Learning And Memory Flashcards
Post-tetanic stimulation
Very short 60sec
brief + high f discharge of NT (60sec)
=increase probability of AP in post-synaptic cell
1. Higher stimulation
2. Ca+2 enters the pre cell
3. More vesicles are able to fuse at synaptic cleft
4. Leads to greater NTs released
5. higher probability that post cell will have an AP
Procedural Memory
Non- declarative memory, can by long-term
Reflexive memory
Implicit memory
(Automatic skills) -riding bike’
Cerebellum = motor skills
NA= non-motor skills (habits)
Declarative Memory
EXPLICIT memory, can be used for long-term
Consciously recollecting learned facts and experiences
1. Episodic
2. Semantic
Episodic memory
Type of declarative
Memory of an event
Semantic Memory
Type of declarative
Memory of words, language, and rules
Working memory
A subset of short-term FOR RETRIEVAL of long-term memory
Memory or facts and such for use at the moment
Ex: recall a fact you can use to answer a test
1. Central Executive (PFC)- fact I need
2. Phonological Loop- auditory info + rules/words of the event ->PFC
3. Visuospatial Loop - visual mems or all ->PFC
Neuronal Plasticity
CNS is altered
More branches to new cells, more synapses
2 types of Plasticity
- Change synaptic Function:
- POST-TETANIC POTENTIATION
- LONG-TERM POTENTIATION - Change structure of the neuron:
- GAIN/LOSS synapses
- DENTRITE changes
- SOME changes
Long-Term Potentiation in post cell
Has to last 30min- several hours
Changes in the pre and post neuron = makes them higher sensitive to a NT, Last hours
- EAA binds to NMDA +Non-NMDA
- Na+ flows into the cell (depol. Opens NMDA .more NA+)
- Ca+2 follows
- CA+2 binds to Calmodulin= cAMP increase
- AMPA receptors get phosphorylated
- Na+ flows in even more= HIGHER AP + sensitivity
Long-Term potentiation from post cell to pre cell
Has to last more then 30min - hours
Changes in the pre and post neuron = makes them higher sensitive to a NT
- EAA binds to NMDA +Non-NMDA
- Na+ flows into the cell (depol. Opens NMDA .more NA+)
- Ca+2 follows
- CA+2 binds to Calceineurin= NOS increase
- Increase NO, flows into pre cell
- cGMP increase + increase NT release from pre cell
Gain/loss of function
Dendrites and soma structurally change
proteins increase in pre and post cell:
NT synthesis enzymes
NT receptors
Growth+synapse formation
CREB
Change in structure on neuron that is permanent
In Long-term potentiation + gain/loss and dendrite/soma structure changes
- Encoding
Attending(focus) to new info
Linking the new info to previous mems
Emotions linked (if we care its worthy to us to remember)
- Storage of information
And areas of the brain that hold this info
Retention of info over time (SHORT-TERM) IS LIMITED
USES LONG-TERM POTENTIATION
Hippocampus
Parahippocampal cortex (also does surprise)
Prefrontal cortex
Some to amygdala
- Consolidation
And brain regions for this
SHORT-LONG
Making memory permanent REPEATED IN THE PAPEZ CIRCUIT +temporal lobe+hippocampus
Physical changes in the synaptic structures
USES LONG-TERM P and STRUCTURAL PLASTICITY
Stored where the new synapses are made which is in the area of the brain associated with the type of info (sound-auditory cortex)
- Retrieval
Recall + use memory (cortex area)
->Neocortex (where all the pieces come from)
->parahippocampal cortex (all come together here)
-> hippocampus (holds it in short-term working memory =reconstruct memory using place cells)
-> parahippocampal cortex (prolongs life of short-term memory)
-> back to cortex ( to make it long term)
Bring info to working memory
Can be modified and lost
Ex: practice questions when studying for test
cAMP increase causes what
Gene transcription of CREB TF——> physical change of neurons
cAMP made in LTP
How to block memories
You block protein synthesis of those memories
Alzheimer’s Disease targets what part of the brain
Nucleus Basalis of Meynert
Connects the neocortex to the Amygdala (short-term memory)
Papez Circuit 4 members
- Hypothalamus and Mammillary Bodies (physiological response to memory or event)
- Anterior Thalamus (sensory info comes here)
- Cingulate Cortex (emotion)
- Hippocampus (short-term)
LTP and Plasticity are both made
Long-term memories don’t use
The limbic system
Issues of retrieval of long-term memory
All the individual pieces (what I saw, smelled, heard, felt) are all stored in their pwn cortex and need to come together
When can info or memory be lost or altered
While you are actively receiving the memory
Pathway is altered
.Central Executive area
PFC
Phonological Loop area
Brocas and Wernickes area
Visuospatial
Occipital cortex for vision
SPATIAL MEMORY is done where and uses what
ONLY HIPPOCAMPUS
Long-term memory of space
Uses pyrimidal place cells of CA1= fire more when you are closer to the object
(When you remember something by thinking about where I was when I learned something)
Place cells location and function
Input from where
in Hippocampus, where in my visual field is this object
Uses pyrimidal place cells of CA1= fire more when you are closer to the object
(Ex: When you remember something by thinking about where I was when I learned something)
Get info from Grid cells
Grid Cells location and function
And input from where
ONLY ACTIVE when you’re in the area
In the Entorhinal cortex (olfaction happens here also)
Make a map of the place I’m at (triangular and hexagonal map)
Get info from border neurons and head direction cells
Border cells
Fire at edges, like walls
Head direction cells
Shows where head was oriented
RETRIEVAL OF SPACE
place cells
