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ANAT242 > Lecture 20- Receptors > Flashcards

Lecture 20- Receptors Flashcards

1
Q

What do polyribosomes do?

A

Translate mRNA free in cytosol

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2
Q

What is the post synaptic density?

A

An electron dense area, packed with proteins

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3
Q

What is ATP like?

A

Nucleotides can act as extracellular
signalling molecules
* ATP can act as a neurotransmitter
* Remember its really important role in energy
metabolism, and a source of phosphate groups
* ATP is co-stored and co-released with
classical neurotransmitters
* ATP acts on purinergic receptors
* both ion channel and G-protein coupled

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4
Q

Do all vesicles have only one type of receptor?

A

No some vesicles have mixed categories

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5
Q

What is an example of an enzyme linked receptor? How does it work?

A

Receptor tyrosine kinases”
* Cytosolic domain with intrinsic enzyme (enzyme part of receptor)
activity
or
* Direct association with an enzyme (enzyme close by)

  • Note: each subunit of an enzyme-linked receptor usually has only one
    transmembrane domain.
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6
Q

For receptor tyrosine kinases is the kinase part of the receptor?

A

No, but it is an important part of the complex

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7
Q

What is brain derived neurotrophic factor an example of? How does it work? What is it’s function?

A

-An enzyme-linked receptor

How does it work:
-Neurotrophins bind to TrkB receptors (which are dimers which have a neurotrophic binding site externally and an intrinsic tyrosine kinase domain inwardly)

Function:
-Brain derived neurotropic factor (BDNF) is a neurotrophin
-Neurotrophins are proteins required for the development of the nervous system
-BDNF was first identified as a survival promoting protein and is a member of the
neurotrophin family of growth factors
-High levels of BDNF are found in the hippocampus
-BDNF plays an important role in neuronal
plasticity

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8
Q

How is BDNF synthesized and packaged/ released?

A
  • Synthesized as the precursor proBDNF
  • ProBDNF is not an inactive precursor, it is a signalling protein in its own right
  • Both are released in an activity dependent
    manner

-BDNF is is packaged into dense core vesicles

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9
Q

What is BDNF associated with?

A

BDNF expression is associated with
* normal and pathological aging
* psychiatric disease

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10
Q

What lifestyle choice enhances the expression of BDNF

A
  • Exercise enhances the expression of
    BDNF in normal and pathological
    conditions.
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11
Q

How do the constituted and regulated pathways of BDNF release from vesicles have opposing functions?

A

Regulated pathway:
-Increased mature BDNF
causes…
-Pro survival effects
-Facilitates LTP

Constitutive pathway:
-Increase in pro BDNF
causes…
-Pro-apoptotic effects
-Facilitates LTD

Pro and mature forms of BDNF have opposite effects

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12
Q

At the ionic /cellular level how does BDNF/ TrkB work?

A
  • BDNF undergoes Ca2+ influx-dependent
    release from pre and postsynaptic sites
  • act on ligand-gated ion channels
  • voltage-gated ion channels
  • second-messenger pathways
  • which mediate fast and slow synaptic transmission in neurons

This has multiple actions in the cell

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13
Q

What does it mean when we say Brain derived neurotropic factor (BDNF)
Alters “local protein synthesis” and gene expression….

A

-Change last for long time

-Regulate the transmission of MRNA and synapses

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14
Q

What is Endocannabinoids an example of? What are they and what do they do?

A

-It’s a presynaptic target
- Anandamide and arachidon-oylglycerol (2-AG)
-Endogenous ligand for the cannabis receptors (CB1 and CB2)
-small lipid soluble molecules
-synthesized in postsynaptic terminals in response to Ca2+ influx
-acts as a retrograde signal to the presynaptic terminal
-activates CB1 receptors which are coupled to G-proteins
-There are more CB1 receptors than any other
G-protein-coupled receptor in the brain

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15
Q

What does medical marijuana do? What is it an example of?

A

-“medical marijuana” to stimulate appetite in
patients with chronic diseases, cancer and
AIDS, via enhancing the sense of smell
-Is a Endocannabinoid

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16
Q

What are some fast acting receptors?

A

Ligand-gated ion channels
* milliseconds
* have intrinsic ion channels (ligand gated
ion channels)
* channel opens to allow influx or efflux of
ions
* excitatory or inhibitory depending on ion
involved and its direction of movement

17
Q

What are some examples of neurotransmitter that act on ligand gated/ fast acting receptors?

A

Glutamate and GABA

most CNS synapses are mediated by the
amino acids:
* glutamate (Glu),
* gamma-aminobutyric acid (GABA), or
* glycine (Gly)

18
Q

What does GABA stand for and what are the two types of receptors that it can act on? (what are these receptors types)

A

GABA: Gamma aminobutyric acid
GABA-A receptors: ionotropic
GABA-B receptors: metabotropic

19
Q

How is GABA synthesized? What does this mean in terms of localizing GABA?

A
  • GABA is an amino acid but it is not found in proteins
  • GABA is synthesized in GABA’ergic neurons by glutamic acid decarboxylases
    (GADs).
  • GADs therefore are good markers for GABA’ergic neurons
20
Q

What cycle exists with GABA?

A

-Synthesized in the GABAergic neuron (presynaptic terminal). Goes from glutamine to glutamate then GABA
-GABA then loaded into vesicles via a neurotransmitter
-Goes across clef interacts with receptors on post synaptic neuron
-Then taken up by astrocytes for metabolism
-Glutamine is returned to the presynaptic terminal via the astrocyte so the process can repeat (recycling mechanism)

21
Q

Where are GABA-A receptors located?

A
  • Widespread- CNS and PNS, e.g.
  • Limbic system
  • Eye
  • Amygdala
  • Neurons, oligodendrocytes and
    Schwann cells
  • NMJ
22
Q

Are GABA-A receptors diverse?

A

Yes, there is a huge variety of subunits that can make them up

23
Q

What is the structure of GABA receptors like?

A

-Each segment= a subunit
-Between subunits are GABA binding sites which are not specific to the subunit
-Across the membrane there is an Extracellular end terminal, 4 transmembrane domains and intracellular end terminal

24
Q

What type of electrical potential are GABA-A receptors associated with? What happens?

A

Inhibitory Postsynaptic Potential (IPSP)
* Activation of GABA (or glycine)-gated ion
channels causes an IPSP.
* An inhibitory postsynaptic potential (IPSP) is a
transient hyperpolarization of the postsynaptic
membrane potential caused by the presynaptic
release.
* Via opening of Chloride ion channels and resulting influx of Cl-
* Results in inhibition of the target cells
* More negative inside, and thus less likely to fire
* GABA’ergic interneurons
* Modulatory effects within a network

25
Q

What do Benzodiazepines & ethanol so with regards to GABA?

A

Enhance it’s natural effect

26
Q

What is the activity at GABA-A receptors like?

A
  • Synaptic and extrasynaptic sites
  • Mediate phasic and tonic inhibition
  • In phasic inhibition, GABA is released from
    presynaptic terminals and binds to
    postsynaptic GABAARs
  • In tonic inhibition, ambient extracellular
    GABA binds to extrasynaptic GABAARs
    and modulates resting membrane
    potentials and cell excitability
27
Q

What are drugs that enhance GABA action? What do pet scans show about GABA activity in people with anxiety disorders?

A
  • Drugs that enhance GABA action are anxiolytic - reduce anxiety (or panic)
  • People with anxiety disorders can have
    reduced GABA activity
  • The figures shows the level of GABA receptors in a person with a panic disorder
    (right) relative to a person who does not.
28
Q

What type of receptor are GABA-B receptors?

A

G-protein coupled receptors

29
Q

Where are GABA-B receptors located in the brain?

A

-Widespread in the brain
-* Located both pre synaptically and postsynaptically,

30
Q

What are GABA-B receptors associated with?

A

*GABAB receptor associated with epilepsy,
spasticity, schizophrenia, anxiety, depression,
cognitive deficits, and addiction

31
Q

Where acetylcholine receptors located in the brain?

A

Widespread location
* transmitter at the neuromuscular junction,
autonomic ganglia, postganglionic
parasympathetic synapses
* interneurons in striatum and cortex
* and a diffuse modulatory system - neurons
originate in midbrain and project to cortex,
hippocampus and amygdaloid complex

32
Q

What is the action of choline acetyltransferase/ acetylcholinesterase and therefore what is a potential treatment for disease involving acetylcholine?

A

choline taken up into nerve terminal
* ACh synthesized by choline
acetyltransferase
* ACh transported into vesicles
* following synaptic release ACh degraded by
acetylcholinesterase

  • Acetylcholine esterase inhibitors are used as
    one of out only therapies for Alzheimer’s disease (not broken down as fast means sits in synapse for longer)
  • Target for insecticides
  • Chemical weapons and drugs
33
Q

What are the different types of acetylcholine receptors?

A

-Can be metabotropic or ionotropic
-Homomeric nAChRs: Form a calcium channel which is very important
-There is also heteromeric nAChRs

The subunits mixing and matching is what creates these different subunits

34
Q

How is the idea of same signal, different responses illustrated by Acetylcholine?

A

-The specific way a cell responds to an extracellular signal depends on
its receptors and intracellular machinery used to interpret the signal.
-For example, with acetylcholine on a heart muscle cell it results in a decreased rate and force of contraction. On a salivary gland cell it causes secretion. On a Skeletal muscle cell it results in contraction

35
Q

What is Muscarinic AchR like?

A
  • Sensitive to muscarine
  • G-protein coupled (GPC)
  • Found for example in:
  • Glia
  • Heart muscle
  • Salivary glands
36
Q

What is Nicotinic AchR like?

A
  • Sensitive to nicotine
  • ligand gated ion channel
  • mediate fast synaptic transmission
  • occur in high density at neuromuscular
    junction
    ~ 20,000 µm2
  • sensitive to a-bungarotoxin
37
Q

Where are acetylcholine receptors located? Where are sodium channels located?

(in the postsynaptic membrane)

A

-On crest of junctional folds (post synaptic membrane) so can act quickly when acetylcholine is released
-Sodium channels at base of junctional fold

ANAT242 (25 decks)

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