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Neuro Endocrine 2 > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What are the Monoamines

A

neurotransmitters created by modifying a single amino acid

Epinephrine
Norepinephrine
dopamine
serotonin
histamine
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2
Q

Where is norepinephrine made

A

Locus ceruleus

other pontine/medullary areas

Wakefulness/alertness

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3
Q

WHere is Epinephrine made

A

Medulla

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4
Q

How is Epinephrine and norepinephrine made

A

Derived from tyrosine

tyrosine is converted to dopamine which is converted to norepi then to epi

Tyrosine hydoxylase conversion of tyrosine to DOPA is the rate limiting step

Dopa is moved into vesicles where NE is created and then Phenolethanolamine N Methyl transferase converts the NE to the Epi

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5
Q

What inhibits the movement of Epi and NE being moved into vesicles by VMAT1 and VMAT2

A

Reserpine

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6
Q

How is the action of Epi and Ne limited

A

Reuptake

Enzymatic degradation via monoamine oxidase and Catechol-O-methyltransferase

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7
Q

What do Epinephrine and Norepinephrine bind too

A

alpha and beta adrenergic receptors

serpentine receptors

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8
Q

Where do you find dopamine

A

Basal ganglia
hypothalamus and limbic system
cortex

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9
Q

How is dopamine made

A

precursor to epinephrine made from tyrosine via tyrosine hydroxylase

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10
Q

What does dopamine bind to

A

5 receptor types which are serpentine receptors

D1 and D5: increase cAMP

D2: decrease cAMP and increase potassium efflex

D3 and D4: decrease cAMP

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11
Q

WHere do you find serotonin

A

Hypothalamus and limbic system

Cerebellum

Raphe nuclei

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12
Q

How do you make serotonin

A

derived from tryptophan via tryptophan hydroxylase

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13
Q

How do you limit Serotonin

A

reuptake

Enzymatic degradation via monoamine oxidase and Catechol-O-methyltransferase

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14
Q

what are the receptors of serotonin

A

7 receptors, 6 are serpentine receptors, and one is ionotropic

5HT3 (ionotropic) does Na influx in the area postrema (vomiting)

5HT6: antidepressant effect

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15
Q

Where do we find histamine

A

Tuberomammillary nucleus of the thalamus

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16
Q

How do you make histamine

A

derived from histidine via histidine decarboxylase

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17
Q

How do you limit histamines action

A

reuptake

Enzymatic degradation via diamine oxidase and Catechol-O-methyltransferase

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18
Q

Whate are the receptors of histamine

A

3 serpentine receptors

H1: PLC activation

H2: increase cAMP

H3: presynaptic, decrease histamine release

H1 involved in wakefulness

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19
Q

Where are neurons that make acetylcholine

A

The striatum of basal ganglia: caudate and putamen

these can be found in the midbrain and the pons

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20
Q

How is acetylcholine made and broken down

A

Synthesis of choline and acetate

moved into vesicles via Vesicular Ach Transporter protein (VAchT)

then removed from synapse via acetylcholinesterase

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21
Q

What are the receptors of Aceytylcholine: muscarinic

A

5 muscarinic receptors

Serpentine/metabotropic

M1: neuronal, and increases Ca++

M4: presynaptic autoreceptor, striatum of basal ganglia: decrease cAMP

M5: cerebrovasculature; dopaminergic neurons of basal ganglia: increase IP3/DAG

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22
Q

What are the receptors of Acetylcholine nicotinic receptors

A

located at the NMJ

synapse between pre and post ganglionic cells in autonomic ganglia

various subunits and by changing the subunits changes the properties of the channel and in some central synapses creates a nicotinic channel that allows more calcium in

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23
Q

What is the major role of GABA and where is it found

A

Major inhibitory amino acids in the CNS

widely distributed throughout the higher levels of the CNS

Spinal cord has least GABA of all locations

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24
Q

What roles is GABA critical in

A

Consciousness

Motor control

Vision

25
Q

How is GABA synthesized and removed

A

synthesis from glutamate via glutamate decarboxylase

Transported into vesicles via Vesicular GABA transporter protein

removed via GAT

  • GAT1 is found on the presynaptic terminal
  • GAT2 is found on the glial cells surrounding the synapse (GAT2 will also convert GABA to glutamine and release it the ECF where it will be taken to presynaptic cell and reconverted to GABA
26
Q

GABA a Receptors

A

Ionotropic (Cl conductance

generates an IPSP

Modulates: Benzodiazepine, ethanol, steroids, general anesthetics like propfol

27
Q

GABA b receptors

A

Metabotropic

Gi/Go protein coupled

activate a K+ channel and close down and inhibit Ca++ channel

located:
Presynaptic: regulate NT release
Postsynaptic: inhibition of post synaptic cell

28
Q

Where is Glycine found and what is its function

A

Spinal cord

and much less in higher areas of the CNS

Function: mediate many spinal inhibitions

29
Q

How is glycine produced and removed from the synapse

A

Produced via unmodified amino acid

romoved from the synapse via the GAT proteins

30
Q

What is the receptor of glycine, and what blocks this receptor

A

Ionotropic: Chloride

Influx of chloride leads to ipsp

Ethanol, and general anesthetics also bind to these receptors

Stychnine: binds to it and blocks this glycine receptor

31
Q

Where are purines found in the CNS

A 
found virtually everywhere in the central nervous system especially: 
cortex
cerebellum
hippocampus
basal ganglia
32
Q

P1 receptors of Purines

A

Ligand: Adenosine

Postsynaptic locations: does sleep induction
general inhibition of neural function

Presynaptic locations: Inhibition of neurotransmitter release

33
Q

P2 receptors of Purines

A

P2X: Ionotropic
Ligand: ATP
Manysuptypes

P2Y: Metabotropic
Ligand: ATP, ADP, UTP, UDP
Gi/gq coupled

Functions:
Learning and memory (co release with EAA)
modification of locomotor pathways

34
Q

What are the 4 peptides included in the peptide family, and what are their general functions

A

endorphins
enkephalins
dynorphins
nociceptine

Modification of nociceptive inputs (cutaneus senses)
Mood/Affect (Neurophysiology of emotion/drug addiction)

35
Q

Where are opioids found in the CNS

A

Basal ganglia
hypothalamus
pontine and medullary sites

36
Q

What are the 4 pre precursor molecules

A

Proopiomelanocortinin

Pro-enkephalin

Pro-dynorphin

Orphanin FQ

37
Q

What is the synthesis and removal of the opioids

A

synthesis: standard protein synthesis in the cell body

removal from trough/cleft via reuptake

and ezymatic destruction via: enkephalinase and aminopeptidase

38
Q

What does the Mu receptor do

A

for opioids

Metobotropic recceptor
Gi/Go

Leads to an increase inpotassium efflux and hyperpolarization

Activation causes:
analgesia
respiratory depression
euphoria
constipation
sedation
39
Q

What does the Kappa receptor do

A

for opioids

Serpentine receptor
Gi/Go

Decreases calcium influx

Produces
Analgesia
Dysphoria
diuresis
miosis
40
Q

What does the Delta receptor do

A

it is for opioids

decreases Calcium influx

it is a serpentine receptor
Gi/Go

Produces analgesia when activated

41
Q

What are endocannabinoids

A

Anandamide

2-Arachidonylglycerol (2AG)

42
Q

Where are endocannabinoids found in the CNS

A

Basal ganglia: mood, motor performance

Spinal cord: modulation of nociception

Cortex: neuroprotection

Hippocampus: Memory formation

Hypothalamus: Control of body energy/hunger

43
Q

What are the synthesis pathways of endogenous cannabinoids

A

Derived from membrane lipids: Arachidonic acid

Anadamide: Derived from N-arachidonyl phosphatidyl ethanol (NAPE)

2-AG: Derived from arachidonyl-containing phosphatidyl inositol bis phosphate (PIP2)

since 2-AG plays an important role for Arachidonic acid, pharmalogical manipulation of 2-AG production has wide reaching effects beyond those of the endocannabinoid system

44
Q

Cannabinoid receptor # 1

A

found in uniform distribution: striatum, thalamus, hypothalamus, cerebellum, lower brainstem

found in non uniform: cortex, amygdala, hippocampus

45
Q

effects of the Cannabinoid receptor 1

A

found on pre-synaptic terminals of EAA and GABA releasing synapses

reduces EAA and GABA release

help with neuroprotection/ mood/ nociception

done via Gi coupled protein

Anamide and 2-AG are equally effective

46
Q

Cannabinoid receptor 2

A

Initially reported as peripheral receptors found primarily on macrophages
also found on microgila

Highly inducible in response to injury or inflammation

binds 2-AG better than AEA

47
Q

Degradation of the endocannabinoids at the synapse

A

2 way pathway:

Hydrolysis

  • Anandamide via Fatty acid amide hydrolase
  • 2-AG monoacyl glycerol lipase

Oxidation: via cyclooxygenase and lipoxygenase pathway

48
Q

what are the two amino acids apart of the EAA

A

Glutamate: derived from alpha ketoglutarate, and its metabolic and transmitter pool is strictly seperated

Aspartate: Often co-localized with glutamate,
serves as neurotransmitter on its own in visual cortex and pyramidal cells
Metabolic and transmitter pool strictly seperated

49
Q

NMDA receptor

A

N-Methyl-D-Aspartate receptor
Ionotrophic

GLutamate and apsartate all activate them in the body

when activate allows for an influx of calcium

Has multiple modulatory sites
-glycine binding site

50
Q

How does Glycine and Magnesium interact wiht the NMDA receptor

A

Glycine site: required co-agonist, but it alone cannot open the channel
Both EAA and glycine must be present for the channel to open

Magnesium site:
Found within the channel itself
blocks the channel at resting membrane potential
Prevents cacium influx when the channel opens
makes the NMDA receptor both ligand and voltage gate

51
Q

How does PCP interact with the NMDA receptor

A

Horse tranquilizer

blocks the channel

52
Q

How does the Non-NMDA receptor work and what are their names

A

AMPA
Kainate

ionotropic but allows a Na+ influx

Contains modulatory sites
-Benzodiazepines bind to a modulatory site and reduces the amount of sodium influx

Glutamate/Aspartate are the endongenous ligands

AMPA is the exogenous agent

53
Q

What is the difference between the non-NMDA and NMDA epsp that they produce

A

Non-NMDA produce a typical exitatory post synaptic potential that is relative short onset and duration

While activation of the NMDA receptors produces a “long” latency epsp with a long duration

54
Q

what are the functions of the non-NMDA and the NMDA receptors

A

Non-NMDA:
primary sensory afferents
upper motorneurons

NMDA:
critical in short and long term memory function
synaptic plasticity in many forms

55
Q

EAA metabotropic receptors

A

Group 1: Gq
(mGlu1, mGlu5)

Group 2: Gi
(mGlu2 mGlu3)

Group 3: Gi
(mGlu4, mGlu6, mGlu7, mGlu8)

these exist in both pre and post synapses
presynaptic: control NT release
Post-synaptic: learning, memory, motor systems

56
Q

What limits the action of EAA

A

glial cells: convert EAA back to glutamine

Nitric oxide

57
Q

What are the neural functions of Nitric oxide

A

Memory:

  • long term potentiation
  • in hippocampus and cerebellum

Cardiovascular and respiratory control
-pons and medulla

58
Q

Effects of NO and downside

A

used for free radicals to breakdown bacteria

also used for relaxation of the bloodvessels

however:
Very unstable
makes free radicals
high concentrations it is toxic to neurons

Neuro Endocrine 2 (24 decks)

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