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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
What are the neural functions of NO?
``` Memory -long term potentiation -in hippocampus and cerebellum -elsewhere Cardiovascular and respiratory control -pons and medulla Potent vasodilator in the CVS ```
26
What is the immunological role of NO?
Macrophages -> toxic to bacteria
27
What is the downside of NO?
Vary unstable - has a short half life Leads to production of free radicals In high concentrations it becomes toxic to neurons and kills them
28
What are the monoamines?
Class of NTs that includes all those that are created by modifying single amino acids Includes epinephrine, NE, dopamine, serotonin and histamine
29
Where does norepinephrine synthesis occur and what is its role as a NT?
Locus ceruleus, other pontine/medullary areas Role: wakefulness/altertness (Independent of the ANS)
30
Where does epinephrine synthesis occur and what is its role?
Medulla | Role: modulatory
31
Describe the synthesis of epinephrine and NE
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
32
What moves NE and epinephrine into vesicles during synthesis?
VMAT1 and VMAT 2 | Inhibited by reserpine (leads to synaptic failure)
33
What limits the actions of epinephrine and NE?
Reuptake | Enzymatic degradation of monoamine oxidase or catechol-O-methyl transferase
34
Where is monoamine oxidase found?
Outer surface of mitochondria | Metabolites release into ECF
35
Where is a catechol-O-methyl transferase (COMT) found?
Glial cells/post synaptic membrane | Have polymorphisms that are associated with increased risk of psychiatric disorders including anxiety and depression
36
What do epinephrine and NE bind to?
Two general classes of receptors including alpha and beta adrenergic receptors Both are serpentine receptors
37
Where can dopamine synthesis be found?
``` Basal ganglia (motor control) Hypothalamus and limbic system (endocrine and emotional control aka mood) Cortex ```
38
How is dopamine made?
Precursor to epinephrine and NE
39
How are the actions of dopamine limited?
Reuptake | Catabolism by MAO and COMT -> release to ECF
40
What does dopamine bind to?
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)
41
Where is serotonin (5HT) found?
Cerebellum (modification of motor activity) Hypothalamus and limbic system (mood) Brainstem raphe nuclei (modification of motor and sensory activity)*
42
How is serotonin made?
Derived from tryptophan | Tryptophan hydroxylase
43
How are the actions of serotonin limited?
Reuptake | Catabolism of MAO and COMT
44
What are the receptors for serotonin?
7 receptor types 5HT 1, 2, 4, 5 and 6 One ionotropic receptor: 5HT3 (Na influx)
45
What role does 5HT3 receptor play?
Located in area postrema | Illicit vomiting when activated
46
What is the role of 5HT6 receptor?
Anti depressant effects
47
Where is histamine found?
Tuberomammillary nucleus of hypothalamus | Critical for wakefulness
48
How is histamine made?
Derived from histidine | Histidine decarboxylase
49
How are the actions of histamine limited?
Reuptake | Catabolism diamine oxidase and COMT
50
What receptors does histamine bind to?
3 receptor types Serpentine receptors: H1 (PLC activation), H2 (increases cAMP associated with gastric acid release), H2 (presynaptic R that decreases histamine release)
51
Which histamine receptors are more abundant in the brain?
More H1 and 3 | H1 involved in wakefulness
52
What are the two major inhibitory amino acids?
GABA (gamma-amino butyric acid) and glycine
53
Where is GABA found?
Widely distributed throughout higher levels of CNS Cortex, cerebellum, basal ganglia Spinal cord has the least GABA of all
54
What is GABA critical in?
Consciousness, motor control and vision (retina)
55
How is GABA synthesized?
From glutamate Important enzyme: glutamate decarboxylase (GAD) Transported into vesicles by vascular GABA transporter protein (VGAT)
56
What removes GABA from the synapse after synthesis?
GAT (GABA transporter) | Two forms: GAT1 (on the presynaptic terminal) and GAT2 (on glial cells surrounding the synapse)
57
What happens when GABA is taken up into the presynaptic membrane by GAT1?
The GABA is repackaged into vesicles as is
58
If GAT2 (on astrocytes) takes up GABA what happens?
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
Describe GABA-A receptors
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
Where are a large number of extra synaptic GABA-A receptors found?
On neurons of the cortex | Believed to be the site of action for a number of general anesthetics including propofol
61
Describe GABA-B receptors
Metabotropic | Gi/Go protein coupled which activate a K channel (GIRK) and close down/inhibit a Ca channel
62
Where are GABA-B receptors located?
Pre synaptically where they regulate NT release | and post synaptically where they inhibit the post synaptic cell
63
Where is glycine found?
Spinal cord (major) Brainstem (medulla) Much less in higher areas of CNS
64
What is the function of glycine?
Mediates many spinal inhibitions
65
How is glycine produced?
The unmodified amino acid
66
How is glycine removed from the synapse?
``` GAT proteins (same as GABA) Recycling ```
67
Which receptors does glycine bind to?
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
What are the purines?
ATP, ADP and adenosine
69
Described purine synthesis and vesicular storage
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
Where are purines found?
Virtually everywhere in the CNs | Special mention to cortex, cerebellum, hippocampus and basal ganglia
71
What are the two major classes for purine receptors?
P1 (aka A receptors) | P2 receptors
72
Describe P1 receptors
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
Describe the P2 receptors
P2X receptors are ionotropic and ligand is ATP | P2Y is metabotropic with ATP, ADP, UTP and UDP as ligands + coupled to Gi/Gq
74
What are the functions of P2 receptors?
Learning and memory (co-release with EAA) | Modification of locomotor pathways
75
Describe peptide transmitters
Are peptides made in the soma and transported down the axon via fast axonal transport Includes opioids, tachykinins (substance P), CCK and somatostatin
76
The opioids are a family of peptides that include what?
The endorphins (endogenous morphines), enkephalins, dynoprhins and nociception
77
Where are opioids found?
Basal ganglia Hypothalamus Multiple pontine and medullary sites
78
What are the general functions of the opioids?
Modification of nociceptive inputs (cutaneous senses) | Mood/affect (neurophysiology of emotion/drug addiction)
79
What are the 4 precursor molecules for the opioids?
Proopiomelanocortinin (POMC - the precursor molecule of ACTH) -> beta-endorphins Pro-enkephalin Pro-dynorphin Orphanin FQ -> nociception
80
What does pre-enkaphalin form?
Tyr-gly-gly-Phe-X X = methionine = Met-enkephalin X = leucine = leu-enkephalin
81
How are the opioids synthesized?
Standard protein synthesis in the cell body
82
How are the opioids removed from the trough/cleft?
Probably reuptake | Enzymatic destruction via enkephalinase or aminopeptidase
83
What are the opioid receptors?
``` Mu receptor (metabotropic) Kappa receptors (serpentine) Delete receptor (serpentine) ```
84
What does activation of the Mu receptor (for opioids)?
Analgesia, respiratory depression, euphoria, constipation and sedation Can decrease dyspnea
85
What does the kappa (opioid) receptor produce?
Analgesia And Dysphoria | Diuresis (increased water loss via urine) and miosis
86
What does the delta (opioid) receptor produce when activated?
Analgesia
87
All opioid receptors are what?
Metabotropic (serpentine) and activate second messenger systems with ligand binding All connect to Gi/Go proteins
88
The Mu receptor leads to what?
An increase in K efflux and hyperpolarization
89
The delta and kappa receptors lead to what?
A decrease in Ca influx
90
What are the endocannabinoids?
Exogenous effects through THC | Endogenous effects through anandamide and 2AG
91
Where are endocannabinoids distributed?
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
How are the endocannabinoids synthesized?
Derived from membrane lipids (arachidonic acid) Occurs in presynaptic terminal The synthesis of anandamide and 2AG are separate
93
What is anandamide derived from?
N-arachydonoyl phosphatidyl ethanol (NAPE
94
What is 2AG derived from?
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
What are the cannabinoid receptors?
Cannabinoid receptor 1 and 2 (CB1 and CB2)
96
Describe cannabinoid receptor 1 (CB1)
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
Where is CB1 distributed?
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
Where is the synaptic location for the cannabinoid receptors?
``` 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
How is the CB1 relevant for neurophysiology?
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
Describe the CB2 receptor
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
How are the endocannabinoids degraded?
Two different pathways: hydrolysis or oxidation
102
Describe the hydrolysis pathway of degradation of the endocannabinoids
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
Describe the oxidation pathway of endocannabinoid degradation
Via cycloxoygenase and lipoxygenase pathway (both AEA and 2AG) Associated with prostaglandins

NE Exam 2 (19 decks)

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