Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
Neuroplasticity |
The nervous system's potential for physical or chemical change that enhances its adaptability |
|
Learning |
A change in an organism's behavior as a result of experience |
|
Memory |
The ability to recall or recognize previous experience |
|
Memory Trace |
A mental representation of a previous experience |
|
Pavlovian Conditioning |
Learning procedure whereby a neutral stimulus (such as a tone) comes to elicit a response because of its repeated pairing with some event (such as the delivery of food)
-AKA Classical Conditioning or Respondent Conditioning |
|
Conditioned Stimulus
Unconditioned Stimulus |
CS -In Pavlovian conditioning, an originally neutral stimulus that, after association with an unconditioned stimulus (UCS), triggers a conditioned response
UCS -A stimulus that unconditionally - naturally and automatically - triggers a response |
|
Conditioned Response
Unconditioned Response |
CR In Pavlovian conditioning, the learned response to a formerly neutral conditioned stimulus
UCR In classical conditioning, the unlearned, naturally occurring response to the unconditioned stimulus, such as salivation when food is in the mouth |
|
CS, UCS, CR, UCR
-A tone (__) is associated with a painless puff of air (__) to the participant's eye
-Blinking is normal reaction (__) to a puff of air
-Learning occurs when blinking occurs in response the CS alone (__) |
-A tone (CS) is associated with a painless puff of air (UCS) to the participant's eye
-Blinking is normal reaction (UCR) to a puff of air
-Learning occurs when blinking occurs in response the CS alone (CR) |
|
Fear Conditioning |
Learned association, a conditioned emotional response, between a neutral stimulus an a noxious event such as a shock |
|
Operant Conditioning |
Learning procedure in which the consequences (such as obtaining a reward) of a particular behavior (such as pressing a bar) increase or decrease the probability of the behavior occurring again
Aka Instrumental Conditioning |
|
What are the 2 categories of memory? |
Implicit Memory Unconscious Memory -Subjects can demonstrate knowledge, such as a skill, conditioned response, or recalling events on prompting, but cannot explicitly retrieve the information
Explicit Memory Conscious Memory -Subjects can retrieve an item and indicate that they know that the retrieved item is the correct item |
|
Amnesia
Can they perform an implicit or explicit memory? |
Partial or total loss of memory
They can perform implicit memory tests |
|
Learning Set |
An understanding of how a problem can be solved with a rule that can be applied in many different situations |
|
Declarative Memory VS Procedural Memory |
Declarative Memory Ability to recount what one knows, to detail the time, place, and circumstances of events; often lost in amnesia
Procedural Memory Ability to recall a movement sequence or how to perform some act or behavior |
|
What Makes Explicit and Implicit Memory Different? |
Implicit = Bottom Up or data-driven manner -Information is encoded in the same way it was perceived -PASSIVE ROLE
Explicit = Top Down or conceptually-driven manner -The subject reorganizes the information before it is encoded -ACTIVE ROLE |
|
Priming |
Using a stimulus to sensitize the nervous system to a later presentation of the same or a similar stimulus
-Often used to measure implicit memory |
|
Where is Short-Term and Long-Term Memory processed? |
Short-Term Frontal Lobes
Long Term Temporal Lobes |
|
Martin + Colleagues
Which brain regions activates recalling color and action words? |
Color --> activates a region in the ventral temporal lobe
Action words --> activates a region in the middle temporal gyrus |
|
Episodic Memory |
Autobiographical memory for events pegged to specific place and time contexts |
|
Episodic Amnesia
E.g. Patient K.C |
-Inability to recall any personally experienced events
-Associated with frontal lobe injuries or reduced blood flow to the frontal lobes |
|
Dissociating Memory Circuits
E.g. H.M |
-Suffered severe amnesia -Could not recall anything that had happened after the surgery (no explicit memory)
-Still had implicit memory |
|
Impaired Implicit Memory and Intact Explicit Memory
Patient J.K |
-Developed Parkinson's disease --> damage to basal ganglia |
|
List 7 of the main structures for Explicit Memory |
-Medial Temporal Region (Hippocampus, Amygdala, Entorhinal Cortex, Parahippocampal Cortex, Perirhinal Cortex)
-Frontal Cortex |
|
Parahippocampal Cortex |
Receives connections from parietal cortex; believed to be involved in visuospatial processing |
|
Perirhinal Cortex |
Receives connections from the visual regions of the ventral stream; believed to be involved in visual object memory |
|
Entorhinal Cortex |
Receives projections from Parahippocampal and Perirhinal cortices; integrative function - first area to show cell death in Alzheimer's disease |
|
Visuospatial Memory |
Using visual information to identify an object's location in space |
|
How does the hippocampus correlate to spatial memory? |
Good spatial memories = bigger hippocampi |
|
What are 2 benefits of the neocortex projecting to the entorhinal cortex, at which it projects back to the neocortex? |
1. Signals from the medial temporal regions back to the cortical sensory regions keep the sensory experience alive in the brain: the neural record outlasts the actual experience 2. Pathway back to the neocortex means it is kept apprised of the information being processed in medial temporal regions |
|
All sensory systems project to which part of the brain region? Long term or short term? |
Frontal Lobes (Short Term) |
|
Tracing the Explicit Memory Circuit
Korsakoff's Syndrome |
Permanent loss of the ability to learn new information (anterograde amnesia) and to retrieve old information (retrograde amnesia)
Caused by diencephalic damage from chronic alcoholism or malnutrition that produces a vitamin B1 deficiency |
|
Retrograde Amnesia |
(Old Memories)
Inability to remember events that took place before the onset of amnesia |
|
Anterograde Amnesia |
(New Memories)
Inability to remember events subsequent to a disturbance of the brain |
|
Mishkin + Colleagues
What were the 4 brain structures that they proposed were neural circuit for explicit memory? |
-Temporal Lobe -Frontal Lobe -Medial Thalamus -Basal Forebrain-Activating Systems |
|
How does the hippocampus consolidate new memories? |
In consolidation, or stabilizing a memory trace after learning, memories move from the hippocampus to diffuse regions in the neocortex |
|
Mishkin + Colleagues
What were the 4 brain structures that they proposed were neural circuit for implicit memory? |
-Basal Ganglia -Ventral Thalamus -Substantia Nigra -Premotor Cortex |
|
Why does Mishkin believe that implicit memories are unconscious? |
Because the connections between the basal ganglia and cortex are unidirectional.
-Basal ganglia receives information from the cortex, but does not project back to the cortex -For memories to be conscious, there must be feedback to the cortex. Medial temporal lobe projects back to the cortex, so explicit memories are conscious |
|
Emotional Memory |
Memory for the affective properties of stimuli or events
-Could be implicit or explicit |
|
What is critical for emotional memory?
What if it is damaged? |
Amygdala
-Damage to the amygdala abolishes emotional memory but has little effect on implicit or explicit memory |
|
What are 6 structures that create the circuit for emotional memory? |
-Amygdala -Medial Temporal Cortex -Brainstem -Hypothalamus -Periaquaductal Gray Matter (PAG) -Basal Ganglia |
|
Memory is associated with the change of what? |
The change that takes place at the synapse |
|
Associative Learning |
Linkage of two or more unrelated stimuli to elicit a behavioral response |
|
Long-Term Potentiation (LTP) |
Long-lasting increase in synaptic effectiveness after high frequency stimulation of EPSP
-A part in associative learning |
|
LTP
Explain 3 ways in which EPSP increase in size |
1. More neurotransmitter must be released from the presynaptic membrane 2. Postsynaptic membrane must become more sensitive to the same amount of transmitter 3. Or both changes must take place |
|
Long-Term Depression (LTD) |
Decrease in EPSP size -Neuron becomes less active in response to repeated stimulation -Requires Ca 2+ entry : decrease responsiveness and numbers of AMPA receptors |
|
Does LTP or LTD create or clear memory? |
LTP creates memories, while LTD clears out old memories |
|
LTP
What are the 2 different types of receptors that Glutamate acts on on the postsynaptic membrane? |
AMPA -Normally responds to glutamate
NMDA -Doubly gated channels -Normally blocked by magnesium (Mg 2+) ions |
|
What neural processes underlie the persistent, long-term changes of learning? |
-Ca 2+ enters postsynaptic neuron and activates a second messenger (e.g cyclic AMP) -cAMP alters gene expression in nucleus, which physically alters synapse: Structural changes in the synapse (Dendritic spines) Formation or loss of synapses |
|
Which 4 part of the brain is capable of generating neurons? |
-Olfactory Bulb -Hippocampal Formation -Neocortex (Frontal and Temporal Lobes) |
|
How does learning effect hippocampal volume? |
Memory improvement and structural changes in the hippocampus extend well into adulthood |
|
In an enriched environment, how does it influence the brain? |
-Increases brain weight -More dendrites, astrocytes, blood capillaries, synapses per neuron -Increase mitochondrial volume (greater metabolic activity) |
|
Specific sits in the DNA of neurons involved in specific memories might exist in what way? |
Methylated or Non Methylated States |
|
How does hormone correlate to plasticity? Estrogen, Dendritic, Neocortex, Testosterone |
-High lvl of estrogen = more dendritic spines in the hippocampus -Low lvl of estrogen = more dendritic spines in neocortex, but fewer dendritic spines in the hippocampus -Low lvl of testosterone = more dendritic spines in neocortex |
|
Glucocorticoid |
Release from the adrenal cortex in times of stress
-Steady levels of glucocorticoids = prolong stress (neurotoxic) -Stress can kill hippocampal cells |
|
Nerve Growth Factor (NGF) |
Neurotrophic factor that stimulates neurons to grow dendrites and synapses and, in some cases, promotes the survival of neurons |
|
Brain-Derived Neurotrophic Factor (BDNF) |
-May enhance plastic changes, such as the growth of dendrities and synapses -Increases when animals learn to solve problems |
|
Sensitization |
An increased number of receptors, synapses, and dendrites |
|
Behavioral Sensitzation |
Escalating behavioral response to the repeated administration of a psychomotor stimulant, such as amphetamine, cocaine, or nicotine
AKA drug-induced behavioral sensitization |
|
Principles of Brain Plasticity (List 7) |
1. Behavioral change reflects change in the brain 2. All nervous systems are plastic in the same general way 3. Plastic changes are age-specific 4. Prenatal events can influence brain plasticity throughout life 5. Plastic changes are brain-region dependent 6. Experience-Dependent Changes Interact (Metaplasticity) 7. Plasticity has Pros and Cons |
|
Traumatic Brain Injury (TBI) |
Damage to the brain that results from a blow to the head |
|
What are the 3 possible ways to recover from brain injury? |
1. Learn new ways to solve problems 2. Reorganize the brain to do more with less 3. Generate new neurons to produce new circuits |
|
Epidermal Growth Factor (EGF) |
Neurotrophic factor that stimulates the subventricular zone to generate cells that migrate into the striatum and eventually differentiate into neurons and glia. |