Exam 3 Neurobiology

What are the 6 steps of synaptic transmission?

1. Action potential arrives at presynaptic terminal

2. Depolarization of the terminal

3. Opening of voltage-gated Ca2+ channels

4. Ca2+ influx

5. Vesicle fusion

6. Neurotransmitter release

NMJ neurotransmitter

Acetylcholine (ACh)

What receptor is at the NMJ?

Nicotinic ACh receptor

What is required for the NMJ to open?

Requires 2 ACh molecules to open

What is the ion flow in the NMJ?

Na+ in, K+ out

What is the net effect in the NMJ?

Depolarization → end plate potential (EPP)

What is end plate potential (EPP)?

• always depolarizing

• leads efficiently to action potential

• EPP is due to Na+ and K+ flowing through the same channel

Excitatory postsynaptic potential (ESPS)

• depolarization

• neurotransmitters: glutamate

• ions: Na+ influx

• effect: brings neuron closer to the threshold

Inhibitory postsynaptic potential

• hyperpolarization

• nuerotransmitters: GABA, Glycine

• ions: Cl- influx

• effect: moves neuron away from threshold

• IPSPs involve Cl- channels

What is the definition of synaptic integration?

The process by which multiple synaptic inputs combine in a neuron.

What are the two types of synaptic integration?

• spatial summation: different synapses

• temporal summation: same synapse over time

What is shunting inhibition?

reduces current flow to axon hillock

What are the properties of GPCRs?

• slow, long-lasting effects

• modulate synaptic strength

• can activate GIRK channels → hyperpolarization

• not ion channels themselves

What are the two types of non-associative learning?

• habituation: decreased response

• sensitization: increased response

What are the two types of associative learning?

• classical conditioning (pavlov): stimulus assosciation

• instrumental conditioning (thorndike): behavior = reward

what is declarative memory?

facts/events

what is procedural memory?

skills/habits

Hippocampus function

memory formation, spatial learning

Prefrontal cortex function

working memory

LIP cortex function

spatial working memory

H.M. case

• bilateral temporal lobectomy

• anterograde amnesia

• working memory and procedural memory intact

place cells

specific location

grid cells

spatial grid

what are the two behavioral tests?

• radial arm maze

• morris water maze

What happens with hippocampal lesions?

• revisits same arm repeatedly

• poor spatial learning

What is Hebb’s theory?

• cells that fire together wire together

• memory = cell assemblies

• sensory/spatial representation distributed across cortical and subcortical areas

What is long term potentiation (LTP)?

long lasting increase in synaptic strength

LTP mechanism

Induction: high-frequency stimulation

• NMDA receptor activation

• Ca2+ influx

• activation of CaMKII and PKA

• insertion of AMPA receptors and AMPA receptors increases conductance

LTP structural changes

increased number and size of dendritic spines

What is long-term depression (LTD)?

long lasting decrease in synaptic strength

What is the induction and function of LTD

• low-frequency stimulation (LFS)

• memory erasure and behavioral flexibility

NMDA receptor

• blocked by Mg2+ at rest

• requires glutamate binding and depolarization via AMPA

What is CREB-1?

activates transcription

What is CREB 2?

represses transcription

What is CaMKII

Activated by Ca²⁺ influx, strengthens synapses by increasing AMPA receptor activity and insertion

What is PKMs?

active kinase that maintains long-term potentiation by keeping AMPA receptors at the synapse

What is adenylyl cyclase?

Converts ATP to cAMP in response to signaling, linking neurotransmitter activity to intracellular memory pathways

What is PKA?

Activated by cAMP, it phosphorylates proteins and transcription factors (like CREB) to drive gene expression for long-term memory