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FALL 2023 > Bio Psych Exam #1 > Flashcards

Bio Psych Exam #1 Flashcards

1
Q

Biological psychology definition

A

the relationship between the brain and behavior

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2
Q

Molecular neuroscience

A

what is happening in the brain at individual chemical levels (pharmaceuticals, understanding basis of neurological and psychological disorders)

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3
Q

Systems neuroscience

A

how do we see, hear and move → how do these systems come into play

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4
Q

Affective and social neuroscience

A

what is happening in the brain when you are feeling emotions or in social settings

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5
Q

Basic functions of the brain

A

1) Create a sensory reality
2) Integrate information
3) Produce behavior
In → integrate → out

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6
Q

10 principles of the nervous system

A
  1. The nervous system produces movement in a perceptual world that the brain constructs (different brains have different perceptions – color blindedness)
  2. Neuroplasticity is the hallmark of nervous system functioning (learning)
  3. Many brain circuits are crossed (interaction of activation)
  4. The brain is symmetrical and asymmetrical (language and spatial)
  5. Brain systems are organized hierarchically and in parallel
  6. The brain divides sensory input for object recognition and movement
  7. Brain functions are localized and distributed
  8. The nervous system works by juxtaposing excitation and inhibition
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7
Q

Parts of the Central Nervous system

A
  1. Brain
  2. Spinal cord
    **function: controls and mediates behavior
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8
Q

Parts of the Peripheral Nervous system

A
  1. somatic nervous system
  2. autonomic nervous system
  3. enteric nervous system
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9
Q

Somatic nervous system

A

Cranial and spinal nerves

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10
Q

Autonomic nervous system

A

Regulates organs and glands → parasympathetic and sympathetic nervous system

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11
Q

Enteric Nervous system

A

control the gut → highly related to stress

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12
Q

Who is the father of modern neuroscience

A

Santiago Ramon y Cajal:
- pathologist from Spain → first one to look at neurons under a microscope
- When two different brain cells come together, they don’t actually touch → very important

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13
Q

Parts of a neuron

A
  1. dendrites
  2. cell body (soma)
  3. axon
  4. end/terminal buttons
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14
Q

Dendrites

A

look like tree branches
- where we receive information
- Includes dendritic spines: the bumpy part → take in information from other cells and funnels it to the cell body – spines give more surface area so we can have more connections

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15
Q

Cell body of a neuron

A
  • Contains nucleus + other typical cell structures
  • Computation happens here: decides what will happen and sends the signal down the axon to the ends
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16
Q

Axon of a neuron

A
  • Goes from the cell body to the ends
  • Myelinated: coated in myelin (a fat) → insulation
  • Ends are called “terminal buttons”
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17
Q

Synapses

A

the space/gap between neurons
- Includes terminal buttons on one side (end of the axon) and the surface of the dendrite of the adjacent cell on the other side
- Contiguous not continuous

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18
Q

Myelin

A

acts as insulation for the electrical AP
- without myelin, electrical activity would bleed out and not get very far
- in breast/whole milk = helps build this in the brain for babies
- when myelin is degraded it causes multiple sclerosis (MS)

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19
Q

Types of neurons

A
  • all have the same structure but look different
    1) sensory neurons
    2) interneurons
    3) motor neurons
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20
Q

Histology definition

A

Study of tissues under a microscope

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21
Q

Use of histology

A
  • Different ways to stain cells which can show us different things
    1) Nissl staining: shows cell bodies (violet)
    2) Golgi staining: cell bodies and dendrites
    3) Individual neurons with electron microscope → allows us to see synapse
    4) Multi-photon microscope
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22
Q

What do glial cells do (broadly)?

A

The glue: holding everything together and doing the “boring” functions – support, connect, protect

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23
Q

Types of glial cells

A

1) astrocyte: form a barrier that prevents toxic substances from entering the brain (“blood-brain barrier”)

2) Oligodendroglial cell and Schwann cell: form the myelin sheath over the axon
2a) Oligodendroglial / oligodendrocytes: in the central nervous system (CNS)
2b) Schwann cells: in the peripheral nervous system (PNS)

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24
Q

How do neurons talk to each other?

A

electrochemical transmission

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25
Q

oscilloscope

A

tool that looks at the inside of a cell’s electrical potential (intracellular recording)
- measures in millivolts
- put a micro-electrode into the axon and it records changes in membrane potential

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26
Q

What generates the resting membrane potential?

A

Movement of charges ions

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27
Q

What is the resting membrane potential (and why)?

A

-70mV
1) Potassium: on the inside of the cell BUT can leave the cell easily through its many leaky channels → why it is more negative as the anions can not move (always on the inside)
2) Outside: we do have chloride (-) but we have much more sodium (+) (there are sodium leaky channels but not as many as potassium so most Na +remain on the outside)
3) Sodium potassium pump: pumps out three Na+ for two K+ in → net result is -1
**no free diffusion - have a seperation of charge

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28
Q

What is inside of the cell at resting potential

A

1) potassium ions (K+)
2) anions (A-)

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29
Q

What is outside of the cell at resting potential

A

1) sodium ions (Na+)
2) Chloride ions (Cl-)

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30
Q

Methods for ion movement

A

1) membrane channels: specific to certain ions - always open
2) gates: open and close
3) pumps: sodium and potassium pump

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31
Q

What are graded potentials?

A

small voltage fluctuation (1-5 mv change)

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32
Q

Hyperpolarization

A

Even more extreme voltage: inside even more negative, outside becomes even more positive → moves away from 0)

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33
Q

Depolarization

A

Getting closer to equilibrium (0) → (-70 goes to -65 etc.)

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34
Q

Threshold potential for an AP

A

-50mV

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35
Q

Graded potentials and their product

A

Hyperpolarizations and depolarizations fight it out → if the resting membrane potential reaches -50mV, it triggers voltage-activated channels: open and close based on voltage – configuration of the gates change to allow Na+ in and K+ out

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36
Q

What happens when membrane potential reaches the threshold?

A

1) voltage gated channels open: sodium floods the cell (fast) and potassium leaves (slowly) – makes inside of the cell more positive
2) keeps happening until we get to +40mV
3) once we hit a peak (+40mV) sodium channels close and potassium continues to leave the cell until we get back to baseline (-70mV) – this is overshot a bit so it dips below baseline and then comes back

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37
Q

Absolute refractory period

A

no way to trigger another AP → both for depolarization and repolarization
- During the rising (depolarization) and falling phase (repolarizing)

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38
Q

Relative refractory period

A

Can make an AP work (but hard, generally doesn’t happen) → only during hyperpolarization
- during the overshoot phase

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39
Q

How does an action potential move?

A

Saltatory conduction:
-The action potential does not take us from cell A to cell B → takes us down the axon of the same cell
- The Na+ from 1 AP causes some local depolarization of adjacent areas of that membrane → continues to the end
- Node of ranvier: gaps in between the myelin → where the action potentials take place

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40
Q

Can you have half an action potential?

A

all or none → a neuron is either firing or it is not

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41
Q

Can action potentials flow in two ways?

A

NO - always going to go from the cell body, down the axon to the terminal
It’s how we get information down the cell so it can synapse with the next cell and talk to it – based on saltatory conduction

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42
Q

Postsynaptic potentials definition

A

how the action potential starts

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43
Q

Types of Postsynaptic potentials

A

1) Excitatory postsynaptic potentials (EPSPs) → positively charged; causes depolarization

2) Inhibitory postsynaptic potentials (IPSPs) → negatively charged; cause hyperpolarization

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44
Q

Temporal summation

A

Temporal = time
Ex: if 5 EPSP come in at the same time: you get a bonus (amplified)

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45
Q

Spatial Summation

A

Spatial = space
Ex: if 5 EPSP come in all right next to each other, you get another bonus (amplified)

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46
Q

Excitatory neurons

A

More Na+ channels open
Influx of Na+ is depolarization (inside of the cell becomes more positive than it once was) → get an increase in the likelihood of reaching the threshold potential

**EPSP

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47
Q

Inhibitory neurons

A

More K+ channels open (leave inside) or Cl- channels open (go inside)
Causes hyperpolarization: inside of the cell becomes even more negative than it once was

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48
Q

Can neurons be excitatory AND inhibitory?

A

no - usually one or the other

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49
Q

Why do we need the chemical part of electrochemical transmission?

A

If electricity entered the synaptic gap it would diffuse away and not enter the other cell

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50
Q

Presynaptic membrane:

A

encloses molecules that transmits chemical message

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51
Q

Postsynaptic membrane

A

contains receptor molecules that receive chemical messages

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52
Q

Vesicles

A

contain chemicals – neurotransmitters

53
Q

Postsynaptic receptors:

A
  • Neurotransmitter is released from the synaptic vesicle in the presynaptic cell
  • Attaches to the postsynaptic receptors and the process repeats
54
Q

How is a neurotransmitter created?

A
  • Synthesized from precursors (raw materials)
  • Comes from food we eat
  • Large neuropeptides: synthesized in cell body
  • Transported to the axon terminals
55
Q

How are neurotransmitters released?

A

1) packaged into vesicles
2) Along axon terminal, there are voltage-gated calcium (Ca2+) channels → Ca2+ hangs out outside the cell around the axon terminal
3) Axon potential reaches the end (last node / terminal button) → voltage of presynaptic membrane changes → this change opens up calcium channels
4) Calcium floods into the cell rapidly and causes the vesicle to fuse to the presynaptic membrane → leads the neurotransmitters to be released (exocytosis)
5) Neurotransmitter diffuses across the synaptic cleft ultimately binding to a receptor on the postsynaptic cell

56
Q

Types of receptors

A

1) ionotropic receptors
2) metabolic receptors
3) autoreceptors

57
Q

Ionotropic receptors

A
  • Aka ligand-gated ion channels
  • When a neurotransmitter binds to the channel, it changes the channel’s shape and allows ions to transfer through its pore
  • Neurotransmitters never enter the cell → bind to the receptor but don’t go inside
    Job is to open up the channels so the charged ions can go inside
58
Q

Metabotropic Receptors

A

“G-protein coupled receptors”
- SLOWER than ionotropic
- Bundle of G protein on the membrane receptor: when the neurotransmitter binds to the receptor, it activated the G protein
- Parts of the G protein (alpha subunit) breaks off and opens the ion channel

59
Q

Autoreceptors

A

On the presynaptic membrane to regulate the amount of neurotransmitter released → usually causes less neurotransmitters to be released
- Allows for adjustment: if there is too much and it can’t bind to the postsynaptic receptors, it binds to the autoreceptors and signals to the cell to not make so much next time

60
Q

How are neurotransmitters removed from the cell?

A

1) through diffusion
2) enzymatic breakdown
3) reuptake ((back into the presynaptic cell and repurposed)
4) glial cell uptake

61
Q

Electrical Synapses

A

“gap junctions”
- minority in mammals (most chemical synapses)
1) 2 half channels align perfectly to create a pore → ions can directly pass between the two cells
- Synchronizes electrical activity among populations of neurons

62
Q

Pros and Cons of Chemical Synapses

A

Pros: plasticity → foundation of learning and memory (allows us to change)
Cons: slow, requires more energy, requires neurotransmitters (body has to make these)

63
Q

Pros and Cons of Electrical Synapses

A

Pros: fast (tunnel for ions), bidirectional, passive (not a lot of energy required), nothing required (no neurotransmitters needed)
Cons: no mechanisms for plasticity

64
Q

Learning definition

A

relatively persistent or even permanent change in behavior that results from an experience

65
Q

Hebbian learning

A

“neurons that fire together wire together”

-They more that cells fire together their efficiency is increased and they are more likely to trigger each other
-encompasses both habituation and sensitization (non associative learning)
- alters how much Ca2+ is released which alters NT levels which impacts EPSP

** ONLY for chemical synapses (not electrical synapses)

66
Q

Synaptic learning

A

1) Changing to be less common (habituation)
2) Changing to be more common (more likely to fire; sensitization)
3) Changing qualities

67
Q

Habituation

A

Neurons “learned” response weekends with repeated presentations

  • It learned that the response to a stimulus (wearing a shirt) weaken as you continue to wear a shirt
  • Neurons are not dead: they are still able to receive/fire action potentials
    BUT EPSPs get smaller → harder to reach the threshold for an action potential

**form of non associative learning: not pairing it with an outside behavior (NOT any type of conditioning)

68
Q

What causes EPSP to get smaller in habituation?

A
  • Less neurotransmitters are released in the synapse → fewer channels are opened
  • Less NT is released because less Ca2+ entering the cell → thus less binding to vesicles and releasing them → thus less NT released into the synapse and weaker EPSP
69
Q

Sensitization

A

Examples: smells or sounds you despise → these stand out to you more than other smells or sounds
Sensory system is sensitized: you become hyper attuned to certain stimuli
Your sensory system learned such that the response to a stimulus was strengthened with repeated presentations
- Neurons are again not dead → BUT EPSP gets larger this time

70
Q

Why doe EPSP get larger in sensitization?

A
  • NT often bind to metabotropic receptors (g protein coupled receptors)
  • Activated cyclic adenosine monophosphate (cAMP) on the presynaptic side
  • cAMP makes potassium channels less responsive → since K+ can’t leave as much, the depolarization lasts longer →
    AP lasts longer (more time for the calcium channels to remain open)
  • Longer Ca2+ channels open, more NT released, larger EPSP
71
Q

Changing the number of synapses in synaptic learning

A

Well habituated or well sensitizes → we can get longer lasting effects by changing the size of the synapse and how many there are
Ca2+ sends instructions to nuclear DNA that says “start making more synapses, more dendritic spines, larger synapses etc”
cAMP is used to carry these instructions to the DNA (it is the messenger)

**More synapses there are → more likely they are paired together
Less synapses there are → less likely they are paired together and fire together

72
Q

Small molecule Neurotranmitters

A

1) Acetylcholine (ACh)
2) Amines (catecholamines + serotonin)
3) Amino Acids

73
Q

Acetylcholine (ACh)

A
  • Choline: comes from food (prominent in eggs) → converted to ACh through different enzymes
  • broken down by enzymes (acetylcholinesterase (AChE)
  • If we inhibit this enzyme: we have too much ACh in the synapse → muscles contract too much and they exfoliate, you can’t control breathing and you die
  • Present where neurons meet muscles (including heart)
    Important for plasticity and memory
    With ACh: we have muscle contraction
    Without ACh: we get paralysis and problems with memory
74
Q

Types of Catecholamines

A

1) Dopamine (DA)
2) Norepinephrine (NE)
3) Epinephrine (EP)

75
Q

Dopamine (DA)

A
  • Death mechanism: reuptake and enzymatic breakdown (MAO, COMT)
  • If you block the receptor that is an antipsychotic
    If you block the enzyme that breaks it down, dopamine hangs out in the synapse for longer → antidepressants
    Genetic variants in how much of these enzymes naturally exist (especially COMT
76
Q

Norepinephrine

A

Death mechanism: reuptake and enzymatic breakdown (MAO, COMT)
Thought to be involved in sleep and alertness → arousal / fight and flight
If we block it: lowers heart rate → beta blockers (heart medication)
ADHD drugs: influence this

77
Q

Epinephrine (EP)

A

Death mechanism: reuptake and enzymatic breakdown (MAO, COMT)
All fight or flight things

78
Q

Serotonin (5HT)

A
  • Amine but not catecholamine
  • Amines: catecholamines and serotonin
  • Made from L-tryptophan
  • Important for mood, aggression, respiration, appetite
79
Q

Amino Acid Neurotransmitters

A

1) Glutamate
2) GABA

80
Q

Glutamate

A
  • Excitatory
  • Located throughout the brain
  • Important for learning and memory (NMDA and AMPA receptors)
    Death mechanism: glial uptake
    Excitotoxicity: if glutamate keeps firing (triggers EPSP) and can’t shut off, we get cell death
    Related to epilepsy and seizures: longer a seizure lasts, you get cell death via this mechanism
81
Q

GABA

A
  • Inhibitory: receptors are ligand gated Cl-channels
  • Death mechanism: glial uptake
    Used to treat epilepsy and seizures
82
Q

Activating Neurotransmitter Systems

A
  • Pathways of a single neurotransmitter: generally: cell bodies start low and the axons go up and around → have particular pathways they like
  • Cellular organization: Cell bodies are in the brainstem, Axons are distributed
    1) Cholinergic activating system
    2) Dopaminergic activating system
    3) Noradrenergic activating system
    4) Serotonergic system
83
Q

Can neurotransmitters be excitatory AND inhibitory?

A

neurotransmitters CAN act as either excitatory or inhibitory depending on which receptor it binds to
- Dopamine: can be either excitatory or inhibitory depending on the receptor

84
Q

Superior / Dorsal

A

towards the top

85
Q

Inferior / Ventral

A

towards the bottom

86
Q

Anterior

A

towards the front

87
Q

Posterior

A

towards the back

88
Q

Latreal

A

lateral: going left and right –> usually based on the patient so flipped in imaging <—– or —–>
Medial: towards the midline of the body (—–> or <—–)

89
Q

Dimensions (planes)

A

1) coronal plane
2) horizontal/axial plane
3) sagittal place

90
Q

Horizontal / axial plane

A

**cut along the x axis (if looking at the brain from the side) – like lifting the top to see straight down
Can see:
- anterior / posterior (front/back)
- lateral and medial (left and right)

Can not see:
- dorsal (superior) or ventral (inferior)

91
Q

Sagittal Plane

A

** cut down the hemisphere split
Can see:
- Anterior and posterior (front/back)
- Dorsal (superior) and ventral (inferior)
Can not see:
- left/right (lateral)

92
Q

Coronal Plane

A

** cut along the y axis (if the brain is to the side) – like how you would cut an apple
Can see:
- Dorsal and ventral
- lateral/medial (left right)
Can not see:
- anterior/posterior

93
Q

Cerebral cortext

A

The surface of the brain

94
Q

Texture of the cerebral cortext

A

Bumpy:
- Gyrus: party that gyrates out → the bumps
Sulcus: the part the sinks down → the cracks
Allows us to fit more in a small amount of space (think of crumpling a piece of paper

95
Q

Colors of the brain

A

1) Gray matter: anything that is NOT a myelinated axon
- Usually cell bodies → where processing happens

2) White matter: myelinates axons → like a highway (how things travel)

96
Q

Thickness of cerebral cortex

A

Neocortex: “new”
- Has 6 layers
- Most superficial portions of the cerebral cortex
- Each layer has a different type of cell
- Cytoarchitectonic maps: Brodmann areas (early 1900s)

Allocortex: “older”
- 3 or 4 layers (layers decrease as you go further in)
- Inner portions of the brain → not the cortex necessarily

97
Q

Occipital lobe

A

back of the head
function: vision

98
Q

Temporal lobe

A

Sides of the head (where temples are)
Main functions:
- Hearing
- Language
- Memory

99
Q

Parietal lobe

A

Top-ish of the head (where a yamaka goes)
Main functions:
- Somatosensory (how do we feel things)
- Attention
- Spatial information

100
Q

Frontal Lobe

A

Closest to forehead
Main functions:
- Planned motor movements
- Integration
- Decision making
- Executive functions

101
Q

Lateral sulcus

A

separates the temporal lobe from the frontal, occipital and parietal lobe – the one that runs horizontal above the temporal lobe

*aka sylvian fissure

102
Q

Central sulcus

A

Separates the frontal lobe from the parietal lobe
- runs vertical from the top of the brain to the temporal lobe

103
Q

interhemispheric / longitudinal fissure

A

separates the right and left hemispheres

104
Q

Insula

A
  • controversial 5th lobe
  • if you peel back the area between the temporal and frontal lobe (along the lateral sulcus) it is inside here
    Main functions:
  • Emotion
  • integrate ion of emotion and cognition
105
Q

Parts of the Forebrain Telencephalon

A

“end brain”
1) cerebral cortext
2) basal ganglia
3) limbic system

106
Q

Basal ganglia

A

parts: caudate nucleus + petamen + globus pallidus
controls: voluntary movements and reward processing

107
Q

Corpus callosum

A

“tough body”
~200 million heavily myelinated axons
- Joins the right and left hemisphere

108
Q

Limbic System

A

parts:
- cingulate cortex (belt shape)
- amygdala (almond shape)
- hippocampus (seahorse shape) – memory
related to motivated / goal-oriented behaviors

109
Q

Forebrain: diencephalon parts

A

“interbrain”

1) thalamus: collection of nuclei
Relay station → especially for sensorimotor information

2) hypothalamus: controls homeostasis; Links CNS with endocrine system

110
Q

Midbrain

A

*part of the brainstem
mainly: substantia nigra – produces dopamine

111
Q

Hindbrain

A

1) cerebellum
2) pons
3) medulla

112
Q

Cerebellum

A
  • Inferior to the cerebrum
  • Posterior to the brain stem

Main functions:
- Coordinating movement
- Balance

113
Q

Pons

A

deals with sleep, respiration, swallowing

114
Q

Medulla

A

Respiration, heart rate, vomiting, consciousness – manages automatic processes

115
Q

Brain stem parts

A

1) pons
2) medulla
3) midbrain (diencephalon)

116
Q

Meninges

A

three layer protection to the brain and the spinal cord

117
Q

Layers of meninges

A
  1. Dura mater: outermost → scalp and skill
  2. Arachnoid mater: spongier, thinner later – subarachnoid: space that follows into different sulci
  3. Pia mater: very thin, follows folds and grooves
118
Q

Ventricular system

A

set of 4 cavities in the brain (cerebral ventricles) which produces, transports and excretes cerebrospinal fluid (CSF)

119
Q

Why is CSF important?

A
  • CSF is basically saltwater → it is the fluid that surrounds the brain and spinal cord
  • Floats for protection
  • Fluid is created in the brain

Lateral ventricles → filled with fluid, CSF will flow from lateral ventricles into a 3rd and 4th ventricle → some will flow up and around to surround the brain and some will go down to the spinal cord
If too much fluid: needs to be drained

120
Q

Circulatory system

A

1) arteries: carry oxygenated blood and glucose form the heart to the brain → supply brain with blood
2) veins: carry deoxygenated blood, lactic acid from brain to heart

121
Q

Carotid arterial system

A
  1. Inter carotid artery goes up through the neck to the base of the brain
  2. Branches to eyes (ophthalmic branch)
  3. Goes superiorly to middle cerebral artery → lots of lateral parts of the cortex + basal ganglia
  4. Common place for strokes
  5. Goes superiorly to the anterior cerebral artery → supplies denial and superior parts of the frontal lobe and anterior parietal lobe
122
Q

Vertebral arterial system

A
  1. Vertebral artery goes up through the neck to the base of the brain (but more posterior)
  2. Supplies cerebellum and brainstem
  3. Posterior cerebral artery: thalamus + hypothalamus *diencephalon), midbrain, some of the deep medial structures (hippocampus, medial portion of occipital lobe etc)
123
Q

Circle of Willis

A
  • Redundancy of pathways→ if one part fails we have backups (to a certain point)
  • in the inferior surface of the brain
124
Q

Circulatory system takeaways

A
  1. Some regions get more direct blood supply than others
  2. Regions in between territory served by the different cerebral arteries are in some danger
  3. Border zones or watershed regions → prone to stroke
125
Q

What is the threshold potential

A

-55mV

126
Q

Hindbrain parts

A

Pons + medulla + cerebellum

127
Q

Brainstem

A

pons + medulla + midbrain + diencephalon

128
Q
A

FALL 2023 (5 decks)

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