serotonin
  • GABA
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20
Q

Which neurotransmitters are involved in Parkinson’s?

A
  • not enough dopamine
  • acetylcholine
  • serotonin
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21
Q

Which neurotransmitters are classified as monoamines?

A
  • Dopamine (DA)
  • Norepinephrine (NE)
  • Serotonin (5-HT)
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22
Q

Which neurotransmitters are classified as catecholamines?

A
  • Dopamine (DA)
  • Norepinephrine (NE)
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23
Q

What is a common precursor of all catecholamines?

A
  • Tyrosine (amino acid)
  • Serves as the starting point in the biosynthesis of catecholamines such as dopamine, norepinephrine, epinephrine
  • All catecholamines are synthesized from tyrosine
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24
Q

How is dopamine synthesized

A

tyrosine, L-DOPA, dopamine

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25
Q

How is norepinephrine synthesized?

A

tyrosine, L-DOPA, dopamine, norepinephrine, (epinephrine)

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26
Q

How is serotonin synthesized?

A

tryptophan, 5-HTP, serotonin (5-HT)

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27
Q

How is GABA synthesized?

A

glutamine, glutamate, GABA

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28
Q

How is glutamate synthesized?

A

glutamine, glutamate

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29
Q

How is acetylcholine synthesized?

A

choline, acetyl-CoA, acetylcholine

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30
Q

vMAT

A
  • vesicular monoamine transporter
  • packages monoamines and puts them into the synaptic vesicle for release during neuronal signaling
  • NT involved: DA, NE, 5-HT (monoamines)
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31
Q

vGLUT

A
  • vesicular glutamate transporter
  • packages glutamate and puts them into synaptic vesicles for release during
  • NT involved: glutamate
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32
Q

vChAT or vAChT

A
  • vesicular acetylcholine transporter
  • packages glutamate and puts it into synaptic vesicles for release during neuronal signaling
  • NT involved: acetylcholine
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33
Q

vGAT

A
  • vesicular GABA transporter
  • packages GABA and puts it into synaptic vesicles for release during neuronal signaling
  • NT involved: GABA
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34
Q

DAT

A
  • dopamine transporter
  • located on presynaptic neuron
  • regulates levels of dopamine in the synapse
  • transports excess dopamine back into the presynaptic neuron (reuptake)
    NT involved: dopamine
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35
Q

SERT

A
  • serotonin transporter
  • located on the presynaptic neuron
  • regulates levels of serotonin in the synapse
  • transports excess serotonin back into the presynaptic neuron (reuptake)
    NT involved: serotonin
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36
Q

NET

A
  • norepinephrine transporter
  • located on the presynaptic neuron
  • regulates the levels of norepinephrine in the synapse
  • transports excess norepinephrine back into the presynaptic neuron (reuptake)
    NT involved: norepinephrine
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37
Q

CHT

A
  • choline transporter
  • located on the presynaptic neuron
  • regulates the levels of choline in the synapse
  • transports excess choline back into the presynaptic neuron (reuptake)
  • NT involved: norepinephrine
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38
Q

EAAT

A
  • excitatory amino acid transporter
  • located on the presynaptic neuron
  • regulates the levels of excitatory neurotransmitters (glutamate) in the synaptic cleft
  • transports excess glutamate back into the presynaptic neuron (reuptake)
    NT involved: glutamate
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39
Q

GAT

A
  • GABA transporter
  • located on the presynaptic neuron
  • regulates the levels of GABA in the synapse
  • transports excess GABA back into the presynaptic neuron (reuptake)
    NT involved: GABA
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40
Q

ionotropic receptors

A
  • receptor protein that includes and ion channel that is opened when the receptor is bound by a neurotransmitter molecule
  • typically ligand-gated ion channels though which ions pass in response to a neurotransmitter
  • 4 or 5 subunits that assemble in the cell membrane
  • contain an intrinsic ion channel that opens in response to NT or drug binding
  • not coupled to second messengers
  • fast
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41
Q

metabotropic receptors

A
  • receptor protein that DOES NOT contain an ion channel, but when activated uses a second-messenger system to alter the functioning of the postsynaptic cell
  • requires G proteins and second messengers to indirectly modulate ionic activity in neuron
  • 1 subunit
  • activate G proteins in response to NT or drug binding
  • coupled to second-messengers
  • slower
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42
Q

Where is cerebrospinal fluid made?

A

Lateral ventricles

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43
Q

DA receptors

A

D1-D5 (metabotopic)

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44
Q

5-HT receptors

A

5-HT1-7 (metabotropic except 5-HT3)

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45
Q

GABA receptors

A

GABA a (ionotropic), GABA b (metabotropic)

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46
Q

Anandamide receptors

A

CB1 and CB2 (metabotropic)

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47
Q

NE receptors

A

NE alpha (-), beta (+) (metabotropic)

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48
Q

Ach receptors

A

nACh (ionotropic), mACh (metabotropic)

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49
Q

Glutamate receptors

A

AMPA, NMDA, kainate (ionotropic), mGLU

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50
Q

Mechanism of action for alcohol

A
  1. activates GABAa receptors
  2. inhibits glutamate neurotransmission
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51
Q

Mechanism of action for morphine

A
  1. inhibits GABA release
  2. disinhibition of dopamine
52
Q

Mechanism of action for cocaine

A
  1. blocks dopamine reuptake
    (DAT, SERT, NET blocker)
53
Q

Mechanism of action for methamphetamine

A
  1. inhibits dopamine, norepinephrine, and serotonin reuptake
54
Q

Mechanism of action for LSD

A
  1. acts as partial agonist and activates/binds to serotonin receptors
55
Q

Mechanism of action for psilocybin

A
  1. acts as partial agonist and activates/binds to serotonin receptors
56
Q

2 factors that contributed to the opioid epidemic

A
  1. overprescribing of opioid pain medication
  2. aggressive marketing and false advertising by pharmaceutical companies
57
Q

How is cocaine made? Where does it come from?

A

extracted from the coca plant

58
Q

What illicit drugs used to be legal in the US and what were they prescribed/used for?

A
  1. cocaine: used for pain management, local anesthetic, asthma, nasal decongestant
  2. heroin: used as a cough suppressant, pain management, general anesthetic
  3. marijuana: used for nausea relief, pain management, sedative, recreational use
59
Q

Explain how neurons communicate in detail

A
  1. action potential:
    - electrical potential difference across the plasma membrane of excitable cells such as neurons, muscle cells, and some endocrine cells
  2. runs down the length of the dendrite and then is propagated down the length of the axon in order to get to the presynaptic terminal
    - always leads to depolarization of membrane
    - large amplitude
    - refractory period
    - summation is not possible
    - triggered by membrane depolarization to threshold
  3. synaptic transmission:
    - synaptic transmission is the potential difference across the postsynaptic membrane of a neuron
    - occurs across the postsynaptic membrane
    - small amplitude
    - no refractory period
    - can be summed across time and space
    - triggered by neurotransmitters
60
Q

name 10 ways drugs affect synaptic neurotransmission

A
  1. drug serves as NT precursor
  2. drug inhibits NT synthesis
  3. drug prevents storage of NT in vesicles
  4. drug stimulates release of NT
  5. drug inhibits release of NT
  6. drug stimulates postsynaptic receptors
  7. drug blocks postsynaptic receptors
  8. drug stimulates autoreceptors; inhibits release of NT
  9. drug blocks autoreceptors; increases release of NT
  10. drug inhibits NT degradation
  11. drug blocks reuptake
61
Q

Where are the cell bodies of DA located?

A
  • substantia nigra
  • ventral tegmental area (VTA)
62
Q

Where are the cell bodies of 5-HT located

A
  • rostral pons
  • upper medulla oblongata
63
Q

Where are the cell bodies of Ach located

A
  • basal forebrain
  • medial septal nucleus
  • dorsal motor nucleus of the vagus (DMNV)
  • preganglionic autonomic neurons
  • somatic motor neurons
  • peripheral ganglia
  • enteric nervous system
64
Q

Where are the cell bodies of NE located

A
  • pons
65
Q

Name DA pathways, where they originate, and where the neurons project

A
  1. mesolimbic pathway (reward pathway)
    - origin: cell bodies of dopaminergic neurons in the mesolimbic pathway primarily located in the VTA (midbrain)
    - projection: limbic system- reward, motivation, addiction
  2. mesocortical pathway (prefrontal cortex pathway)
    - origin: dopaminergic neurons in the mesocortical pathway also originate in the VTA
    -projection: prefrontal cortex and other cortical areas- executive functions, decision making, memory
  3. nigrostriatal pathway:
    - origin: substantia nigra
    - projection: striatum- motor control and coordination
  4. tuberinfundibular pathway:
    - origin: hypothalamus
    - projection: pituitary gland- regulates hormone levels
66
Q

why are d3 receptors excellent for anti-addiction drugs?

A

D3 receptors are receptors for dopamine, if you block them you can reduce cravings and relapse

66
Q

what are 3 major problems with d3 antagonists?

A
  1. side effects
  2. cause motor impairment
  3. increase blood pressure
67
Q

why is cocaine an indirect DA agonist?

A
  • cocaine increases dopamine in the brain by blocking reuptake (inhibits DAT)
    (it does not directly bind to dopamine receptors to activate them like an agonist would)
68
Q

partial agonist

A

-high binding affinity, low activation
- binds to a receptor and activates it, but produces a submaximal response compared to a full agonist

69
Q

direct agonist

A

mimics the effect of the NT

70
Q

indirect agonist

A

inhibits NT reuptake

71
Q

inverse agonist

A

produces the opposite effect as agonist (naloxone)

72
Q

competitive (direct) antagonist

A

prevents neurotransmitter from binding

73
Q

noncompetitive (indirect) antagonist

A

binds to allosteric site, interferes with neurotransmission

74
Q

why are people more likely to overdose from fentanyl than morphine

A

fentanyl is highly potent and causes respiratory depression (affects the medulla)

75
Q

why do women get intoxicated faster than men?

A
  1. women have higher body fat an lower water than men of the same weight and alcohol is water soluble and not fat soluble (more concentrated in women’s blood stream)
  2. women have lower levels of alcohol dehydrogenase (ADH)- slows down rate at which alocohol is broken down and eliminated from the body
  3. hormone differences
  4. body size and weight
76
Q

what is wernicke’s encephalopathy?

A
  • neurological disorder caused by thiamine (vitamin B) deficiency in the brain
  • often associated with chronic alcoholism
  • causes: thiamine deficiency; can result from chronic alcoholism, inadequate dietary intake, malabsorption disorders, or other medical conditions
  • symptoms: mental confusion, ocular abnormalities, lack of muscle coordination, difficulties with fine motor skills
  • if left untreated, can progress to korsakoff’s syndrome
77
Q

korsakoff’s syndrome

A
  • long term consequence of untreated wernicke’s encephalopathy
  • chronic and debilitating neurological disorder that primarily affects memory and cognitive function
  • causes: thiamine deficiency; alcohol interferes with thiamine absorption and utilization leading do deficiency that can result in brain damage
  • symptoms: severe memory impairment, confabulation, executive functioning deficits, personality changes, lack of insight, eye muscle weakness, lack of muscle coordination
78
Q

what is fetal alcohol syndrome? what causes it? symptoms?

A
  • happens when a person consumes alcohol during pregnancy
  • symptoms:
    1. facial deformities
    2. heart defects
    3. stunted growth
    4. brain damage and cognitive impairments
    5. health problems (kidney failure, heart defects, skeletal abnormalities)
79
Q

Which drug produces nodding off?

A

opioids

80
Q

Which drug produces teeth grinding?

A

(meth)amphetamines

81
Q

Which drug produces decreased respiratory function?

A

opioids

82
Q

Which drug produces enhanced sexual drive?

A

ecstasy, ketamine

83
Q

Which drug produces hallucinations?

A

LSD, psilocybin, ketamine, scopolamine, cocaine

84
Q

Which drug is a local anesthesia?

A

fentanyl, cocaine

85
Q

Which drug produces pupil constriction?

A

opioids

86
Q

Which drug produces pupil dilation?

A

marijuana, cocaine, (meth)amphetamine

87
Q

how are endocannabinoids, such as anandamide and 2-AG, different from traditional neurotransmitters?

A
  • endocannabinoids are not stored in vesicles like traditional neurotransmitters
  • they are synthesized on-demand in the postsynaptic neuron in response to certain stimuli
  • once synthesized, they are released and act as retrograde messengers (they travel back across the synapse to modulate neurotransmission)
88
Q

why are marijuana edibles often sold as baked good full of butter/shortening/ vegetable oil?

A

THC is fat soluble

89
Q

what is fake weed? how is it different from natural marijuana?

A
  • synthetic marijuana is much more potent
  • chemical composition is different, produces a much greater high
  • increase risk of anxiety/panic attack and death
90
Q

through which mechanism does cannabis work and how does it increase firing of mesolimbic DA neurons

A
  • high binding affinity (THC fits perfectly into CB1 receptors and yet cannot produce the same effect as a full agonist)
91
Q

what is a function of dendrites?

A

dendrites receive signal from the axon of another cell/neuron

92
Q

where are dendrites located

A
  • end of a neuron
93
Q

do dendrites have receptor sites?

A
  • receptors are located on the dendrites where neurotransmitter bonds
94
Q

dendrites and neuroplasticity

A
  • go under plastic changes
  • long term potentiation: reduction in efficacy of synapses that last for hours or longer
  • long-term depression: strengthening of neuronal synapses based on recent patterns of activity
95
Q

what is neuroplasticity?

A
  • the ability of neural networks in the brain to change through growth and reorganization
  • experience based changes in the function of neurons
96
Q

what is the difference between neurons with myelinated vs unmyelinated axons?

A

myelinated axon:
- has myelin sheath and nodes of ranvier
- faster conduction (sheath insulates and electrically isolates segments of the axon which speeds up transmission)
- energy efficiency (reduces the amount of energy required to maintain the resting potential and propagate action potentials)
- faster saltatory conduction (nodes of ranvier)
- found in larger neurons

unmyelinated axon:
- lack of myelin
- slower conduction
- higher energy requirements
- found in smaller neurons

97
Q

what are vesicles?

A

membrane bounds sacs or small organelles found within cells

98
Q

where are vesicles located?

A

throughout the cell, functions are diverse and specialized

99
Q

what is the function of vesicles?

A

play essential roles in various cellular processes by serving as transport carriers, storage for organelles, and sites for specific biochemical reactions.

100
Q

what is the function of schwann cells? where are they located?

A
  • glia cell found in the PNS
  • create myelin sheath, attacks multiple axons (oligodendrocyte)
101
Q

which structures are a part of the basal ganglia?

A

basal ganglia: motor processing
- striatum (caudate nucleus, putamen)
- globus pallidus
- subthalamic nucleus
- substantia nigra

102
Q

what structures are a part of the mesolimbic system?

A

mesolimbic system: emotions, motivation, learning, memory, decision making, planning, addiction
- ventral tegmental area (VTA)
- hippocampus
- amygdala
- septal nuclei
- olfactory bulb
- prefrontal cortex

103
Q

what structures are a part of the brain stem?

A
  • midbrain
  • medulla
  • pons
104
Q

angiography

A

x-ray of head with dye present in cerebral blood vessels
- useful to diagnose vascular diseases

105
Q

computerized axial tomography (CAT/CT)

A

a measure of x-ray absorption at several positions around the head
- maps tissue density
- useful to study structures
- measures growth abnormalities/ tumors but cannot see small detail structures
- only takes horizontal images

106
Q

magnetic resonance imaging (MRI)

A

produces high-resolution images using magnetic energy
- useful to study structures

107
Q

diffusion tensor imaging (DTI)

A

alternative application of MRI that exploits fractional anisotropy– the diffusion of water in axons– to visualize axonal connections between regions

108
Q

electroencephalogram (EEG)

A

test that measures electrical activity in the brain using small metal discs (electrodes) attached to the scalp
- need an experienced scientist to interpret brain waves

109
Q

positron emission tomography (PET)

A

uses a radioactive tracer to produce images of brain activity; identifies brain regions that contribute to specific functions

110
Q

functional magnetic resonance imaging (fMRI)

A

detects small changes in brain metabolism, such as oxygen use, in active brain areas

111
Q

transcranial magnetic stimulation (TMS)

A
  • induces a strong localized magnetic field that triggers a weak current in the brain
  • can excite or inhibit neuronal activity
112
Q

what are the divisions of the PNS?

A

autonomic: involuntary (controls self-regulated action of internal organs/glands)
- sympathetic nervous system (arousal): fight or flight response system
- parasympathetic nervous system (calming): rest and digest system, shuts everything down

somatic:
- sensory input
- motor output (controls skeletal muscles)

113
Q

which division of the PNS is highly activated during anxiety?

A
  • sympathetic nervous system
  • increased heart rate and blood pressure
114
Q

which division of the PNS is suppressed by opiates?

A
  • sympathetic nervous system
  • slowed heart rate, lowered blood pressure, decreased alertness
115
Q

which division of the PNS is stimulated by psychostimulants?

A
  • sympathetic nervous system: increased heart rate and blood pressure, dilated pupils, increased alertness, increased sweating
116
Q

which NT systems are implicated in depression?

A

a depletion of the NTs serotonin, norepinephrine, and dopamine in the CNS

117
Q

what type of medications are prescribed for depression? mechanisms of action? side effects?

A
  1. selective serotonin reuptake inhibitors (SSRI)
    - side effects: nausea, insomnia, sexual dysfunction, serotonin syndrome (diarrhea, sweat, chills, tremors, muscle spasms)
    - mechanism of action: affects the transporters, inhibits reuptake of serotonin
  2. serotonin and norepinephrine reuptake inhibitors (SNRI)
    - side effects: nausea, drowsiness, fatigue, constipation
    - mechanism of action: affects transporters, inhibits reuptake of serotonin and norepinephrine
  3. classic tricyclics (TCAs)
    - side effects: constipation, dry mouth, blurry vission, irregular heartbeat, hypotension, arrythmia; fatigue, sedation
    - mechanism of action: blocks norepinephrine and serotonin reuptake AND also an antihistamine (anti-HAM)
  4. monoamine oxidase inhibitors (MAOIs)
    - side effects: nausea, dizziness, restlessness, weight gain, reduced libido
    - mechanism of action: prevents monamines from breaking down, inhibits the activity of monoamine oxidase enzymes
    - SEVERE REACTIONS WITH FOODS HIGH IN TYRAMINE
118
Q

what other major CNS disorders can be treated with antidepressants and why?

A
  • anxiety and eating disorders
  • both usually mean there is a low level of tryptophan/serotonin and antidepressants increase levels of serotonin
119
Q

what classes of antidepressant drugs does not work in part by blocking the reuptake of serotonin?

A
  1. tricyclic antidepressants (TCAS)
    - blocks reuptake of serotonin and norepinephrine (and also acetylcholine?) but is also an antihistamine
  2. monoamine oxidase inhibitors (MAOIs)
    - inhibits action of monamine oxidase that breaks down monamines

(snri if only talking about serotonin)

120
Q

if a person is lacking tryptophan in their diet, what psychological disorder are they at risk for?

A
  • anxiety
  • depression
121
Q

what is cannabidioil?

A

CBD- compound found in marijuana
- doesn’t get people high
- hemp consists of lots of CBD
- medical benefits

122
Q

which drugs produce analgesia?

A

fentanyl and morphine
- analgesia is the inability to feel pain

123
Q

which drug is used to reverse opioid overdose?

A

naloxone (narcan)
- inverse agonist and produces the opposite effect as agonists

124
Q

which drugs are used to treat opioid addiction and how are they different?

A
  1. methadone
    - most effective (abstinence rate goes from 12 to 18%)
    - must be supervised
    - reduces cravings
  2. buprenorphine
    - longer duration, 1-3x a week
    - reduces cravings and withdrawal
  3. naltrexone
    - long lasting
    - doesn’t eliminate cravings
    - better for highly motivated people
    - poor compliance
    - causes dysphoria
125
Q

date rape drugs:

A
  • scopolamine
  • rohypnol (benzo)
126
Q

how does ketamine, scopolamine, and psilocybin work? which is used during surgery? prescribed for depression? was used in the mk ultra program?

A

ketamine: indirect noncompetitive antagonist
- dissociative anesthetic used for clinical depression

LSD: used in mk ultra program

scopolamine: mACh antagonist
- causes powerful hallucinations

psilocybin: psychedelic drug
- rapidly dephosphorylated in the body psilocin, an agonist for serotonin receptors

Biopsychology (2 decks)

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