Biopsychology Exam 1

Front 1

Biological Psychology

Back 1

study of the physiological, evolutionary, and developmental mechanisms of behavior and experience

Front 2

Aristotle's Four Kinds of Causality

Back 2

material cause = physiological cause of bx = mechanism
formal cause = topography
efficient cause = evolutionary cause of bx = genetic development
final cause = functional cause of bx = why
also: developmental cause of behavior = maturation of behavior

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Functions of Psychology

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1. Describe behavior
2. Predict behavior
3. Explain behavior (cause and effect)
4. Explain the mechanisms of behavior (how cause and effect works)

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Dualism of Behavior (Cartesian)

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Voluntary behaviors: initiated by the mind, made by choice, and only in humans
Involuntary behaviors: initiated by stimuli, made by reflex, in humans and animals

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Reflex

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mechanism by which a specific stilmulus elicits a specific response

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Dualism of Being (Cartesian)

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Mind: not physical, not subject to laws of physics
Body: physical, subject to laws, predictable

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Cartesian Dualism: Content of Mind

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Images: representations of stimuli, acquired
Ideas: universal thoughts, innate

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Monism of Being

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Materialism: mind and body both physical
Mentalism: mind and body both mental
Identity: mind and body are each both physical and mental

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Monism of Behavior?

Back 9

all behaviors are thus both mental and physical, as are all experiences of the world

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Nervism

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all physiological functions are governed by the nervous system

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Gene

Back 11

unit of heredity that maintains its structural identity from one generation to the next that consists of a sequence of DNA that occupies a specific location on a chromosome and determines a particular characteristic in an organism

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Chromosome

Back 12

strand of DNA and associated proteins in the nucleus of eukaryotic cells that carries the genes and functions in the transmission of hereditary information

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Sex-linked Genes

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genes that are on sex chromosomes; secondary sex characteristics, as well as others such as color vision

Front 14

Sex-limited Genes

Back 14

genes located on other chromosomes but whose influence is determined by the sex of the individual

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Evolution

Back 15

change in the frequencies of genes in a population; can be due to mutation or recombination; does not imply progress or an increase in complexity

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Mutation

Back 16

change within the DNA sequence of an individual gene

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Recombination

Back 17

reassortment of genes along or between chromosomes; results in genetic combinations not present in the parent

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Heredity

Back 18

genetic transmission of characteristics from parents to offspring

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Heritability

Back 19

estimate of how much variance in some characteristic is due to variance in heredity; is a value for the characteristic

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Fitness

Back 20

number of copies of an individual's genes that endure in later generations

Front 21

Gene

Back 21

unit of heredity that maintains its structural identity from one generation to the next that consists of a sequence of DNA that occupies a specific location on a chromosome and determines a particular characteristic in an organism

Front 22

Chromosome

Back 22

strand of DNA and associated proteins in the nucleus of eukaryotic cells that carries the genes and functions in the transmission of hereditary information

Front 23

Sex-linked Genes

Back 23

genes that are on sex chromosomes; secondary sex characteristics, as well as others such as color vision

Front 24

Sex-limited Genes

Back 24

genes located on other chromosomes but whose influence is determined by the sex of the individual

Front 25

Evolution

Back 25

change in the frequencies of genes in a population; can be due to mutation or recombination; does not imply progress or an increase in complexity

Front 26

Mutation

Back 26

change within the DNA sequence of an individual gene

Front 27

Recombination

Back 27

reassortment of genes along or between chromosomes; results in genetic combinations not present in the parent

Front 28

Heredity

Back 28

genetic transmission of characteristics from parents to offspring

Front 29

Heritability

Back 29

estimate of how much variance in some characteristic is due to variance in heredity; is a value for the characteristic

Front 30

Fitness

Back 30

number of copies of an individual's genes that endure in later generations; determined by genetic variation and natural selection

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General Process Approach

Back 31

assumption that all diverse behavioral/physiological phenomena are products of more fundamental mechanisms (general processes); this is the only scientific justification for animal research

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Neuron Doctrine

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hypothesis that the brain is composed of separate cells that are distinct structurally, functionally, and metabolically

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Neuron

Back 33

cell that receives information and transmits it to other cells

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Glia

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cells of the nervous system that do not transmit information but perform other supportive functions

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Motor Neurons

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send information to musculature; aka projection neurons

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Sensory Neurons

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send information from sensory receptors to the brain; aka projection neurons

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Interneurons

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neurons that lie within a particular structure and do not send information to another structure

Front 38

Soma/Cell Body

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contains nucleus and other organelles

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Dendrites

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INPUT of the cell, receives information form other cells

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Axon

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sends information from the cell body down to the presynaptic terminals

Front 41

Presynaptic Terminals

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OUTPUT of the cell, translates the information into a chemical signal for transmission to other cells

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Plasma Membrane

Back 42

separates the inside of the cell from the outside; sandwich of phospholipids

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Astrocytes

Back 43

glia that clean up dead neurons and help to synchronize neurons by taking up and releasing neurotransmitter metabolites

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Microglia

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glia that clean up waste materials, fungi, viruses

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Oligodendrocytes

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glia that build up myelin coverings around axons in the CNS

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Schwann Cells

Back 46

glia that build myelin coverings around axons in the PNS

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Radial Glia

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glia that guide neurons during development

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Central Nervous System (CNS)

Back 48

inside the cranium or spinal column

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Peripheral Nervous System (PNS)

Back 49

outside the cranium and spinal column

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Blood-Brain Barrier (BBB)

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collective term for the various physical/chemical mechanisms that protect the brain from the circulating blood; includes: tightly packed epithelial cells of vasculature and particular transport mechanisms

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Advantages of BBB

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1. brain is protected from toxins coursing through the vasculature
2. immune cells cannot get in to attack and kill neurons

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Disadvantages of BBB

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1. active transport is necessary for getting glucose and other molecules into the brain, so use energy
2. immune system is compromised
3. must use glucose as energy source because other sugars are too large

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Electric Potential

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difference in electrical charge across a barrier

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Resting Potential

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electrical difference between the inside and outside of the cell when it is at rest; average is -70mV for neurons

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Action Potential

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electrical difference between the inside and outside of the cell when it is active

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Graded Potential

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electrical difference between the inside and outside of the cell when it has received a chemical signal but is not in an active state

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Sources for Potentials of the Nervous System

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1. Na/K Pump: protein in the cell membrane that spends 1 ATP to pump 2 K into the cell while 3 Na ions are pumped out
2. K leak: at rest, the membrane is slightly permeable to K, so it tends to leak out
3. Intracellular proteins: tend to be negatively chraged, cause the inside of the cell to be negative with respect to the outside

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Concentraion Gradient

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difference in the particular concentrations of an ion inside and outside the cell; another source of potential energy because of tendency of ions to move from high concentration to low

Front 59

Electrochemical Potential or Gradient

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for each ion species, both electrical and chemical forces act together to produce this

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Na+

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has a strong electrochemical potential driving it into the cell because:
1. inside of the cell is negative
2. much more Na outside than inside

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K+

Back 61

more conflicted than Na because:
1. inside negativity attracts
2. outside has less K

Front 62

Action Potential

Back 62

mechanism that the cell uses to transfer an input signal down its axon so that is can be given to yet another cell; results because inputs from other cells cause changes in the internal voltage of the target cell (depolarize)

Front 63

Threshold

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membrane becomes active at about -40mV; will have an action potential; strength of the action potential is independent of the stimulus that initiates it, once threshold is crossed, it goes full strength

Front 64

Local Anesthetics

Back 64

work by blocking the Na channel which prevents the action potential and keeps signals from being transmitted from sensor neurons up into the brain; blocks other axons indiscriminately (like motor neurons)

Front 65

General Anesthetics

Back 65

work by opening K channels wider than usual which prevents the action potential by keeping the membrane potential more negative

Front 66

Absolute Refractory Period

Back 66

immediately after action potential, no amount of stimulation will cause another because Na channels are still inactive; prevents backfiring

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Relative Refractory Period

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for some additional time, only a very strong stimulus can cause another because Na channels can be opened, but K channels are still open, so hyperpolarized

Front 68

Two Factors that Control "Direction" of Action Potential

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1. soma and dendrites lack voltage-gated Na channels, so AP can't go back into soma
2. once Na gates open at a point in the axon, they can't open again for some time (inactive), so AP can't go back and forth along axon

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Ways Myelin Insulation Helps to Speed Up Action Potential

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1. myelin prevents constant K leak from the axon
2. axons tend to concentrate Na channels in Nodes of Ranvier, increasing the efficiency of regenerating the potential

Front 70

Chemical Synapse

Back 70

when the AP reaches the presynaptic terminal, the cell releases a chemical NT that carries the signal to other cells

Front 71

K+

Back 71

more conflicted than Na because:
1. inside negativity attracts
2. outside has less K

Front 72

Action Potential

Back 72

mechanism that the cell uses to transfer an input signal down its axon so that is can be given to yet another cell; results because inputs from other cells cause changes in the internal voltage of the target cell (depolarize)

Front 73

Threshold

Back 73

membrane becomes active at about -40mV; will have an action potential; strength of the action potential is independent of the stimulus that initiates it, once threshold is crossed, it goes full strength

Front 74

Local Anesthetics

Back 74

work by blocking the Na channel which prevents the action potential and keeps signals from being transmitted from sensor neurons up into the brain; blocks other axons indiscriminately (like motor neurons)

Front 75

General Anesthetics

Back 75

work by opening K channels wider than usual which prevents the action potential by keeping the membrane potential more negative

Front 76

Absolute Refractory Period

Back 76

immediately after action potential, no amount of stimulation will cause another because Na channels are still inactive; prevents backfiring

Front 77

Relative Refractory Period

Back 77

for some additional time, only a very strong stimulus can cause another because Na channels can be opened, but K channels are still open, so hyperpolarized

Front 78

Two Factors that Control "Direction" of Action Potential

Back 78

1. soma and dendrites lack voltage-gated Na channels, so AP can't go back into soma
2. once Na gates open at a point in the axon, they can't open again for some time (inactive), so AP can't go back and forth along axon

Front 79

Ways Myelin Insulation Helps to Speed Up Action Potential

Back 79

1. myelin prevents constant K leak from the axon
2. axons tend to concentrate Na channels in Nodes of Ranvier, increasing the efficiency of regenerating the potential

Front 80

Chemical Synapse

Back 80

when the AP reaches the presynaptic terminal, the cell releases a chemical NT that carries the signal to other cells

Front 81

Electrical Synapse

Back 81

in cells that are packed so tightly that they share ion channels so that when they open up, the electrical potential of one cell is communicated directly to the other; coordinate activity in the superchiasmatic nucleus

Front 82

Local Neurons

Back 82

cells without APs; usually sensory neurons;
can't transmit signals very far and only communicate with cells in the immediate vicinity;
depolarization travels passively, thus the potential is proportional to the input signal (graded potential)

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Synapse

Back 83

gap between two neurons

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Presynaptic Neuron

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neuron that delivers the synaptic transmission

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Postsynaptic Neuron

Back 85

neuron that receives the message

Front 86

Why is conduction in a reflex arc slower than the sum of conductions along each component axon?

Back 86

1. translation of the electrical to chemical signal
2. time it takes for chemical to diffuse across synapse and activate next cell

Front 87

EPSP (Excitatory Postsynaptic Potential)

Back 87

graded depolarization; typically produced by receptors that allow Na to enter the postsynaptic cell

Front 88

IPSP (Inhibitory Postsynaptic Potential)

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graded hyperpolarization; typically produced by receptors that either allow K to leave the cell or allow Cl to enter the cell

Front 89

Spatial Summation

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if a cell receives inputs from two different locations, the inputs can sum to produce a response

Front 90

Temporal Summation

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if a cell receives input from a single other cell, repeated inputs from that cell can sum to produce a response if close enough in time

Front 91

Disinhibition

Back 91

process by which one neuron "excites" another by inhibiting the neuron that typically inhibits it, thus allowing it to be excited

Front 92

Steps of Chemical Communication

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1. neuron synthesizes NTs either in cell body or at presynaptic terminal
2. NTs synthesized in body transported to presynaptic terminal
3. AP causes Ca to enter which helps dock the vesicles to the presynaptic membrane
4. NT diffuses across synapse and attaches to receptors on the postsynaptic cell
5. once receptor is modified, NT is released from binding site
6. presynaptic cell takes up leftovers

Front 93

Categories of NTs

Back 93

1. amino acids
2. peptides
3. acetylcholine
4. monoamines
5. purines
6. gases

Front 94

Amino Acids (AAs)

Back 94

acid molecules that contain an amine group; ex. GABA and glutamate

Front 95

Glutamate

Back 95

AA that is major excitatory NT in brain; opens Na channel

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GABA

Back 96

AA that is major inhibitory NT in brain; opens Cl channel

Front 97

Peptides

Back 97

chains of AAs; ex. endorphins

Front 98

Acetylcholine

Back 98

similar to AA, but has a different terminal group (acetyl) instead of amine; involved in reward circuitry, learning, and memory

Front 99

Monoamines

Back 99

contain the amine group but are not acidic; ex. catecholamines such as epinephrine, norepinephrine, and dopamine, and indoleamines such as serotonin and melatonin

Front 100

Dopamine

Back 100

monoamine very important for motor control; implicated in schizophrenia

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Norepinephrine

Back 101

very widespread distribution; implicated in many different processes

Front 102

Serotonin

Back 102

implicated in depression

Front 103

Purines

Back 103

adenosine and its derivatives;
adenosine is very tiny, largely inhibitory, and increased levels signal increased tiredness

Front 104

Gases

Back 104

NO and others, possibly act as retrograde transmitters;
NO can be produced in the postsynaptic cell, diffuse through membranes, and get into presynaptic cell to send signal to change synapse

Front 105

Receptors

Back 105

the effect of any NT depends entirely on the receptor on the postsynaptic cell;
any given NT may:
1. excite the cell
2. inhibit the cell
3. initiate a complex metabolic reaction inside the cell

Front 106

Ionotropic Effects

Back 106

receptors are attached directly to ion channels; activation of the receptor causes the channel to open and change the potential of the target cell; direct

Front 107

Metabotropic Effects

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receptors are attached to secondary intracellular mechanisms (proteins), often a G-protein which activates another molecule like cAMP that acts as a second messenger to activate any number of metabolic processes; indirect

Front 108

Possible Metabotropic Effects

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changes in the structure/function of proteins:
1. enzymes
2. cytoskeletal proteins
3. vesicular proteins
4. receptors
5. gene regulatory proteins

Front 109

Acetylcholinesterase

Back 109

breaks acetylcholine up into choline, which diffuses back into the presynaptic cell, and acetate, which is sucked up by glia

Front 110

Monoamine Recycling

Back 110

taken up without any breakdown by active transport by an monoamine pump

Front 111

Agonists

Back 111

drugs that mimic or enhance the effects of endogenous NTs

Front 112

Antagonists

Back 112

drugs that block the effects of endogenous NTs

Front 113

Inverse Agonists

Back 113

drugs that bind to a receptor and do the opposite of what normal NTs usually do; usually at synapses where cell has a lot of spontaneous activity

Front 114

Affinity

Back 114

how well a drug binds to a particular type of receptor

Front 115

Efficacy

Back 115

how well a drug activates a particular receptor type

Front 116

Common Mechanism of Drugs of Abuse
(The Dopamine Hypothesis)

Back 116

all increase levels of dopamine in the synapses of the nucleus accumbens, as do natural rewards

Front 117

Group that Depresses CNS and Behavior

Back 117

1. Alcohol
2. Barbiturates
3. Non-barbiturate hypnotics
4. Anxiolytics

Front 118

Additive Effects

Back 118

of alcohol and barbiturates; really mutiplicative or factorial

Front 119

Cross Tolerance

Back 119

if tolerant to one, will have some tolerance to other

Front 120

Alcohol

Back 120

no accepted medical uses;
behavioral effects: disinhibition, sedative effects, stupor, respiratory depression and lethality in high doses
neurochemical effects: facilitates GABA receptors, inhibits Na channels, decreases serotonin activity, increases dopamine activity by disinhibiting release of dopamine in nucleus accumbens

Front 121

Marijuana

Back 121

medical uses: glaucoma, antiemetic, anticonvulsant, enhance appetite, analgesic
behavioral effects: disinhibition, euphoria, perceptual changes, recent memory impairment, and impairment of complex motor tasks
neurochemical effects: activation of endogenous cannabinoid receptors that are G-protein couples metabotropic receptors and are inhibitory; also, disinhibition of cells firing on the nucleus accumbens, thus increasing dopamine release there

Front 122

Amphetamine

Back 122

medical uses: obesity, narcolepsy, attention deficit disorder
psychomotor stimulant effects: arousal, euphoria, and decreased fatigue
autonomic functions: excitatory effects of increasing BP, body temperature, and bronchodilation
neurochemical effects: increases dopamine output and reverses monoamine transporter

Front 123

Cocaine

Back 123

local anesthetics because decrease pain perception by blocking Na channels;
pshychomotor effects: euphoria and irritation
autonomic effects: restricts blood vessels and increases blood pressure
neurochemical effects: increases dopamine output and blocks monoamine transporter

Front 124

Other Stimulants

Back 124

Nicotine: activates Ach receptor on cell that releases dopamine, so releases lots
Caffeine: blocks adenosine at presynaptic receptors; adenosine normally inhibits NT release, so disinhibition, but at cell surface

Front 125

Opiates

Back 125

exogenous molecules that are alkaloids found in the opium poppy

Front 126

Opioids

Back 126

compounds with opiate-like actions including opiates, morphine, heroin, endorphins, etc.

Front 127

Opiates (effects)

Back 127

behavioral effects: inhibit pain transmission, relaxation of mood, euphoria
other effects: nausea, respiratory depression, GI effects, cough suppression, motor effects
long-term: severe withdrawl symptoms, persistent craving despite withdrawl
neurochemical effects: activate endogenous opioid receptors and disinhibit dopamine release

Front 128

Opiate Addiction

Back 128

very severe withdrawl symptoms, and withdrawl symptoms are guaranteed to include enhanced pain perception; very immune to treatment

Front 129

Opponent Process Theory

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Solomon and Corbit; assumption: physiology is homeostatic in nature; emotions/drug reactions produced by external environment are counteracted by the body by an opponent process

Front 130

Ventricular Zone (VZ)

Back 130

cells that line the wall of the neural tube; place that produces neurons, which will travel along radial glia to their cortical destinations

Front 131

Symmetric Division

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formation of progenitors in VZ; exponential development of cells

Front 132

Assymetric Division

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formation of neurons; 1 neuron and 1 identical stem cell

Front 133

Neocortical Expansion (Rakic)

Back 133

mutation of regulatory genes is responsible for an expanded mature cortical sheet without an expansion in the number of neurons per column

Front 134

Radial Unit Hypothesis (Rakic)

Back 134

cortex is composed of a series of columns, each composed of a radial unit (each radial glia directs the formation of one column of cortex);
for any given mature cortical cell, the column location (x and y) is determined by the location of the progenitor within the VZ, while the depth (z) is determined by the birthdate

Front 135

Evolutionary Expansion (Rakic)

Back 135

determinant of cortical sheet size is the number of progenitor cells contributing neurons to the cortex

Front 136

Two Basic Phases of Cell Proliferation

Back 136

1. Symmetric division in the VZ (which increases surface area - an increase of only a few days in this phase could mean an exponential increase in cells)
2. Asymmetric division in the VZ

Front 137

Cortical Reorginization

Back 137

after injury, areas that lose their input begin to process stimuli that would normally be processed by adjacent cortex

Front 138

Somatosensory Pathway

Back 138

Cortex
⬆
Thalamus
⬆
Medulla

Front 139

Pons

Back 139

deafferated zone responded to face stimulation

Front 140

Three Possible Mechanisms for Reorganization (Plasticity)

Back 140

1. Sprouting in the thalamus
2. Sprouting in thalamocortical connections
3. Sprouting in cortico-cortical connections

Front 141

Florence

Back 141

examined reorganization in macaques with "accidental" injuries using tracers;
found that there were new cortico-cortical connections formed, not new thalamo-cortical connections

Front 142

Pons 2

Back 142

in deafferented animals, thalamus showed evidence of reorganization;
thus, type of reorganization depends on type of injury

Front 143

Phantom Limb Pain

Back 143

sensation/pain; perceptually wil feel as if it's still there;
changes in connectivity take some time;
perception and awareness center activated because hand neurons are being activated by face area