Brain Basics II - Neurotransmission

During ________ neuron is ready to receive and fire and action potential

Resting

When EPSPs happen the neuron gets slightly more _______

positive

During depolarization, after reaching ________, neuron rapidly gets more ______ while firing an action potential

threshold, positive

During repolarization the neuron rapidly returns to a _________ internal state

negative

During the undershoot the neuron becomes super _________ (more than at rest)

negative

During the depolarization stage, EPSPs due to excitation from the __________________ interaction

neurotransmitter-receptor

How does the inside of the cell become more positive during depolarization?

Voltage-Gated Sodium Channels open allowing an influx of Na+

What happens after the Voltage-Gated Sodium Channels open depolarizing the cell?

Voltage-Gated Potassium Channels open allowing K+ to flow out of the cell

What happens at the peak of depolarization?

Voltage-Gated Sodium Channels inactivate

What happens after the action potential, right after the peak of depolarization?

Voltage-Gated Potassium Channels remain open allowing for K+ to flow out of the cell

What happens at the end of repolarization during the undershoot phase?

Voltage-Gated Potassium Channels allow for more K+ to move out of the cell than at resting membrane potential

During the refractory period ____________ actively move Na+ out of the cell and K+ inside of the cell and __________ that allow K+ to flow into the cell.

Sodium Potassium Pumps, Leak channels

When the action potential arrives at the axon terminal the _____________ opens

Voltage-Gated Calcium Channels

What happens to the neurotransmitter at the postsynaptic membrane?

Excitation

What are the 3 ways neurotransmitters get removed from synapses?

1. Breakdown from enzymes

2. Reuptake via transports back into the presynaptic neuron

3. reuptake by glial cells from breakdown or reuse

Neurotransmitters have to be __________ substances, processed by _______, able to bind and interact with postsynaptic membrane (___________), cause changes to the postsynaptic cell (____ or ________), and alter ___________ between neurons.

chemical, neurons, have an effect, hyper- depolarization, communication

Glutamate and GABA are examples of ___________

Amino acids

String of amino acids

Neuropeptides

Acetylcholine is an example of a ______

Ester

Drugs can ____ or _______ the amount of neurotransmitter synthesized by a cell, altering how neurotransmitters interact with their receptors.

add, subtract

Drugs can ____ neurotransmitter vesicles from obtaining the neurotransmitter, altering how neurotransmitters interact with their receptors.

block

Drugs can stimulate/block neurotransmitter ________ into the presynaptic cleft, altering how neurotransmitters interact with their receptors.

release

Drugs can stimulate/block autoreceptors which will add or subtract further neurotransmitter _______ into the synaptic cleft, altering how neurotransmitters interact with their receptors.

release

Drugs can _____ reuptake, altering how neurotransmitters interact with their receptors

block

Drugs can stimulate/block _________, altering how neurotransmitters interact with the postsynapse

receptors

Drugs can block ______ of neurotransmitters altering how neurotransmitters interact with the postsynapse.

degradation

Neurotransmitters are an example of an endogenous chemical that is produced _____ the body.

inside

Endogenous chemicals act on endogenous receptors to ______ change (depolarization, hyperpolarization, changes in gene expression).

exert

Drugs are an example of exogenous substances that are produced ______ the body.

outside

Exogenous substances can act on endogenous receptors to make them more _____, _____ their activity , or _______ their activity

active, block, modify

______ increase activity fully

Full agonist

_______ increase activity less than fully.

Partial Agonists

Maximal response of binding, bind to the same spot as the endogenous ligand (neurotransmitter)

Full agonist

Less maximal response, does not bind to exactly the same spot as then endogenous ligand (neurotransmitter)

Partial Agonist

Drug doesn’t compete with the endogenous neurotransmitter for binding, they can bind at the same time

Allosteric Modulator, Indirect Agonist

___________ have no effect on activity.

Antagonists

When a drug is bound to the receptor there is less than normal responding when a substrate binds (prevention of a response)

Antagonist

Drug competes for the same binding site as an endogenous ligand (neurotransmitter)

Competitive Antagonist

Drug does not compete for the same binding site as an endogenous ligand (neurotransmitter)

Noncompetitive Antagonist

Which type of antagonist responsible for substrate binding being blocked?

Competitive Antagonist

Which type of antagonist is responsible for a substrates binding reaction being blocked?

Noncompetitive Antagonist

Drug forms “permanent” or very long lasting bonds with the receptor and can modify it in such as way that it no longer binds to its endogenous substrate

Reversible Antagonist

___________ decrease activity.

Inverse Agonist

Receptors that have spontaneous activity (active without any substrate binding to it)

Inverse Agonist

When an inverse agonist binds to a receptor it _________ it

inactivates