Kenyon: Neurotransmission Flashcards by Megan Foggia

What’s this?

A single transmembrane, multimeric protein binds the neurotransmitter and is the channel.

ligand-gated ion channels aka ionotropic receptors

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T/F: By mixing and matching subunits, there is an enormous number of potential ionotropic receptors

True!

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What’s this?
Binding of the neurotransmitter activates trimeric G-proteins that directly and indirectly influence the opening and closing of ion channels

GPCRs or metabotropic receptors

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What’s this?
Hundreds of potential receptor types for a given neurotransmitter made by mixing and matching subunits.
Binding of the neurotransmitter opens a channel.
The response is limited to a change in membrane potential unless the channel allows Ca2+ through.

ionotropic receptors

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What's this?
A couple (

metabotropic receptors

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What’s this?
Binding of the ligand (neurotransmitter?) activates a tyrosine kinase that indirectly influence the opening and closing of ion channels

enzyme-linked receptors

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T/F: Unconventional neurotransmitters have receptors, too.

True

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ACh
Postsynaptic effect?
Precursor?
Removal mechanism?
Type of vesicle?

excitatory
choline + acetyl CoA
AChE
small, clear

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Glutamate
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

excitatory
transporters
small, clear

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GABA
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

inhibitory
transporters
small, clear

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Glycine
Postsynaptic effect?
Removal mechanism?
Type of vesicle?

inhibitory
transporters
small, clear

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Catecholamines
Postsynaptic effect?
Precursor?
Removal mechanism?
Type of vesicle?

excitatory
tyrosine
transporters, MAO
small, dense-core

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Serotonin
Postsynaptic effect?
Precursor?
Rate-limiting step in synthesis?
Removal mechanism?
Type of vesicle?

excitatory
tryptophan
tryptophan hydroxylase
transporters, MAO

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Histamine
Postsynaptic effect?
Removal mechanism?

excitatory

transporters

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ATP
Postsynaptic effect?
Precursors?
Removal mechanism?

excitatory
ADP
hydrolysis to AMP and adenosine

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Neuropeptides
Postsynaptic effect?
Precursors?
Removal mechanism?
Type of vesicle?

excitatory/inhibitory
amino acids
proteases
large, dense-core

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Endocannabinoids
Precursors?
Rate-limiting step in synthesis?
Type of vesicle?

membrane lipids
enzymatic modification of lipids
none

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Nitric oxide
Precursors?
Rate-limiting step in synthesis?
Removal mechanism?
Type of vesicle?

arginine
NO synthase
spontaneous oxidation
none

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Where is ACh found?
What synthesizes it?
How is it inactivated?
How is choline recovered?

neuromuscular junction, preganglionic autonomic ganglia, post-ganglionic parasympathetic neurons, many CNS neurons;
choline acetyltransferase;
extracellular acetylcholineterase;
Na+/choline transporter

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Nicotinic AChR are (blank) receptors.
How many different muscle nACh receptors are there?
How many different neuronal nACh receptors are there?

ionotropic;
two kinds;
a zillion kinds

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Two kinds of nicotinic AChR in muscle?

Pentamers in fetal mammals (and Torpedo)

Pentamers in adult mammals

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Where are ACh, nicotine, curare, and bungarotoxin binding sites located?

on the alpha1 subunits

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Muscarinic AChR are (blank) receptors.

metabotropic

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Where are mACh receptors found?

neurons
smooth muscle
cardiac muscle

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The principle fast excitatory neurotransmitter in the nervous system. Half of the synapses in the brain have receptors for this neurotransmitter.

glutamate

What collects glutamate after its release into the synaptic junction? What cells are involved in its removal and inactivation?

EAATs; glial cells

3 ionotropic glutamate receptors?

AMPA NMPA kainate receptors

All ionotropic glutamate receptors pass (blank). Some specialize in passing (blank). All mediate (blank).

cations; Ca++; EPSPs

Neurons receiving glutamatergic input commonly have a mix of (blank) receptors that mediate kinetically distinct responses

ionotropic

What ions can pass through an NMDA receptor? What is the implication of this?

Na+, K+, Ca++ | there is potential for both depolarization and activation of Ca+ dependent processes

What is a complication with NMDA receptors?

Mg++ blocks the channel if the membrane portential is negative **NDMA receptors alone may not do anything at the resting potential

How can you relieve the block of Mg++ on the NMDA ion channel?

depolarize the neuron **Mg++ will pop out of the channel | activate neighboring AMPA receptors & depolarize the neuron **synaptic plasticity

Upon (blank), no Mg++ blocks the channel pore of the NMDA receptor

depolarization

With postsynaptic depolarization caused by activation of AMPA receptors there is Ca2+ entry through NMDA receptors that can activate many things including (blank)

long-term potentiation

What enables NMDA receptors to pass Ca++ and triggers biochemical events that don't happen in NMDA alone?

AMPA depolarization

The power of a glutamate synapse is adjustable. After high frequency stimulation, stimulation of the pathway results in a larger EPSP. This effect lasts a long time (hours). What is this referred to as?

long-term potentiation

The combination of activation of both AMPA and NMDA receptors is required for (blank) entry. Once you have (blank) in the picture, anything is possible.

Ca++; Ca++

What is this? Reduced blood flow --> high levels of extracellular glutamate --> elevates Ca++ -->kills neurons with glutamate receptors

excitotoxicity

coupled to various types of G-proteins regulating multiple cellular processes including the opening and closing of ion channels

metabotropic glutamate receptors

A major inhibitory neurotransmitter.

GABA

How is GABA inactivated? What are the ionotropic receptors that commonly mediate IPSPs? What activates GABA(a)? What is the metabotropic receptor?

inactivated by uptake; GABA(a) and GABA(c) Benzodiazepines GABA(b)

(blank) (Valium® and Librium®) activate ionotropic GABA receptors reducing anxiety. (blank) (phenobarbital, pentobarbital) activate some ionotropic GABA receptors in anesthesia. Some effects of (blank) are mediated by ionotropic GABA receptors

Benzodiazepines Barbiturates alcohol

The other inhibitory neurotransmitter that also activates ionotropic Cl- channels. Particularly important in the spinal cord where they are blocked by strychnine

Glycine

List some biogenic amines.

catecholamines (dopamine, norepi, epi) histamine serotonin

What's the rate limiting enzyme in the formation of the catecholamines?

tyrosine hydroxylase | tyrosine --> DOPA --> dopamine --> norepi --> epi

How is dopamine inactivated? What inhibits its inactivation?

Na+ dependent uptake; cocaine

Dopaminergic neurons projecting from (blank) to corpus striatum (caudate and putamen) are important in coordinating movements (Parkinson’s Disease)

substantia nigra

Dopaminergic neurons projecting from substantia nigra to (blank) (caudate and putamen) are important in coordinating movements (Parkinson’s Disease)

corpus striatum

The neurotransmitter released by sympathetic post-ganglionic neurons. Also important in the CNS

Norepi

How is norepi inactivated?

NET * *also transports dopamine * *inhibited by amphetamines

A transmitter in the CNS. Inactivation mechanism is uptake but the transporter is not identified (yet). a- and b-adrenergic receptors (metabotropic). Adrenergic neurons are located in lower brainstem (medulla). They project to hypothalamus and thalamus. The function is not clear.

epinephrine

``` A neurotransmitter in the CNS. Very important PERIPHERALLY as well allergic responses pain itch Metabotropic receptors Inactivation mechanism is uptake ```

histamine

Disregulation of (blank) pathways in the CNS is linked to psychiatric disorders. (blank) is also important in pain and in the GI tract.

serotonergic; serotonin

What is serotonin synthesized from? What enzyme is involved?

tryptophan; tryptophan-5-hydroxylase

How is serotonin inactivated?

by a specific transporter (SERT) | **inhibited by Prozac and other anti-depressants

(blank) receptors 5-HT1, 5-HT2, 5-HT4 – 5HT7 do the usual things. (blank) receptors 5-HT3 are nonselective cation channels.

metabotropic | ionotropic

What are the purines?

ATP ADP AMP adenosine

(blank) transmission is important in the periphery (smooth muscle) and in the central nervous system (mechanosensation and pain). (blank) is released along with all the other neurotransmitters (co-transmission). There are important purinergic receptors with different sensitivities to each of the purines. Extracellular ecto-5’ nucleotidases convert the ATP to a soup of purines. Thus, one has a mix of purines (ATP, ADP, AMP, adenosine) hitting a mix of receptors.

purinergic; | ATP

``` Genes encoding (blank) have a signal sequence that targets the pre-propeptides to the ER and Golgi. **processed to produce more than one ```

neuropeptides

List some neuropeptides

brain/gut peptides *substance P opioid peptides *endorphins, enkephalins, dynorphins pituitary peptides hypothalamic peptides

Virtually all receptors of neuropeptides are (blank) receptors that do the usual G-protein coupled things.

metabotropic

(blank) can travel to affect distant neurons. | The effects of (blank) are slow and long lasting.

neuropeptides