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NE Exam 2 > Neurotransmitter Systems > Flashcards

Neurotransmitter Systems Flashcards

1
Q

Where are neurotransmitters made?

A

In cell bodies in the brain

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2
Q

Where are the receptors for the NTs located?

A

Usually outside the CNS (may travel a long distance)

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3
Q

What do the raphe nuclei make?

A

Serotonin

Meaning the cell bodies that make this NT (serotonergic) are within the raphe nuclei

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4
Q

What are the excitatory amino acids?

A

Glutamate and Aspartate

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5
Q

What are the different NT systems?

A

Excitatory amino acids, monoamines, cholinergic, inhibitory amino acids, purines, opioids and endocannabinoids

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6
Q

What is glutamate?

A

Derived from alpha ketoglutarate

Metabolic and transmitter pool strictly separate

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7
Q

What is Aspartate?

A

Often co-localized with glutamate
Serves as NT on its own in visual cortex and pyramidal cells
Metabolic and transmitter pool strictly separated

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8
Q

Where are the EAA located?

A

Most important excitatory NT system in the brain

Widely distributed throughout the CNS

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9
Q

What are the receptors for the EAA?

A 
Both ionotropic (allows ions in) and metabotropic receptors (G-protein coupled) 
Several kinds of each
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10
Q

What are the ionotropic EEA receptors?

A

NMDA (N-methyl-D-aspartate) receptor

Non-NMDA receptors including AMPA and kainate (primarily Na influx).

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11
Q

What is the NMDA receptor?

A

NMDA is an exogenous agent that activates this receptor
Glutamate, aspartate, etc all active them in the body
When activated the channel allows influx of Ca
Has multiple modulators sites (glycine binding site, PCP binding site and magnesium binding site)

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12
Q

Describe the glycine binding site of the NMDA receptor

A

Is a required co-agonist but it alone cannot open the channel
Both EAA and glycine must be present for the channel to open

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13
Q

Describe the Mg binding site of the NMDA receptor

A

Within the channel itself
Blocks the channel at resting membrane potentials
Prevents Ca influx when the channel opens
Makes the NMDA receptor both ligand and voltage gated

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14
Q

Describe the PCP binding site on the NMDA receptor

A

Horse tranquilizer and hallucinogen

Blocks the channel preventing Ca influx

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15
Q

Describe the AMPA (non-NMDA) ionotropic receptor for EAA

A

Exogenous agent AMPA activated
Glutamate/Aspartate are the endogenous ligands
Modulator sites as well
Na influx when open
Benzodiazepines bind to a site on the extracellular face of the protein
-Reduces the amount of Na that enters

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16
Q

Describe the kainate non-NMDA ionotropic receptor

A

Allows for Na and some Ca entry

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17
Q

What is the result of EAA ligands binding to ionotropic receptors?

A

Activation of the non-NMDA receptors produces a typically excitatory synaptic potential (epsp) with a relatively short onset and duration
While activation of the NMDA receptors produces a long latency epsp (due to Na leaving) with a long duration (due to Ca influx)

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18
Q

Describe the co-localization of non-NMDA and NMDA receptors on the post-synaptic membrane (EAA)

A

EAA released
Binds to both types of receptors
Both non-NMDA and NMDA channels open, Na flows in via the non-NMDA channels and Ca cannot enter the NMDA channel because of the Mg
The non-NMDA receptor activation produces the typical epsp
The epsp can provide a sufficient depolarization to cause the Mg to leave the NMDA channel
Ca now enters the NMDA channel producing the longer lasting epsp

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19
Q

Non-NMDA receptors do exist on post synaptic membranes without what?

A

NMDA receptors in some systems

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20
Q

What is the function of non-NMDA ionotropic receptors?

A

Primary sensory afferent

Upper motor neurons (pre-motor neurons)

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21
Q

What are the functions of NMDA ionotropic receptors?

A

Critical in short and long term memory formation

Synaptic plasticity in many forms

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22
Q

What are the three groups of EAA metabotropic receptors?

A

Group 1: coupled to Gq

Groups 2 and 3: coupled to Gi

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23
Q

What doe pre-synaptic metabotropic EAA receptors control?

A

NT release

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24
Q

What are post synaptic metabotropic EAA receptors involved with?

A

Learning, memory and motor systems

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25
Q

What are the neural functions of NO?

A 
Memory 
-long term potentiation 
-in hippocampus and cerebellum 
-elsewhere 
Cardiovascular and respiratory control 
-pons and medulla 
Potent vasodilator in the CVS
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26
Q

What is the immunological role of NO?

A

Macrophages -> toxic to bacteria

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27
Q

What is the downside of NO?

A

Vary unstable - has a short half life
Leads to production of free radicals
In high concentrations it becomes toxic to neurons and kills them

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28
Q

What are the monoamines?

A

Class of NTs that includes all those that are created by modifying single amino acids
Includes epinephrine, NE, dopamine, serotonin and histamine

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29
Q

Where does norepinephrine synthesis occur and what is its role as a NT?

A

Locus ceruleus, other pontine/medullary areas
Role: wakefulness/altertness
(Independent of the ANS)

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30
Q

Where does epinephrine synthesis occur and what is its role?

A

Medulla

Role: modulatory

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31
Q

Describe the synthesis of epinephrine and NE

A

Derived from tyrosine (along with dopamine)
Tyrosine -> L-DOPA -> dopamine -> NE -> epi
Tyrosine hydroxylase conversion of tyrosine to DOPA is RLS
Then moved into vesicles
NE created
Neurons that have phenoethanolamine-N-methyl transferase (PNMT) covert NE to epi after NE leaves the vesicles
Epinephrine moved back into vesicles

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32
Q

What moves NE and epinephrine into vesicles during synthesis?

A

VMAT1 and VMAT 2

Inhibited by reserpine (leads to synaptic failure)

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33
Q

What limits the actions of epinephrine and NE?

A

Reuptake

Enzymatic degradation of monoamine oxidase or catechol-O-methyl transferase

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34
Q

Where is monoamine oxidase found?

A

Outer surface of mitochondria

Metabolites release into ECF

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35
Q

Where is a catechol-O-methyl transferase (COMT) found?

A

Glial cells/post synaptic membrane

Have polymorphisms that are associated with increased risk of psychiatric disorders including anxiety and depression

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36
Q

What do epinephrine and NE bind to?

A

Two general classes of receptors including alpha and beta adrenergic receptors
Both are serpentine receptors

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37
Q

Where can dopamine synthesis be found?

A 
Basal ganglia (motor control) 
Hypothalamus and limbic system (endocrine and emotional control aka mood) 
Cortex
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38
Q

How is dopamine made?

A

Precursor to epinephrine and NE

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39
Q

How are the actions of dopamine limited?

A

Reuptake

Catabolism by MAO and COMT -> release to ECF

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40
Q

What does dopamine bind to?

A

5 receptor types with multiple subtypes
Metabotropic (serpentine) receptors
Connected to G proteins including D1 and D5 (increase cAMP), D2 (decrease cAMP and increase K permeability/efflux resulting in inhibition), and D3 and D4 (decrease cAMP)

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41
Q

Where is serotonin (5HT) found?

A

Cerebellum (modification of motor activity)
Hypothalamus and limbic system (mood)
Brainstem raphe nuclei (modification of motor and sensory activity)*

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42
Q

How is serotonin made?

A

Derived from tryptophan

Tryptophan hydroxylase

43
Q

How are the actions of serotonin limited?

A

Reuptake

Catabolism of MAO and COMT

44
Q

What are the receptors for serotonin?

A

7 receptor types
5HT 1, 2, 4, 5 and 6
One ionotropic receptor: 5HT3 (Na influx)

45
Q

What role does 5HT3 receptor play?

A

Located in area postrema

Illicit vomiting when activated

46
Q

What is the role of 5HT6 receptor?

A

Anti depressant effects

47
Q

Where is histamine found?

A

Tuberomammillary nucleus of hypothalamus

Critical for wakefulness

48
Q

How is histamine made?

A

Derived from histidine

Histidine decarboxylase

49
Q

How are the actions of histamine limited?

A

Reuptake

Catabolism diamine oxidase and COMT

50
Q

What receptors does histamine bind to?

A

3 receptor types
Serpentine receptors: H1 (PLC activation), H2 (increases cAMP associated with gastric acid release), H2 (presynaptic R that decreases histamine release)

51
Q

Which histamine receptors are more abundant in the brain?

A

More H1 and 3

H1 involved in wakefulness

52
Q

What are the two major inhibitory amino acids?

A

GABA (gamma-amino butyric acid) and glycine

53
Q

Where is GABA found?

A

Widely distributed throughout higher levels of CNS
Cortex, cerebellum, basal ganglia
Spinal cord has the least GABA of all

54
Q

What is GABA critical in?

A

Consciousness, motor control and vision (retina)

55
Q

How is GABA synthesized?

A

From glutamate
Important enzyme: glutamate decarboxylase (GAD)
Transported into vesicles by vascular GABA transporter protein (VGAT)

56
Q

What removes GABA from the synapse after synthesis?

A

GAT (GABA transporter)

Two forms: GAT1 (on the presynaptic terminal) and GAT2 (on glial cells surrounding the synapse)

57
Q

What happens when GABA is taken up into the presynaptic membrane by GAT1?

A

The GABA is repackaged into vesicles as is

58
Q

If GAT2 (on astrocytes) takes up GABA what happens?

A

The GABA is converted into glutamine and released into the ECF where it will be taken up by the presynaptic terminal and recycled into GABA

59
Q

Describe GABA-A receptors

A

Ionotropic (Cl conductance, allows Cl influx when activated)
Activation produces IPSPs in adult neurons
Multiple biding sites modulate including benzodiazepine site, ethanol, certain steroids (these all potentiate its action causing bigger IPSPs)

60
Q

Where are a large number of extra synaptic GABA-A receptors found?

A

On neurons of the cortex

Believed to be the site of action for a number of general anesthetics including propofol

61
Q

Describe GABA-B receptors

A

Metabotropic

Gi/Go protein coupled which activate a K channel (GIRK) and close down/inhibit a Ca channel

62
Q

Where are GABA-B receptors located?

A

Pre synaptically where they regulate NT release

and post synaptically where they inhibit the post synaptic cell

63
Q

Where is glycine found?

A

Spinal cord (major)
Brainstem (medulla)
Much less in higher areas of CNS

64
Q

What is the function of glycine?

A

Mediates many spinal inhibitions

65
Q

How is glycine produced?

A

The unmodified amino acid

66
Q

How is glycine removed from the synapse?

A 
GAT proteins (same as GABA) 
Recycling
67
Q

Which receptors does glycine bind to?

A

Ionotropic (allows Cl in)
Influx of Cl leads to IPSPs
Ethanol and general anesthetics bind to it and potentiate
Strychnine binds to it and blocks it

68
Q

What are the purines?

A

ATP, ADP and adenosine

69
Q

Described purine synthesis and vesicular storage

A

ATP by mitochondria (presynaptic terminal has many mitochondria)
Stored in vesicles (VNUT protein)
Released as ATP
ATP -> ADP -> adenosine (break down occurs in synaptic trough)

70
Q

Where are purines found?

A

Virtually everywhere in the CNs

Special mention to cortex, cerebellum, hippocampus and basal ganglia

71
Q

What are the two major classes for purine receptors?

A

P1 (aka A receptors)

P2 receptors

72
Q

Describe P1 receptors

A

Ligand: adenosine
Postsynaptic locations (sleep induction and general inhibition of neural function - it can stop the heart for a few secs))
Presynaptic locations (inhibition of NT releasE)
Caffein inhibits adenosine receptor

73
Q

Describe the P2 receptors

A

P2X receptors are ionotropic and ligand is ATP

P2Y is metabotropic with ATP, ADP, UTP and UDP as ligands + coupled to Gi/Gq

74
Q

What are the functions of P2 receptors?

A

Learning and memory (co-release with EAA)

Modification of locomotor pathways

75
Q

Describe peptide transmitters

A

Are peptides made in the soma and transported down the axon via fast axonal transport
Includes opioids, tachykinins (substance P), CCK and somatostatin

76
Q

The opioids are a family of peptides that include what?

A

The endorphins (endogenous morphines), enkephalins, dynoprhins and nociception

77
Q

Where are opioids found?

A

Basal ganglia
Hypothalamus
Multiple pontine and medullary sites

78
Q

What are the general functions of the opioids?

A

Modification of nociceptive inputs (cutaneous senses)

Mood/affect (neurophysiology of emotion/drug addiction)

79
Q

What are the 4 precursor molecules for the opioids?

A

Proopiomelanocortinin (POMC - the precursor molecule of ACTH) -> beta-endorphins
Pro-enkephalin
Pro-dynorphin
Orphanin FQ -> nociception

80
Q

What does pre-enkaphalin form?

A

Tyr-gly-gly-Phe-X
X = methionine = Met-enkephalin
X = leucine = leu-enkephalin

81
Q

How are the opioids synthesized?

A

Standard protein synthesis in the cell body

82
Q

How are the opioids removed from the trough/cleft?

A

Probably reuptake

Enzymatic destruction via enkephalinase or aminopeptidase

83
Q

What are the opioid receptors?

A 
Mu receptor (metabotropic) 
Kappa receptors (serpentine) 
Delete receptor (serpentine)
84
Q

What does activation of the Mu receptor (for opioids)?

A

Analgesia, respiratory depression, euphoria, constipation and sedation
Can decrease dyspnea

85
Q

What does the kappa (opioid) receptor produce?

A

Analgesia And Dysphoria

Diuresis (increased water loss via urine) and miosis

86
Q

What does the delta (opioid) receptor produce when activated?

A

Analgesia

87
Q

All opioid receptors are what?

A

Metabotropic (serpentine) and activate second messenger systems with ligand binding
All connect to Gi/Go proteins

88
Q

The Mu receptor leads to what?

A

An increase in K efflux and hyperpolarization

89
Q

The delta and kappa receptors lead to what?

A

A decrease in Ca influx

90
Q

What are the endocannabinoids?

A

Exogenous effects through THC

Endogenous effects through anandamide and 2AG

91
Q

Where are endocannabinoids distributed?

A

Broadly in the CNS
Basal ganglia (mood and motor performance)
Spinal cord (modulation of nociception)
Cortex (neuroprotection)

Hippocampus (memory formation)
Hypothalamus (control of energy/hunger)

92
Q

How are the endocannabinoids synthesized?

A

Derived from membrane lipids (arachidonic acid)
Occurs in presynaptic terminal
The synthesis of anandamide and 2AG are separate

93
Q

What is anandamide derived from?

A

N-arachydonoyl phosphatidyl ethanol (NAPE

94
Q

What is 2AG derived from?

A

Arachidonoyl-containing phosphatidyl inositol bisphoshate (PIP2)
A major source for arachidonic acid in certain tissues especially brain
Consequence: pharmacological manipulation of 2AG production has wide reaching effects beyond those on the endocannabinoid system

95
Q

What are the cannabinoid receptors?

A

Cannabinoid receptor 1 and 2 (CB1 and CB2)

96
Q

Describe cannabinoid receptor 1 (CB1)

A

Neuronal location
Activation associated with the psychoactive responses to the cannabinoid pes
97-99% homology with the mouse and rat versions of the receptor (must be critical)
Polymorphisms lined to occurrence of obesity, ADHD, schizophrenia, depression in Parkinson’s disease
Can form a heterodimer with other NT receptors including dopamine and orexin

97
Q

Where is CB1 distributed?

A

CNS
Uniform distribution in the striatum, thalamus, hypothalamus, cerebellum and lower brain stem
Non uniform distribution (associated with specific neuron types): cortex, amygdala and hippocampus

98
Q

Where is the synaptic location for the cannabinoid receptors?

A 
Largely presynaptic 
Some sources will say exclusively 
Generally away from active zone (where the vesicles are) 
Greater density at inhibitory synapses 
Binds AEA and 2AG with high affinity
99
Q

How is the CB1 relevant for neurophysiology?

A

Found on presynaptic terminals of EAA and GABA releasing synapses
Reduces EAA and GABA release
Via Gi coupled protein
Anandamide and 2AG are equally effective

100
Q

Describe the CB2 receptor

A

Found in the brain and on microglia
Neuronal location (dendrites and within soma) are also reported usually associated with nerve injury
Highly inducible in response to injury or inflammation
Binds 2AG better than AEA

101
Q

How are the endocannabinoids degraded?

A

Two different pathways: hydrolysis or oxidation

102
Q

Describe the hydrolysis pathway of degradation of the endocannabinoids

A

Prevalent neurons
Anandamide (AEA) and 2AG are degraded via two speratate pathways
AEA: fatty acid aside hydroxylase (FAAH - has polymorphism that decrease its activity and decreased cannabinoid and decreased sensitivity to pain) and two forms now known to exist
2AG: monoacylglycerol lipase (MAGL)

103
Q

Describe the oxidation pathway of endocannabinoid degradation

A

Via cycloxoygenase and lipoxygenase pathway (both AEA and 2AG)
Associated with prostaglandins

NE Exam 2 (19 decks)

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