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Neuro Endocrine 2 > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

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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

Study These Flashcards
A

Consciousness

Motor control

Vision

25
How is GABA synthesized and removed
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
GABA a Receptors
Ionotropic (Cl conductance generates an IPSP Modulates: Benzodiazepine, ethanol, steroids, general anesthetics like propfol
27
GABA b receptors
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
Where is Glycine found and what is its function
Spinal cord and much less in higher areas of the CNS Function: mediate many spinal inhibitions
29
How is glycine produced and removed from the synapse
Produced via unmodified amino acid romoved from the synapse via the GAT proteins
30
What is the receptor of glycine, and what blocks this receptor
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
Where are purines found in the CNS
``` found virtually everywhere in the central nervous system especially: cortex cerebellum hippocampus basal ganglia ```
32
P1 receptors of Purines
Ligand: Adenosine Postsynaptic locations: does sleep induction general inhibition of neural function Presynaptic locations: Inhibition of neurotransmitter release
33
P2 receptors of Purines
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
What are the 4 peptides included in the peptide family, and what are their general functions
endorphins enkephalins dynorphins nociceptine Modification of nociceptive inputs (cutaneus senses) Mood/Affect (Neurophysiology of emotion/drug addiction)
35
Where are opioids found in the CNS
Basal ganglia hypothalamus pontine and medullary sites
36
What are the 4 pre precursor molecules
Proopiomelanocortinin Pro-enkephalin Pro-dynorphin Orphanin FQ
37
What is the synthesis and removal of the opioids
synthesis: standard protein synthesis in the cell body removal from trough/cleft via reuptake and ezymatic destruction via: enkephalinase and aminopeptidase
38
What does the Mu receptor do
for opioids Metobotropic recceptor Gi/Go Leads to an increase inpotassium efflux and hyperpolarization ``` Activation causes: analgesia respiratory depression euphoria constipation sedation ```
39
What does the Kappa receptor do
for opioids Serpentine receptor Gi/Go Decreases calcium influx ``` Produces Analgesia Dysphoria diuresis miosis ```
40
What does the Delta receptor do
it is for opioids decreases Calcium influx it is a serpentine receptor Gi/Go Produces analgesia when activated
41
What are endocannabinoids
Anandamide 2-Arachidonylglycerol (2AG)
42
Where are endocannabinoids found in the CNS
Basal ganglia: mood, motor performance Spinal cord: modulation of nociception Cortex: neuroprotection Hippocampus: Memory formation Hypothalamus: Control of body energy/hunger
43
What are the synthesis pathways of endogenous cannabinoids
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
Cannabinoid receptor # 1
found in uniform distribution: striatum, thalamus, hypothalamus, cerebellum, lower brainstem found in non uniform: cortex, amygdala, hippocampus
45
effects of the Cannabinoid receptor 1
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
Cannabinoid receptor 2
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
Degradation of the endocannabinoids at the synapse
2 way pathway: Hydrolysis - Anandamide via Fatty acid amide hydrolase - 2-AG monoacyl glycerol lipase Oxidation: via cyclooxygenase and lipoxygenase pathway
48
what are the two amino acids apart of the EAA
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
NMDA receptor
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
How does Glycine and Magnesium interact wiht the NMDA receptor
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
How does PCP interact with the NMDA receptor
Horse tranquilizer | blocks the channel
52
How does the Non-NMDA receptor work and what are their names
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
What is the difference between the non-NMDA and NMDA epsp that they produce
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
what are the functions of the non-NMDA and the NMDA receptors
Non-NMDA: primary sensory afferents upper motorneurons NMDA: critical in short and long term memory function synaptic plasticity in many forms
55
EAA metabotropic receptors
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
What limits the action of EAA
glial cells: convert EAA back to glutamine Nitric oxide
57
What are the neural functions of Nitric oxide
Memory: - long term potentiation - in hippocampus and cerebellum Cardiovascular and respiratory control -pons and medulla
58
Effects of NO and downside
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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