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Neuroendocrine Exam 2 > Neurotransmitter Systems > Flashcards

Neurotransmitter Systems Flashcards

1
Q

Monoamines

A

Epinephrine, norepinephrine, dopamine, serotonin, histamine

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2
Q

Norepinephrine

A

Locations: locus ceruleus, pontine/medullary areas
Role: wakefulness/alertness

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3
Q

Epinephrine

A

Locations: medulla
Role: modulatory role

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4
Q

Epinephrine and Norepinephrine Synthesis

A
  • derived from tyrosine
  • tyrosine > dopamine > NE > epinephrine
  • Tyrosine Hydroxylase converts tyrosine to DOPA = rate-limiting
  • moved into vesicles then conversion to NE
  • Phenolethanolamine-N-methyl transferase converts NE to epinephrine once NE leaves vesicles
  • epinephrine moves back into vesicles
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5
Q

Vesicular Monoamine Transporter

A

moves epinephrine and norepinephrine into vesicles
VMAT1 and 2
blocked by reserpine = synaptic failure

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6
Q

Limitation of NE and E actions

A
  • reuptake
  • degradation by MOA: mitochondria outer surface
  • degradation by COMT: glial cells/post-synaptic membrane
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7
Q

Monoamine Receptor Classes

A

Alpha adrenergic
Beta adrenergic
many places in brain; both serpantine

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8
Q

Dopamine

A 
basal ganglia (motor control)
hypothalamus and limbic system (endocrine and emotions)
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9
Q

Dopamine Synthesis

A

precursor to NE and E

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10
Q

Limitation of Dopamine Actions

A

reuptake

catabolism by MOA and COMT and released to ECF

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11
Q

Dopamine Receptors

A

5 Metabotropic and G Protein Receptors
D1 and D5: increase cAMP via Gs = excitatory neurons
D2: decreases cAMP = via Gi/o = potassium efflux > cell hyperpolarization > inhibition
D3 and D4: decreases cAMP via Gi/o

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12
Q

Serotonin

A

Hypothalamus and Limbic System: mood
Cerebellum: motor activity
Brainstem Raphe Nuclei: modification of motor and sensory activity esp nociception

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13
Q

Serotonin Synthesis and Termination

A

tryptophan precursor
made by tryptophan hydroxylase
catabolized by MAO and COMT

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14
Q

Serotonin Receptors

A

7 receptor types
5HT3 ionotropic receptor = Na influx and depolarization; present in area postrema
5HT6 ionotropic receptor = anti-depressant effects
5HT7 = limbic system and mood

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15
Q

Histamine

A

tuberomamillary nucleus and hypothalamus

roles in wakefulness

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16
Q

Histamine Synthesis

A

histidine precursor

histidine decarboxylase enzyme

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17
Q

Histamine Termination

A

reuptake

catabolism by diamine oxidase and COMT

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18
Q

Histamine Receptors

A

3 receptor types
H1: PLC activation via Gq pathway; wakefulness
H2: increase cAMP; gastric acid release; least in brain
H3: pre-synaptic; decrease histamine release

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19
Q

Anti-Histamines

A

H1 receptor blockers

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20
Q

Inhibitory Amino Acids

A

GABA

Glycine

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21
Q

GABA

A

major inhibitory AA in brain
more present in higher areas of CNS
least in spinal cord

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22
Q

GABA Function

A

consciousness, motor control, vision

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23
Q

GABA Synthesis

A 
from glutamate 
glutamate decarboxylase (target of autoimmune responses = neuro sx)
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24
Q

GABA Termination

A

VGAT: transports into vesicles
GAT1: remove from synapse; located on pre-synaptic terminal
GAT2: remove from synapse; located on glial cells

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25
GAT1
GABA repackaged into vesicles as is
26
GAT2
- GABA converted to glutamate and then glutamine by glial cell - must be converted to glutamine bc glutamate has excitatory effects - released to ECF and taken up by pre-synaptic terminal and recycled to GABA
27
GABA A Receptors
-ionotropic; Cl conduction for cell entry and hyperpolarization to create IPSPs Benzo binding site: more Cl- entry and cell inhibition Ethanol and steroid binding sites: cause bigger IPSPs extra GABA A receptors in the synapse respond to anesthetics like propofol
28
GABA B Receptors
metabotropic and Gi/Go coupled activate GIRK K+ channel for K to leave cell Inhibit Ca ++ channel and reduce Ca Pre-synaptic location: regulates release of GABA Post-synaptic location: inhibits post-synaptic cell
29
Glycine
Locations: spinal cord, medulla, less in higher areas Function: mediates spinal inhibition Production: unmodified amino acid Termination: GAT proteins and recycling
30
Glycine Receptors
- ionotropic allow Cl influx cause IPSP - potentiated by alcohol and anesthetics = more Cl and more inhibition - blocked by strychine which causes convulsions via increased excitatory activity
31
Purines
- all vesicles have ATP - Location: everywhere in CNS esp cortex, cerebellum, hippocampus, basal ganglia - Production: ATP by mitochondria, stored in vesicles, released - conversion of ATP to adenosine occurs in synaptic trough
32
P1 Purine Receptors
bind adenosine post-synaptic locations: sleep induction, general inhibition of neural function pre-synaptic locations: inhibit NT release
33
P2 Purine Receptors
P2X: bind ATP, ionotropic, allow Ca and Na in P2Y: bind ATP, ADP, UTP, UDP, metabotropic, Gi/Gs coupled Function: learning and memory (co-release with EAA), locomotor pathway modification
34
Opioids
endorphins, enkephalins, dynorphins, nociceptins Location: basal ganglia, hypothalamus, pontine and medullary sites Function: modify nociceptive inputs, mood
35
Opioid Pre-Cursors
Proopiomelanocortinin: pre-cursor to B-endorphines and ACTH Pro-Enkephalin: met-enkephalin, leu-enkephalin Pro-Dynorphin: dynorphin Orphanin: nociceptin
36
Opioid Synthesis and Termination
standard protein synthesis in cell body | removed via reuptake and destruction by enkephalinase and aminopeptidase
37
Mu Receptors
opioid receptor metabotropic Gi/Go increased K efflux and hyperpolarization = inhibit role in analgesia, respiratory depression, euphoria, constipation, sedation
38
Kappa Receptors
opioid receptor serpentine Gi/Go reduced calcium influx = indirect inhibition produces analgesia, dysphoria, diuresis, miosis
39
Delta Receptors
opioid receptor Gi/Go serpentine analgesia
40
Endocannabinoid Active Ingredients
anandamide, 2-arachidonylglycerol
41
Endocannabinoids
Basal ganglia: mood, motor performance Spinal cord: modulation of nociception Cortex: neuroprotection Hippocampus and Hypothalamus
42
Endocannabinoid Synthesis
from arachidonic acid lipids in presynaptic terminal Anandamide Synthesis: from NAPE 2-AG: from PIP2; 2 AG is major source of arachidonic acid in brain so manipulation pharmacologically has wide range effects
43
CB1 Receptor
- neurons - psychoactive response - Gi coupled - binds AEA and 2-AG with high affinity - locations: striatum, thalamus, hypothalamus, cerebellum, brainstem (uniformly); cortex, amygdala, hippocampus (non-uniform) - largely pre-synaptic in EAA and GABA releasing synapses to reduce their release
44
CB2 Receptor
- in microglia - neuronal locations associated with nerve injury - high response to injury/inflammation
45
Anandamide Hydrolysis
via Fatty Acid Amide Hydrolase
46
2-AG Hydrolysis
via mono-acyl glycerol lipase
47
Oxidation of Endocannabinoids
via cyclooxygenase and lipooxygenase (both AEA and 2-AG)
48
EAA
glutamate aspartate: NT in visual cortex and pyramidal cells widely in CNS
49
NMDA Receptor
ionotropic and voltage gated EAA receptor endogenously activated by NMDA exogenously Ca influx Glycine binding site for modulation; required for channel to open but doesn't open channel on its own; needs EAA Mg binding site within channel blocks channel at resting membrane and prevents calcium influx; leaves channel when cell is depolarized PCP binding site blocks channel when hallucinogen PCP binds and prevents Ca entry
50
AMPA Receptor
``` activated by AMPA exogenously asp/glut endogenously ionotropic sodium influx Benzo site: benzos reduce Na influx and decreases excitation ```
51
Kainate Receptor
opened by Kainic acid to allow Na influx and some Ca
52
Non-NMDA Receptor Activation
short EPSP due to Na
53
NMDA Receptor Activation
long latency (bc kicking Mg out) and long duration (bc of Ca influx and how long channel is open)
54
EPSP
- EAA binds to NMDA and non-NMDA receptors - Na flows into non-NMDA - Ca can'r enter NMDA due to Mg - non-NMDA receptor activity induces EPSP - EPSP causes enough depolarization to cause Mg to leave NMDA channel - Ca enters NMDA channel and longer lasting EPSP occurs
55
Non-NMDA Receptor Functions
- sensory afferents | - upper motor neurons
56
NMDA Receptor Functions
short-term and long-term memory formation | synaptic plasticity
57
EAA Metabotropic Receptors
Group 1: Gq Group 2 and 3: Gi Pre-synaptic: control NT release via feedback Post-Synaptic: learning, memory, motor systems
58
EAA Control
EAA in high concentrations = toxic Glial cells take EAA in via active transport Na/K pump and convert to glutamine glutamine diffuses out and is taken into pre-neuron again
59
NMDA Receptors and NO
EAA binds to NMDA receptors and allows Ca ++ into cell Ca activates calcineurin which activates Nitric oxide synthase NOS takes arginine and cleaves NO leaving NO and citruline NO = very lipid soluble and diffuses across cleft
60
Neuronal Functions of NO
Memory: long term potentiation in hippocampus and cerebellum CV and resp control: pons and medulla high concentrations of NO is toxic to neurons bc half life is short and free radicals are produced which harm neurons
61
Non-Neuronal Functions of NO
- released by macrophages bc toxic to bacteria | - EDRF = vasodilator

Neuroendocrine Exam 2 (11 decks)

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