Neurotransmitters and Their Receptors

Question 1

Basic stuff: What are the two main types of synapse in body?

Answer 1

Electrical - like in the heart. Connected cytoplasms. Quick, can’t modulate.
Chemical - what we care about with the neurotransmitters and stuff.

Question 2

What are the two types of potentials that can be induced in the post-synaptic cell?

Answer 2

Excitatory Post-Synaptic Potential (EPSP)

Inhibitory Post-Synaptic Potential (IPSP)

Question 3

What’s another name for ligand-gated ion channel receptors for neurotransmitters?

Answer 3

Ionotropic receptors.

Question 4

What’s another name for neurotransmitter receptors that are GPCRs?

Answer 4

metabotropic receptors

Question 5

What types of ions to excitatory ionotropic receptors usually use? Ligands?

Answer 5

Cations. Glutamate and ACh.

Question 6

What kind of ions do inhibitory ion receptors usually use? Ligands?

Answer 6

Anions. GABA, glycine

Question 7

What’s faster, an ionotropic or a metabotropic receptor?

Answer 7

Ionotropic is faster. Makes sense.

Question 8

How is receptor diversity facilitated in ionotropic receptors?

Answer 8

Receptor subunits can be reshuffled to form receptors with different activities.

Question 9

What can a metabotropic receptor do that an ionotropic receptor can’t? (3 things)

Answer 9

• can amplify signal through 2nd messenger systems
• alter gene expression (and make other cellular change) through 2nd messenger signaling
• sustain signaling for a longer duration

Question 10

Can metabotropic GPCR subunits be recombined?

Answer 10

Nope, they’re a monomer.

Question 11

What 4 things must a neurotransmitter have/do?

Answer 11

• Specific synthesis
• Specific release mechanism
• Post-synaptic effects
• Method for inactivation (degradation, reuptake)

Question 12

What are 3 ways in which neurotransmitter activity can be terminated?

Answer 12

Degradation, reuptake, diffusion.

Question 13

4 types of molecules that can be neurotransmitters?

Answer 13

Amino acids
Small molecules - ACh
“Biogenic amines”
Peptides

Question 14

Serotonin, histamine, and catecholamines. Are these NTs excitatory or inhibitory?

Answer 14

Excitatory. (as are glutamate and ACh, but that’s easy)

Question 15

Are GABA and glycine excitatory or inhibitory NTs?

Answer 15

Inhibitory.

Question 16

What’s the main excitatory CNS NT?

Answer 16

Glutamate!

Question 17

Name 3 ionotropic glutamate receptors.

Answer 17

NMDA, AMPA, and Kainate Receptors.

Question 18

What are the metabotropic receptors for glutamate listed?

Answer 18

mGluRs… okay, that’s not quite profound

Question 19

How can NMDA receptors get blocked? (endogenously, not drugs) Significance?

Answer 19

NMDA channels in hyperpolerized cells can get blocked by Mg2+. Thus NMDA receptors will only work when the cell is repolarized.

Question 20

3 uses for NMDA-R blockers?

Answer 20

Alzheimer’s-Parkinson’s
Anesthetics (ketamine)
Drugs of abuse (PCP)

Question 21

What happens to AMPA and Kainate receptors when you repeatedly stimulate them?

Answer 21

They desensitize.

Question 22

What’s the main inhibitory NT in the brain?

Answer 22

GABA!

Question 23

What are the two main GABA receptors? Ionotropic or metabotropic?

Answer 23

GABA-A - Ionotropic - uses Cl-
GABA-B - Metabotropic
(don’t worry about GABA-C, it’s only in the retina.. but it’s also ionotropic)

Question 24

What allosteric modulators can act on GABA-A? (classes of drugs, name 4)

Answer 24

Barbituates, benzodiazapines, anesthetics, steroids.

Question 25

Contrast GABA-A and GABA-B. Speed? Duration? Ions modulated?

Answer 25

Speed: A is fast, B is slow
Duration: B lasts longer.
Ions: A uses Cl-, B modulates Ca++ and K+

Question 26

What drugs act on GABA-B?

Answer 26

Baclofan (for spasticity)
GHB (date rape…… no good :( )
Ecstasy (a way better idea than date rape, but still a bad idea)

Question 27

So you know about nicotinic and muscarinic receptors for ACh (don’t you? ish?). Are they ionotropic or metabotropic?

Answer 27

Nicotinic is ionotropic.

Muscarinic is metabotropic.

Question 28

When are nicotinic receptors expressed in the brain?

Answer 28

Early in life. Expression declines later.

Question 29

Do cholinergic systems modulate dopanergic systems? (relevant Parkinson’s)

Answer 29

Yes. (But not being a neuro person, I have no idea what this means.)

Question 30

Acronym for cholinergic toxidrome (too much ACh)?

Answer 30

SLUDGE

Salivation, lacrimation, urination, diarrhea, GI distress, emesis

Question 31

What’s the mnemonic for things that cause an anticholinergic toxidrome?

Answer 31

A bunch of “A” things: Atropine, antihistamines, antidepressants, antipsychotics, antiparkinsonian drugs.
(something about hatters, bones, and beets)

Question 32

Where is norepinephrine synthesized? Where does it go?

Answer 32

In the “locus coeruleus.” It goes everywhere.

Question 33

Where is serotonin made? Where does it go?

Answer 33

Made in the raphe nuclei. It goes everywhere.

Question 34

Where is dopamine made? Where does it go?

Answer 34

Made in ventral tegmental area and substatia nigra. Goes to prefrontal cortex, caudate nucleus and putamen, nucleus accumbens. Professor emphasized that it goes to the basal ganglia

Question 35

Where is ACh made (in the brain). Where does it go?

Answer 35

Septal nuclei, nucleus basalis, pontomesencephalotegmental complex (must have been named by a German). Goes… lots of places.

Question 36

What was causing the syndrome of the case of the woman with psychosis, agitation, fever, seizures, unstable heart rate/BP, and abnormal muscle movement.

Answer 36

Autoantibodies against NMDA receptors.

Question 37

What was the root cause of these anti-NMDA-R antibodies?

Answer 37

Ovarian teratomas -> antibodies produced via a paraneoplastic syndrome