What is an example of associative learning?
learning that two events go together - Pavlov’s dog
What is a conditioned vs. unconditioned stimulus?
Unconditioned stimulus (US): Naturally produces a response (food → salivation).
Conditioned stimulus (CS): Originally neutral, but becomes meaningful after pairing with US (bell → salivation).
Describe the sea slug (Aplysia) experiments: what did they do, what did they see, what does it tell us about associative learning?
What they did: Touched the siphon while pairing it with a tail shock.
What they saw: After pairing, the siphon touch produced a stronger gill withdrawal reflex.
What it told us: Associative learning occurs through changes in synaptic strength—specifically increased neurotransmitter release and synaptic facilitation in the sensory → motor neuron pathway.
Difference between short-term sensitization and long-term potentiation (LTP)?
Short-term sensitization:
Lasts minutes.
Mainly presynaptic.
Increased neurotransmitter release (often via serotonin → cAMP → PKA).
Long-term potentiation (LTP):
Lasts hours–days–years.
Mainly postsynaptic.
Increased AMPA receptors, spine growth, and stronger EPSPs.
What is a coincidence detector?
A neuron or receptor that detects two inputs arriving at the same time.
Example: NMDA receptor
how can coincidence detector increase synaptic efficacy
Requires presynaptic glutamate AND postsynaptic depolarization.
This coincidence opens NMDA → Ca²⁺ enters → triggers mechanisms that strengthen the synapse (more AMPA receptors, bigger spines)
What role does calcium play in LTP?
Calcium is the second messenger that initiates LTP.
Enters through NMDA receptors
Activates CaMKII, PKC, and other enzymes
Leads to AMPA insertion, spine growth, and long-term changes.
Other enzymes relevant for short-term sensitization or LTP
Short-term sensitization:
cAMP, PKA, PKC
LTP:
CaMKII (most important),
PKC,
CREB (for long-term structural changes)
After LTP, what aspects of the neuron change?
More AMPA receptors inserted in postsynaptic membrane
Larger dendritic spines
Stronger EPSPs
Can also include new synapse formation
Increased presynaptic NT release (in some cases)
two types of memory
episodic and semantic
What three cells work together to establish context for your memory? what do they do
Place cells – where you are in space
Grid cells – spatial metric/map
Head-direction cells – which way you’re facing
True or false: NDDs are not genetic disorders.
not all are genetic
Difference between monogenic, polygenic, and oligogenic?
monogenic - on mutated gene
oligogeneic - a few genes mutated
polygenic - many genes
biggest effect of mono poly and oligogenic
mono has big effect
oligogenic has moderate effect
polygenic has small effects
Most NDDs involve mutations that affect what part of the neuron?
synapses (synaptic development, stability, communication).
This includes receptors, scaffolding proteins, ion channels, release machinery, and cytoskeleton.
For each example, choose a molecule that could be mutated + how dysfunction leads to NDD phenotypes - cytoskeletal dynamics
Microtubule-associated protein (e.g., MAP2 or tubulin).
Dysfunction: Poor dendrite growth, abnormal axon guidance → impaired circuitry → sensory issues, cognitive delays.
What role do environmental interactions have in NDDs? Use alcohol as an example.
Environment can worsen, trigger, or expose vulnerabilities created by genetics.
Example: Alcohol
Prenatal alcohol exposure disrupts neuron migration, synapse development, and gene expression.
Can interact with genetic vulnerabilities → more severe NDDs (poor motor skills, cognitive deficits, sensory issues).
Gene mutations often affect:
* Cytoskeletal dynamics →
slit/robo
ion conductance and AP dynamics gene mutations affect how
shank proteins
gene mutations affect NT release, binding, reuptake by what
VGluT
gene mutations affect gene plasticity by what
over/under pruning
