Final exam - Fundamentals of Neuroscience

What is the cell membrane made of?

Semipermeable phospholipid bilayer

What are ion channels? What are they made of?

Made of specialized proteins located in cell membranes that act as gateways to let Na+, K+, Ca2+, Cl- to flow in and out of cells

What are ion pumps or exchangers? What are they made of?

Made up of transmembrane proteins that maintain cellular ionic balance by moving ions across the cell membrane against their electrochemical gradient (ex. Na+/K+ ATPase pump)

What are the three compartments of a neuron? What is the purpose of each of them?

Dendrites, cell body, soma

Dendrites: receive signals or NTs from other neurons

Cell body: receives signals from dendrites, triggers impulses

Axon: conducts the action potential

What is the charge of Na+, K+, Cl-?

Na+ and K+ = +1

Cl- = -1

Which ion is more concentrated inside the cell? Outside?

More Na+ outside the cell, K+ inside the cell (salty banana)

What two forces are in equilibrium to produce an equilibrium potential?

Diffusion/chemical force and electrostatic force must be in equilibrium

What conditions need to be in place to produce an equilibrium potential for an ion?

Unequal concentration of specific ions inside vs outside the cell (higher K+ inside, higher Na+ outside)

How does an ion’s equilibrium potential drive its movement once it becomes permeable across the membrane?

Driving force is the electrochemical gradient

What factors determine the membrane potential at any time?

Ion concentration differences (through ion pumps/exchangers) and membrane permeability (opening/closing of ion channels)

Under what circumstances is the resting potential produced?

Leakage channels are open all the time

What is the purpose of a synaptic potential?

Acts as an incoming signal that transmits information between neurons, allowing them to integrate inputs and determine whether to produce an action potential

Under what circumstances is a synaptic potential produced?

Produced when a presynaptic neuron releases NTs into the synaptic cleft which then bind to receptors on the postsynaptic neuron, due to ligand-gated ion channels

What is the purpose of the action potential?

Propagates signals along axon to transmit information throughout the nervous system.

What is the series of events that produce the action potential? Which ion channels open/inactivate/close?

Closed/deactivated: not conducting ions, ready to be opened

Open: conducting ions

Inactivated: closed and not ready to be opened

Under what circumstances does the sodium channel inactivate?

During the peak of the action potential

Why is it important that this process works?

There must be a refractory period to prevent the action potential from travelling backward

What is myelination and its purpose? What type of cells help produce myelination?

Myelination is the fatty coating around cell axons that speeds up cell signaling, formed by Schwann cells

What are the 4 amines and 3 amino acids?

Amines: dopamine, serotonin, epinephrine, norepinephrine

Amino acids: glutamate, GABA, glycine

Acetylcholine

• Main neurotransmitter of the skeletal nervous system

• Acetyl CoA carries acetate → choline acetyltransferase puts them together → vesicular ACh transporter moves it into vesicles → acetylcholine esterase inactivates it → breakdown products are taken up and reused

What are the kinds of acetylcholine receptors?

Nicotinic — ionotropic (ligand-gated ion channels), nicotine binds to these receptors

Muscarinic — metabotropic (G protein-coupled receptors), most common type in the brain

What is myasthenia gravis?

Disease in which muscles are quickly fatigued with repetitive use, patient’s own immune system attacks/blocks nicotinic ACh receptors at the NMJ

Glutamate, GABA, glycene

Glutamate - highly excitatory, can excite nearly every neuron in the central nervous system

GABA - inhibitory NT in the brain

Glycene - inhibitory NT in the spinal cord

How are small molecule neurotransmitters made?

Synthesized in axon terminal by enzymes and transported to the terminal

Ex: acetylcholine (ACh) synthesized from choline/Acetyl-CoA by the enzyme choline acetyltransferase

Where in the neuron are small molecule transmitters made?

Within the presynaptic axon terminal

How are peptide neurotransmitters made?

Peptide neurotransmitters are synthesized through protein synthesis

Where in the neuron are peptide neurotransmitters made?

Cell body/soma

What happens if neurotransmitter synthesis is prevented? How could you prevent it?

Preventing neurotransmitter synthesis halts neuronal communication, leading to potential cell death

Can be prevented with enzyme inhibitor medications

What happens if we increase neurotransmitter synthesis? How could you do this?

Higher synthesis creates a larger pool of neurotransmitters within the presynaptic terminal, potentially leading to enhanced neural communication and improved mood/cognitive functioning

Diet and exercise can increase certain NT synthesis

Which ion is responsible for neurotransmitter release?

Calcium (Ca2+) ions

What has to happen for a NT to be released?

1. Action potential reaches the axon terminal and depolarizes the membrane

2. Voltage-gated Ca2+ channels open, Ca2+ flows in

3. Ca2+ influx triggers the synaptic vesicles to release NT

4. NT binds to receptors on target cell

What happens if NT release is prevented? How could you do this?

Blocked nerve impulses (can cause paralysis), example of this is Botox

What happens if you increase NT release? How could you do this?

There will be more neurotransmitters performing their individual actions, could do this naturally or through medications like SSRIs/SNRIs

What are the two types of neurotransmitter receptors?

Ionotropic and metabotropic

How do ionotropic and metabotropic receptors work?

Ionotropic receptors are ligand-gated ion channels; when NT/ligand binds the pore opens and allows specific ions to flow through

Metabotropic receptors are G-protein coupled receptors; when NT binds a G-protein is activated which activates other membrane proteins like enzymes which allows for intracellular signaling

What happens if you increase NT receptor activation? Decrease it?

Increase it: neuron is more likely to fire, but can cause too much excitement

Decrease it: neuron is less likely to fire, which can impair normal functioning due to the lack of signaling

How can neurotransmitters be inactivated?

Reuptake: recycled back into presynaptic neuron

Enzymatic degradation: broken down and rendered inactive

Diffusion: NT molecules drift away, decreasing concentration

What happens if you prevent NT inactivation? How could you?

There would be an accumulation of NTs in the synaptic cleft which causes overactivated neural pathways and increased signaling (could cause something like a muscle spasm)

How: through MAOIs, SSRIs which are drugs preventing the breakdown and reuptake of NTs

What happens if you increase NT inactivation? How could you?

There would be a reduction in available neurotransmitter to bind to receptors, shortening/weakening the signal sent between neurons

How: increasing activity of proteins that transport NTs back into presynaptic neuron for recycling (MAO, acetylcholinesterase)

How does cocaine interfere with neurotransmitters?

Blocks/binds to dopamine transporter - agonist - (DAT) leading to a massive buildup of dopamine and creating a “high”

How does nicotine interfere with neurotransmitters?

Mimics ACh (agonist) and binds to nicotinic acetylcholine receptors (nAChRs), triggering the release of dopamine and other neurotransmitters

What is a postsynaptic potential?

Change in polarization of a neuron’s membrane, caused by the binding of a neurotransmitter to receptors at a synapse

What makes a PSP excitatory? Inhibitory?

EPSP: excitatory postsynaptic potential; depolarizes membrane, influx of positive ions, usually caused by glutamate

IPSP: inhibitory postsynaptic potential; hyperpolarizes membrane, influx of negative ions/efflux of positive ions, usually caused by GABA or glycine