What were the key discoveries from the case of Henry Molaison (HM) after his hippocampus was removed?
Hippocampus is essential for forming new long-term declarative memories (anterograde amnesia).
Short-term memory was preserved, showing it's independent of the hippocampus.
Procedural memory (e.g., motor skills) remained intact, proving it's handled by other brain systems.
Memory types are distributed, not localized to one brain area.
Hippocampus is not the storage site for old memories, just for consolidation.
lexical memory does not rely on medial temporal structures
Two types of long term memory
What it is: Memory you can consciously recall and describe.
Brain areas involved: Hippocampus, medial temporal lobe.
What it is: Memory that influences behavior without conscious awareness.
Brain areas involved: Basal ganglia, cerebellum, amygdala.
two types of memory?
short term (prefrontal cortex)
long term (modulated by hippocampus and amygdala)
Hebb rule
Neurons that fire together get wired together
cellular basis of learning involves strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires
What is LTP and where to find?
persistent increase in synaptic strength that can be rapidly induced by brief neural activity
makes synapses stronger
= a candidate mechanism for Hebbian learning
hippocampus, PNS(mammals), neocortical&subcortical (mammals)
Which receptor field are involved in LTP (long termn potential)
AMPA (more AMPA -> synapse stronger)
NMDA (start signal LTP)
GABA (balance LTP and neuronal activities)
What changes during synaptic plasticity?
Increased AMPA receptor density in the postsynaptic membrane.
Stronger EPSPs (excitatory postsynaptic potentials) in response to the same presynaptic signal.
Changes in spine morphology (postsynaptic dendritic spines can grow or change shape).
Enhanced neurotransmitter release (in some cases, presynaptic changes too).
What is the mechanism responsible for the induction of synaptic plasticity?
Glutamate binds to AMPA → depolarization.
If the postsynaptic cell is already depolarized, NMDA receptors open → Ca²⁺ influx.
Calcium acts as a trigger:
Activates protein kinases (like CaMKII).
Leads to AMPA receptor insertion, gene expression, and cytoskeletal changes.
This is the induction phase of LTP: Ca²⁺ is the key signal that turns “activity” into long-lasting synaptic strengthening.
What are the rules governing synaptic plasticity?
hebb rule
How is synaptic plasticity maintained?
Short-term (minutes to hours):
Continued AMPA receptor trafficking.
Long-term (hours to days):
Gene expression changes in the nucleus (via CREB, etc.).
What happens during normal glutamatergic synaptic transmission? (signal transmission, strength etc…)
Action potential reaches presynaptic terminal.
Ca²⁺ channels open → Ca²⁺ enters.
Glutamate is released into synaptic cleft.
Glutamate binds to AMPA receptors → Na⁺ in → EPSP.
NMDA receptors are still blocked (by Mg²⁺).
Glutamate is cleared by glial cells or reuptake.
Why is depolarization important for NMDA receptor activation and LTP?
Depolarization (via AMPA receptors) removes the Mg²⁺ block from NMDA receptors.
During strong or repeated stimulation, this allows Ca²⁺ to enter through NMDA → triggers LTP.
Normal depolarization happens often, but only strong depolarization enables LTP.
What is the signaling mechanism underlying LTP?
Strong synaptic activity → NMDA opens → Ca²⁺ influx triggers:
Activation of CaMKII and PKC
Insertion of AMPA receptors into the membrane
Structural spine changes → These changes strengthen the synapse = LTP.
What does LTP requires?
active synapse
depolarization of postsynaptic neuron
remocal of the Mg block
Why does a small amount of stress gelp you learn better?
β-adrenergic receptors are activated by adrenaline/noradrenaline during emotional or attention-demanding situations.This boosts arousal and attention, enhancing activity in the amygdala and hippocampus, which improves memory encoding.
What happens to LTP if you antagonizing GABA
Ehance LTP induction
What are the main types of LTP based on mechanism?
NMDA-dependent LTP: Requires glutamate + strong depolarization → Ca²⁺ influx via NMDA → classic LTP (e.g., in CA1 hippocampus).
NMDA-independent LTP: Found in regions like CA3 (mossy fibers); involves presynaptic changes or mGluRs/cAMP pathways.
What is the difference between early and late LTP?
Early LTP (minutes–1 hr): Needs Ca²⁺, activates CaMKII, adds AMPA receptors, no gene expression.
Late LTP (hours–days): Requires new proteins, gene transcription (e.g., via CREB), and supports long-term memory.
Order the discover of:
A: head direction cells
B: place cells
C: speed cells
D: border cells
E: grid cells
place cells
head direction cells
grid cells
border cells
speed cells
What does grid cell firing patterns modules code
movement distance and direction
What is distance
speed x time
What do mEC track
firiing rate of speed cells are following the animals running speed
what are speed cells importan for
necessary to update grid pattern in accordance with anmials movement
Which cells are importan for spatial information
place cell + head direction cell + grid cell
What is the EC
entorhinal cortex
major input and outpu structure of hippocampal formation
nodal point of cortico-hippocampal circuits
How does the brain create spatial maps using place and grid cells?
The hippocampus uses place cells to estimate location by combining:
Path integration input from grid cells (dead reckoning)
Sensory "sightings" (likely from the lateral entorhinal cortex)
Together, they build a map that tracks familiar locations and plans paths.
Where to find place cells and what is ther function and when are they activated?
location: dorsal hippocampus
function: storing spacial memory
activated: tunde to a specific location
Where to find grid cells and what is ther function and when are they activated?
location: Enthorinal Cortex
function: arrange hexagonal patterns linked to position
activated: distance, angle, landmarks
Where to find boder cells and what is ther function and when are they activated?
function: detection of edges
activated: when in edge
Where to find head direction cells and what is ther function and when are they activated?
location: medial Enthorinal Cortex
function: internal compass
activated: when in animal faces a spec direction
Where to find speed direction cells and what is ther function and when are they activated?
function: speed detection
activated: running speed is represented in firing rate
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