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This document contains key concepts and terms from the NEUR 170 course, organized into flashcards for study and review.
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Resting membrane potential
The typical resting membrane potential of a neuron is -65 mV.
Depolarization
When the membrane potential becomes less negative or more positive.
Hyperpolarization
When the membrane potential becomes more negative.
Action potential rising phase
During this phase, Na⁺ (sodium) flows IN through voltage-gated sodium channels.
Action potential falling phase
During this phase, K⁺ (potassium) flows OUT through delayed rectifier potassium channels.
Undershoot (afterhyperpolarization)
Occurs due to delayed rectifier K⁺ channels staying open too long, allowing excess K⁺ to flow out.
States of a voltage-gated sodium channel
Closed → Activated (open) → Inactivated → De-inactivated (closed but ready).
Absolute refractory period
The period when Na⁺ channels are inactivated and no action potential can be triggered.
Voltage sensor of the S4 segment
Regularly spaced positively charged amino acids (arginine/lysine) move outward when the membrane depolarizes.
Initiation of action potential
Typically initiated at the axon hillock (spike-initiation zone).
Saltatory conduction
Action potential jumping node to node (Nodes of Ranvier) in myelinated axons.
Myelin's impact on conduction speed
Faster than continuous conduction due to insulation of internodal segments.
What triggers vesicle fusion at a chemical synapse?
Ca²⁺ influx through voltage-gated Ca²⁺ channels activates synaptotagmin and SNARE complex.
EPSP
Excitatory PostSynaptic Potential — depolarization of the postsynaptic membrane.
IPSP
Inhibitory PostSynaptic Potential — hyperpolarization of the postsynaptic membrane.
Ionotropic vs metabotropic receptors
Ionotropic is the receptor that IS the ion channel; metabotropic is a GPCR separate from the channel.
Spatial summation
Multiple synapses firing simultaneously, their PSPs add together at the axon hillock.
Temporal summation
Same synapse firing rapidly in succession, voltage changes stack over time.
Autoreceptor
A presynaptic receptor that responds to the neuron's own neurotransmitter, acting as a negative feedback brake.
Agonist
A molecule that binds a receptor and elicits the same effect as the endogenous neurotransmitter.
Antagonist
A molecule that binds a receptor and blocks the actions of the neurotransmitter.
Cholinergic neuron
A neuron that synthesizes and releases acetylcholine (ACh).
Acetylcholine synthesis
Choline + Acetyl CoA, combined by choline acetyltransferase (ChAT).
Catecholamine precursor
Tyrosine is the precursor to all three catecholamines.
Major inhibitory neurotransmitter
GABA is the most important inhibitory neurotransmitter.
NMDA receptor
Only opens when glutamate binds and the membrane is depolarized to ~-30mV.
CB1 receptor
A receptor activated by endocannabinoids synthesized in the POSTSYNAPTIC neuron.
What is a ligand?
Any molecule that binds to a receptor
Which receptor type is faster — ionotropic or metabotropic?
Ionotropic (milliseconds, direct). Metabotropic is slower but produces longer-lasting, widespread effects.
How are small-molecule neurotransmitters packaged differently from peptide neurotransmitters?
Small-molecule NTs: synthesized locally in axon terminal, packaged in small clear synaptic vesicles. Peptides: made in cell body via rough ER/Golgi, packaged in large dense-core vesicles, transported to terminal
What are the four types of chemical synapses by location?
Axodendritic (axon → dendrite), Axosomatic (axon → cell body), Axoaxonic (axon → axon), Axospinous (axon → dendritic spine)
What are the three structural levels of a gap junction from smallest to largest?
Connexin protein → Connexon (6 connexins) → Gap junction (two docked connexons)
What is a Piezo channel and what activates it?
A mechanosensitive cation channel activated by physical/mechanical force (e.g. stepping on something sharp)
What two ingredients make acetylcholine, and what enzyme combines them?
Choline + Acetyl CoA, combined by choline acetyltransferase (ChAT)
What happens if AChE is blocked?
ACh accumulates in the cleft → prolonged receptor activation (used by nerve agents and some Alzheimer's drugs)
What are the three catecholamines?
Dopamine, Norepinephrine, Epinephrine
What enzyme degrades catecholamines?
Monoamine oxidase (MAO)
What is the precursor to serotonin and where does it come from?
Tryptophan, obtained from diet ~ 95% made in the gut
What enzyme converts glutamate into GABA?
Glutamic acid decarboxylase (GAD)
What does Gs do vs Gi in GPCR signaling?
Gs: stimulates adenylyl cyclase → more cAMP → more PKA → cell activation. Gi: inhibits adenylyl cyclase → less cAMP → inhibition
What are the two GPCR downstream pathways?
1) Shortcut pathway: G-protein directly opens nearby ion channel (fast, localized). 2) Second messenger cascade: G-protein → effector enzyme → second messengers (slower, widespread, long-lasting)
What are endocannabinoids and why are they called retrograde messengers
Lipid signals synthesized in the POSTSYNAPTIC neuron that travel BACKWARD to bind CB1 receptors on the PRESYNAPTIC terminal — opposite direction of normal neurotransmission
What triggers endocannabinoid synthesis?
Activation of the postsynaptic neuron → Ca²⁺ influx → endocannabinoids synthesized from membrane phospholipids
What does CB1 receptor activation do?
Activates Gi → suppresses Ca²⁺ channels → reduces neurotransmitter release from the presynaptic terminal
What is the vesicular transporter for glutamate?
vGLUT
What takes up glutamate from the synaptic cleft?
Excitatory Amino Acid Transporters (EAATs) in neurons AND astrocytes