Neurotransmission and Synaptic Plasticity: Key Concepts in Neuroscience

Presynaptic neuron

Sends the signal.

Postsynaptic neuron

Receives the signal.

Synapse

Junction where communication occurs between neurons.

Synaptic cleft

Space between pre- and postsynaptic membranes.

Synaptic vesicle

Stores neurotransmitters before release.

Neurotransmitter

Chemical messenger released from presynaptic terminal.

Neurotransmitter receptor

Protein that binds neurotransmitters on postsynaptic side.

Small molecule neurotransmitter

Synthesized in axon terminal (e.g., ACh, dopamine).

Peptide neurotransmitter

Synthesized in soma; larger and slower acting.

SNARE proteins

Help vesicles fuse with membrane for neurotransmitter release.

Horseradish peroxidase (HRP)

Used to trace vesicle recycling.

Neurotransmitter inactivation

Process that stops neurotransmitter action (e.g., reuptake, degradation).

Calcium (Ca²⁺)

Triggers neurotransmitter release.

EPSP (Excitatory postsynaptic potential)

Na⁺ enters → neuron more likely to fire.

IPSP (Inhibitory postsynaptic potential)

K⁺ exits → neuron less likely to fire.

Reversal Potential

Shows that ACh-gated channels allow passage of both Na⁺ and K⁺, not just one ion.

Temporal summation

Repeated inputs over time add up.

Spatial summation

Multiple inputs from different locations add up.

Acetyl CoA / Choline Acetyltransferase (ChAT)

Used to make acetylcholine (ACh).

Acetylcholinesterase (AChE)

Breaks down ACh in synapse.

Nicotinic ACh receptor

Ionotropic (fast).

Muscarinic ACh receptor

Metabotropic (slow).

Myasthenia gravis

Autoimmune disease reducing ACh receptors → muscle weakness.

Acetylcholine (ACh)

Learning, memory, muscle movement.

Dopamine (DA)

Reward, movement. Too little = Parkinson's.

Serotonin (5-HT)

Mood, sleep. Made from tryptophan.

Catecholamines

Norepinephrine / Epinephrine.

GABA

Main inhibitory NT. Benzodiazepines & barbiturates = agonists.

Glutamate

Main excitatory NT. Important for LTP.

Metabotropic Signaling Steps

1. Neurotransmitter binds to metabotropic receptor 2. G-protein activated (GTP = active; GDP = inactive) 3. Adenylyl cyclase activated 4. cAMP generated (second messenger) 5. PKA phosphorylates target proteins

Signal Amplification

A single receptor activation can produce a large intracellular response via second messengers like cAMP.

Transcription Regulation

Phosphorylation of ion channels = short-term changes. Activation of transcription factors (like CREB) = long-term gene expression → structural/functional change.

CREB (cAMP Response Element-Binding Protein)

Activated by PKA, acts as a transcription factor. Turns on genes needed for synaptic strengthening. Required for long-term potentiation (LTP) and memory formation.

Nicotine

ACh agonist that stimulates nicotinic receptors.

Curare

ACh antagonist that blocks nicotinic receptors.

Barbiturates + Benzodiazepines

GABA agonists that increase inhibition; dangerous together.

Amphetamine / Cocaine

Increase dopamine & NE.

Opioids (morphine, heroin, codeine)

Alters perception.

THC

Cannabinoid receptor agonist.

MAOIs, SSRIs

Increase serotonin; used in depression.

PCP

NMDA receptor blocker that mimics schizophrenia-like symptoms.

Habituation

Repeated stimulus → less Ca²⁺ enters → decreased neurotransmitter release → weaker response.

Sensitization

Increased neurotransmitter release due to serotonin → activates cAMP & PKA → more Ca²⁺ entry.

Long-term facilitation

Requires CREB activation → gene transcription → new synapses.

Long-Term Potentiation (LTP) Induction

Requires glutamate binding NMDA & AMPA receptors, depolarization to remove Mg²⁺ block, Ca²⁺ influx, and CREB activation.

LTP Maintenance

AMPA receptors are added to postsynaptic membrane → stronger future responses.

Induction Phase Key Event

Ca²⁺ enters via NMDA receptor.

Expression Phase Key Event

Increased AMPA activity leads to more Na⁺ entry.

Maintenance Phase Key Event

CREB-mediated gene protein synthesis for memory expression.

Too little dopamine

Leads to Parkinson's disease.

ACh deficiency

Leads to Myasthenia gravis.

Adenylyl cyclase

Activated by G-proteins to produce cAMP.

cAMP

Second messenger activating PKA.

EPSP

Na⁺ entry leads to excitatory response.

IPSP

K⁺ exit leads to inhibitory response.

Reuptake

Neurotransmitter recycled into presynaptic terminal.