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143 Cards in this Set

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Biological Psychology
study of the physiological, evolutionary, and developmental mechanisms of behavior and experience
Aristotle's Four Kinds of Causality
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
Functions of Psychology
1. Describe behavior
2. Predict behavior
3. Explain behavior (cause and effect)
4. Explain the mechanisms of behavior (how cause and effect works)
Dualism of Behavior (Cartesian)
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
Reflex
mechanism by which a specific stilmulus elicits a specific response
Dualism of Being (Cartesian)
Mind: not physical, not subject to laws of physics
Body: physical, subject to laws, predictable
Cartesian Dualism: Content of Mind
Images: representations of stimuli, acquired
Ideas: universal thoughts, innate
Monism of Being
Materialism: mind and body both physical
Mentalism: mind and body both mental
Identity: mind and body are each both physical and mental
Monism of Behavior?
all behaviors are thus both mental and physical, as are all experiences of the world
Nervism
all physiological functions are governed by the nervous system
Gene
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
Chromosome
strand of DNA and associated proteins in the nucleus of eukaryotic cells that carries the genes and functions in the transmission of hereditary information
Sex-linked Genes
genes that are on sex chromosomes; secondary sex characteristics, as well as others such as color vision
Sex-limited Genes
genes located on other chromosomes but whose influence is determined by the sex of the individual
Evolution
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
Mutation
change within the DNA sequence of an individual gene
Recombination
reassortment of genes along or between chromosomes; results in genetic combinations not present in the parent
Heredity
genetic transmission of characteristics from parents to offspring
Heritability
estimate of how much variance in some characteristic is due to variance in heredity; is a value for the characteristic
Fitness
number of copies of an individual's genes that endure in later generations
Gene
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
Chromosome
strand of DNA and associated proteins in the nucleus of eukaryotic cells that carries the genes and functions in the transmission of hereditary information
Sex-linked Genes
genes that are on sex chromosomes; secondary sex characteristics, as well as others such as color vision
Sex-limited Genes
genes located on other chromosomes but whose influence is determined by the sex of the individual
Evolution
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
Mutation
change within the DNA sequence of an individual gene
Recombination
reassortment of genes along or between chromosomes; results in genetic combinations not present in the parent
Heredity
genetic transmission of characteristics from parents to offspring
Heritability
estimate of how much variance in some characteristic is due to variance in heredity; is a value for the characteristic
Fitness
number of copies of an individual's genes that endure in later generations; determined by genetic variation and natural selection
General Process Approach
assumption that all diverse behavioral/physiological phenomena are products of more fundamental mechanisms (general processes); this is the only scientific justification for animal research
Neuron Doctrine
hypothesis that the brain is composed of separate cells that are distinct structurally, functionally, and metabolically
Neuron
cell that receives information and transmits it to other cells
Glia
cells of the nervous system that do not transmit information but perform other supportive functions
Motor Neurons
send information to musculature; aka projection neurons
Sensory Neurons
send information from sensory receptors to the brain; aka projection neurons
Interneurons
neurons that lie within a particular structure and do not send information to another structure
Soma/Cell Body
contains nucleus and other organelles
Dendrites
INPUT of the cell, receives information form other cells
Axon
sends information from the cell body down to the presynaptic terminals
Presynaptic Terminals
OUTPUT of the cell, translates the information into a chemical signal for transmission to other cells
Plasma Membrane
separates the inside of the cell from the outside; sandwich of phospholipids
Astrocytes
glia that clean up dead neurons and help to synchronize neurons by taking up and releasing neurotransmitter metabolites
Microglia
glia that clean up waste materials, fungi, viruses
Oligodendrocytes
glia that build up myelin coverings around axons in the CNS
Schwann Cells
glia that build myelin coverings around axons in the PNS
Radial Glia
glia that guide neurons during development
Central Nervous System (CNS)
inside the cranium or spinal column
Peripheral Nervous System (PNS)
outside the cranium and spinal column
Blood-Brain Barrier (BBB)
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
Advantages of BBB
1. brain is protected from toxins coursing through the vasculature
2. immune cells cannot get in to attack and kill neurons
Disadvantages of BBB
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
Electric Potential
difference in electrical charge across a barrier
Resting Potential
electrical difference between the inside and outside of the cell when it is at rest; average is -70mV for neurons
Action Potential
electrical difference between the inside and outside of the cell when it is active
Graded Potential
electrical difference between the inside and outside of the cell when it has received a chemical signal but is not in an active state
Sources for Potentials of the Nervous System
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
Concentraion Gradient
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
Electrochemical Potential or Gradient
for each ion species, both electrical and chemical forces act together to produce this
Na+
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
K+
more conflicted than Na because:
1. inside negativity attracts
2. outside has less K
Action Potential
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)
Threshold
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
Local Anesthetics
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)
General Anesthetics
work by opening K channels wider than usual which prevents the action potential by keeping the membrane potential more negative
Absolute Refractory Period
immediately after action potential, no amount of stimulation will cause another because Na channels are still inactive; prevents backfiring
Relative Refractory Period
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
Two Factors that Control "Direction" of Action Potential
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
Ways Myelin Insulation Helps to Speed Up Action Potential
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
Chemical Synapse
when the AP reaches the presynaptic terminal, the cell releases a chemical NT that carries the signal to other cells
K+
more conflicted than Na because:
1. inside negativity attracts
2. outside has less K
Action Potential
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)
Threshold
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
Local Anesthetics
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)
General Anesthetics
work by opening K channels wider than usual which prevents the action potential by keeping the membrane potential more negative
Absolute Refractory Period
immediately after action potential, no amount of stimulation will cause another because Na channels are still inactive; prevents backfiring
Relative Refractory Period
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
Two Factors that Control "Direction" of Action Potential
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
Ways Myelin Insulation Helps to Speed Up Action Potential
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
Chemical Synapse
when the AP reaches the presynaptic terminal, the cell releases a chemical NT that carries the signal to other cells
Electrical Synapse
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
Local Neurons
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)
Synapse
gap between two neurons
Presynaptic Neuron
neuron that delivers the synaptic transmission
Postsynaptic Neuron
neuron that receives the message
Why is conduction in a reflex arc slower than the sum of conductions along each component axon?
1. translation of the electrical to chemical signal
2. time it takes for chemical to diffuse across synapse and activate next cell
EPSP (Excitatory Postsynaptic Potential)
graded depolarization; typically produced by receptors that allow Na to enter the postsynaptic cell
IPSP (Inhibitory Postsynaptic Potential)
graded hyperpolarization; typically produced by receptors that either allow K to leave the cell or allow Cl to enter the cell
Spatial Summation
if a cell receives inputs from two different locations, the inputs can sum to produce a response
Temporal Summation
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
Disinhibition
process by which one neuron "excites" another by inhibiting the neuron that typically inhibits it, thus allowing it to be excited
Steps of Chemical Communication
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
Categories of NTs
1. amino acids
2. peptides
3. acetylcholine
4. monoamines
5. purines
6. gases
Amino Acids (AAs)
acid molecules that contain an amine group; ex. GABA and glutamate
Glutamate
AA that is major excitatory NT in brain; opens Na channel
GABA
AA that is major inhibitory NT in brain; opens Cl channel
Peptides
chains of AAs; ex. endorphins
Acetylcholine
similar to AA, but has a different terminal group (acetyl) instead of amine; involved in reward circuitry, learning, and memory
Monoamines
contain the amine group but are not acidic; ex. catecholamines such as epinephrine, norepinephrine, and dopamine, and indoleamines such as serotonin and melatonin
Dopamine
monoamine very important for motor control; implicated in schizophrenia
Norepinephrine
very widespread distribution; implicated in many different processes
Serotonin
implicated in depression
Purines
adenosine and its derivatives;
adenosine is very tiny, largely inhibitory, and increased levels signal increased tiredness
Gases
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
Receptors
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
Ionotropic Effects
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
Metabotropic Effects
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
Possible Metabotropic Effects
changes in the structure/function of proteins:
1. enzymes
2. cytoskeletal proteins
3. vesicular proteins
4. receptors
5. gene regulatory proteins
Acetylcholinesterase
breaks acetylcholine up into choline, which diffuses back into the presynaptic cell, and acetate, which is sucked up by glia
Monoamine Recycling
taken up without any breakdown by active transport by an monoamine pump
Agonists
drugs that mimic or enhance the effects of endogenous NTs
Antagonists
drugs that block the effects of endogenous NTs
Inverse Agonists
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
Affinity
how well a drug binds to a particular type of receptor
Efficacy
how well a drug activates a particular receptor type
Common Mechanism of Drugs of Abuse
(The Dopamine Hypothesis)
all increase levels of dopamine in the synapses of the nucleus accumbens, as do natural rewards
Group that Depresses CNS and Behavior
1. Alcohol
2. Barbiturates
3. Non-barbiturate hypnotics
4. Anxiolytics
Additive Effects
of alcohol and barbiturates; really mutiplicative or factorial
Cross Tolerance
if tolerant to one, will have some tolerance to other
Alcohol
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
Marijuana
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
Amphetamine
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
Cocaine
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
Other Stimulants
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
Opiates
exogenous molecules that are alkaloids found in the opium poppy
Opioids
compounds with opiate-like actions including opiates, morphine, heroin, endorphins, etc.
Opiates (effects)
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
Opiate Addiction
very severe withdrawl symptoms, and withdrawl symptoms are guaranteed to include enhanced pain perception; very immune to treatment
Opponent Process Theory
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
Ventricular Zone (VZ)
cells that line the wall of the neural tube; place that produces neurons, which will travel along radial glia to their cortical destinations
Symmetric Division
formation of progenitors in VZ; exponential development of cells
Assymetric Division
formation of neurons; 1 neuron and 1 identical stem cell
Neocortical Expansion (Rakic)
mutation of regulatory genes is responsible for an expanded mature cortical sheet without an expansion in the number of neurons per column
Radial Unit Hypothesis (Rakic)
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
Evolutionary Expansion (Rakic)
determinant of cortical sheet size is the number of progenitor cells contributing neurons to the cortex
Two Basic Phases of Cell Proliferation
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
Cortical Reorginization
after injury, areas that lose their input begin to process stimuli that would normally be processed by adjacent cortex
Somatosensory Pathway
Cortex

Thalamus

Medulla
Pons
deafferated zone responded to face stimulation
Three Possible Mechanisms for Reorganization (Plasticity)
1. Sprouting in the thalamus
2. Sprouting in thalamocortical connections
3. Sprouting in cortico-cortical connections
Florence
examined reorganization in macaques with "accidental" injuries using tracers;
found that there were new cortico-cortical connections formed, not new thalamo-cortical connections
Pons 2
in deafferented animals, thalamus showed evidence of reorganization;
thus, type of reorganization depends on type of injury
Phantom Limb Pain
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