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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
Q

GAT1

A

GABA repackaged into vesicles as is

26
Q

GAT2

A
  • 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
Q

GABA A Receptors

A

-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
Q

GABA B Receptors

A

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
Q

Glycine

A

Locations: spinal cord, medulla, less in higher areas
Function: mediates spinal inhibition
Production: unmodified amino acid
Termination: GAT proteins and recycling

30
Q

Glycine Receptors

A
  • 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
Q

Purines

A
  • 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
Q

P1 Purine Receptors

A

bind adenosine
post-synaptic locations: sleep induction, general inhibition of neural function
pre-synaptic locations: inhibit NT release

33
Q

P2 Purine Receptors

A

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
Q

Opioids

A

endorphins, enkephalins, dynorphins, nociceptins
Location: basal ganglia, hypothalamus, pontine and medullary sites
Function: modify nociceptive inputs, mood

35
Q

Opioid Pre-Cursors

A

Proopiomelanocortinin: pre-cursor to B-endorphines and ACTH
Pro-Enkephalin: met-enkephalin, leu-enkephalin
Pro-Dynorphin: dynorphin
Orphanin: nociceptin

36
Q

Opioid Synthesis and Termination

A

standard protein synthesis in cell body

removed via reuptake and destruction by enkephalinase and aminopeptidase

37
Q

Mu Receptors

A

opioid receptor
metabotropic
Gi/Go
increased K efflux and hyperpolarization = inhibit
role in analgesia, respiratory depression, euphoria, constipation, sedation

38
Q

Kappa Receptors

A

opioid receptor
serpentine
Gi/Go
reduced calcium influx = indirect inhibition
produces analgesia, dysphoria, diuresis, miosis

39
Q

Delta Receptors

A

opioid receptor
Gi/Go
serpentine
analgesia

40
Q

Endocannabinoid Active Ingredients

A

anandamide, 2-arachidonylglycerol

41
Q

Endocannabinoids

A

Basal ganglia: mood, motor performance
Spinal cord: modulation of nociception
Cortex: neuroprotection
Hippocampus and Hypothalamus

42
Q

Endocannabinoid Synthesis

A

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
Q

CB1 Receptor

A
  • 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
Q

CB2 Receptor

A
  • in microglia
  • neuronal locations associated with nerve injury
  • high response to injury/inflammation
45
Q

Anandamide Hydrolysis

A

via Fatty Acid Amide Hydrolase

46
Q

2-AG Hydrolysis

A

via mono-acyl glycerol lipase

47
Q

Oxidation of Endocannabinoids

A

via cyclooxygenase and lipooxygenase (both AEA and 2-AG)

48
Q

EAA

A

glutamate
aspartate: NT in visual cortex and pyramidal cells
widely in CNS

49
Q

NMDA Receptor

A

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
Q

AMPA Receptor

A 
activated by AMPA exogenously
asp/glut endogenously
ionotropic
sodium influx
Benzo site: benzos reduce Na influx and decreases excitation
51
Q

Kainate Receptor

A

opened by Kainic acid to allow Na influx and some Ca

52
Q

Non-NMDA Receptor Activation

A

short EPSP due to Na

53
Q

NMDA Receptor Activation

A

long latency (bc kicking Mg out) and long duration (bc of Ca influx and how long channel is open)

54
Q

EPSP

A
  • 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
Q

Non-NMDA Receptor Functions

A
  • sensory afferents

- upper motor neurons

56
Q

NMDA Receptor Functions

A

short-term and long-term memory formation

synaptic plasticity

57
Q

EAA Metabotropic Receptors

A

Group 1: Gq
Group 2 and 3: Gi
Pre-synaptic: control NT release via feedback
Post-Synaptic: learning, memory, motor systems

58
Q

EAA Control

A

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
Q

NMDA Receptors and NO

A

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
Q

Neuronal Functions of NO

A

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
Q

Non-Neuronal Functions of NO

A
  • released by macrophages bc toxic to bacteria

- EDRF = vasodilator

Neuroendocrine Exam 2 (11 decks)

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