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Neuro test 2 > 5.1 NT Systems > Flashcards

5.1 NT Systems Flashcards

1
Q

How are monoamines synthesized?

A

created by modifying certain AAs

Catecholamines (DA–> NE–> E) from tyrosine (via tyrosine hydroxylase)

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2
Q

Where are monoamines cell bodies located?

A

DA- SNPC/VTA; Tyr

NE- locus coreolus; Tyr

Epi- brainstem; Tyr

Serotonin- Raphe nuclei; Tryp

Histamine- tuberomammillary nucleus; His

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3
Q

How are cholinergic NTs synthesized?

A

ACh- synthesized by choline and acetate

Moved into clear vesicles via Vesicular Ach Transporter protein (VAchT)

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4
Q

How are cholinergic NTs degraded?

A

ACh- removed from synaptic through via acetylcholinesterase bound to post-synaptic cell membrane

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5
Q

What are the receptor characteristics for the Monoamines?

A

DA- D1, D2, D3

NE/E- Alpha and Beta adrenergics

5-HT: multiple ; 5HT6

Histamine- H1 and H2

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6
Q

What does it mean to say that serotonergic neurons are found in the raphe nuclei?

A

that is where their cell bodies are found; axons travel to different places

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7
Q

Where is ACh found in the brain?

A

found a lot in brainstem

on other side of lateral ventricle= basal ganglia- specifically the striatum- CNS (have lot of cholinergic neurons there)

Also found PNS- NMJ, autonomic pregaglionic synapses, PS post-ganglionic fibers, sympathetic post-ganglionic fibers innervating sweatl glands/muscle vasodilators, amacrine cells

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8
Q

What is the striatum in charge of?

A

control of voluntary motion

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9
Q

What are the midbrain and pons in charge of?

A

baseline excitation to cortex (brain arousal mechanism), REM sleep

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10
Q

What are the receptor characteristics for the cholinergic NT systems?

A

MUSCARINIC (metabotropic= serpentine); at least 5 subtypes

NICOTINIC = located at NMJ, synapses bw pre- and post-ganglionic cells in autonomic ganglia; other central synapses; 5 subunits coded for by 16 different genes

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11
Q

What are the subtypes of Acetylcholine receptor M1*?

A

M1 (neuronal): increase IP3/DAG (Gq)–> increase Ca2+

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12
Q

What are the subtypes of Acetylcholine receptor M4*?

A

presynaptic autoreceptor; striatum of basal ganglia

decrease cAMP (Gi)

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13
Q

What are the subtypes of Acetylcholine receptor M5*?

A

cerebrovasculature; dopaminergic neurons of basal ganglia

increase IP3/ DAG (like M1)

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14
Q

What are the subtypes of Acetylcholine receptor M2 and M3?

A

M2: decrease cAMP (Gi)–> increase K efflux

M3: smooth m. of bronchi, vasculature; endothelial cells of vasc (NO); increase IP3/DAG (Gq) –> increase Ca2+

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15
Q

How are monoamines removed?

A
  1. Reuptake by presynaptic terminal
  2. Two enzymes- MAO and Catchol-Omethyl transferase (COMT*) enzymatic destruction

^For both catecholamines and serotonin

For histamine: diamine oxidase degrades after uptake

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16
Q

What happens if you change the subunits of the nicotinic ACh receptor?

A

you change the properties of the channel

in some central synapses, it creates a nicotinic channel that allows more calcium in

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17
Q

What are the two major inhibitory AAs?

A

GABA (y-amino butyric acid) and glycine

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18
Q

What are some characteristics of GABA?

A

major inhibitory aa NT in CNS

widely distributed through HIGHER levels of CNS: cortex, cerebellum, basal ganglia

spinal cord has least gaba

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19
Q

What is GABA critical in?

A

consciousness, motor control, vision (retina)

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20
Q

How is GABA synthesized?

A

from glutamate

Impt enzyme= glutamate decarboxylase (GAD)

also found in pancreatic islet; Abs found in T1D

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21
Q

How is GABA transported into vesicles and removed from synapse?

A

Transported into vesicles via Vesicular GABA Transporter Protein (VGAT)

removed from synapse via GABA transporter (GAT); NaCl co-transport

two forms = GAT1 (presynaptic terminal) and GAT2 (on glial cells surrounding synapse)`

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22
Q

What happens if GAT1 takes GABA up?

A

it is on presynaptic terminal; so GABA is repackaged into vesicles as is

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23
Q

What happens if GAT2 takes GABA up?

A

on astrocytes; glial cell/astrocyte will take up GABA converted to glutamate and will bring it back/convert it to glutamine and released to ECF, where its taken up by presynaptic terminal and recycled into GABA

repackaged and recycled!!

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24
Q

What are the types of GABA receptors?

A

GABA-A, B, and C

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25
Q

What are the characteristics of GABA-A?

A
  • ionotropic (Cl- conductance)
  • activation produces IPSP in adult neurons
  • multiple binding sites modulate: benzodiazepine site (sedatives), ethanol, certain steroids, which aLL POTENTIATE action of GABA
  • large number of extra-synaptic GABA-A receptors which are believed to be site of action for number of general anesthetics, including propofol
26
Q

What happens when there is a Cl- influx with GABA around?

A

Cl-influx –> hyperpolarizes cells normally but Cl- leaves cell when GABA released

27
Q

What are the characteristics of GABA-B?

A

-metabotropic, Gi/Go protein coupled

activate a K+ channel (GIRK)–> goes out!! with positive charge produces slow IPSP

close down (inhibit) Ca2+ channel

presynaptically –> regulates NT release

post-synaptically –> inhibition of post-synaptic cell

28
Q

Where is Glycine found?

A

spinal cord (major), brainstem (medulla), much less in higher areas of CNS

*almost exclusively on presynaptic side**

29
Q

What is the function of glycine?

A

mediates many spinal inhibitions

30
Q

How is glycine produced and removed from the synapse?

A

Production: unmodified aa

Removal from synapse by GAT Proteins (same as GABA), recycling

31
Q

What is the receptor for glycine like?

A

GlyR: ionotropic (Cl-) like GABA-A

influx of Cl- leads to IPSP

ethanol and general anesthetics bind to it and potentiate

32
Q

What is an antagonist to the glycine receptor? What symptoms occur with blocking?

A

Stychnine binds to it and blocks it; prevents channel from opening

Sx: causes convulsions (all activity normally suppressed isn’t being suppressed anymore)

33
Q

Why are purines long debated?

A

all synaptic vesicles contain ATP, which led to debate that it was required for metabolic function; some NT synthesis is completed in vesicles; recognized as co-transmitter first

34
Q

How are purines synthesized and stored in vesicles?

A

ATP by mitochondria (pre-synaptic terminal has many)

ATP–> ADP–> AMP–> Adenosine occurs in synaptic trough; AMP to adenosine by 5’-nucleosidase

Stored in vesicle (VNUT protein)

35
Q

Where are purines found?

A

Virtually everywhere in CNS (especially in CORTEX, CEREBELLUM, HIPPOCAMPUS, BASAL GANGLIA)

36
Q

What are the purine receptors?

A

Two major classes: P1 ( A receptors) and P2 (P2X, P2Y)

37
Q

What are P1 receptors’ ligand and how does function vary for locations?

A

A receptors

ligand= adenosine

post-synaptic locations= sleep induction; general inhibition of neural function

pre-synaptic locations= inhibition of NT release

38
Q

What are P2 receptors’ ligands?

A

P2X receptor- ionotropic; ligand= ATP; many subtypes

P2Y receptor- metabotropic (like P1); ligand= ATP, ADP, UTP, UDP; Gs/Gq coupled

39
Q

What are the functions of Purines?

A

Learning and memory (co-release with EAA)

modification of locomotor pathways

40
Q

Where are peptide transmitters made and transported? via what transport?

A

NT peptides made in SOMA

transported down AXON via FAST axonal transport

41
Q

What are the peptide transmitters?

A

opioids, tachykinins (SP), cholecystokinin, somatostatin, others

42
Q

What peptides are included in the opioids?

A

endorphins, enkephalins, dynorphins, and nociceptin

43
Q

Where are opioids located?

A

striatum (basal ganglia), hypothalamus, periaqueductal gray, multiple pontine and medullary sites, raphe nuclei in brainstem

44
Q

What are some general functions of opioids?

A

modification of nociceptive inputs (cutaneous senses)

-pain relief, mood, and effect

drug addiction/neurophysiology of emotion!!

45
Q

What are the precursor molecules of opioids?

A

proopiomelanocortinin (PCOM)–> B- endorphins (from ACTH precursor)

Pro-enkephalin–> Tyr-gly-gly-phe-x (Met or Leu)

Pro-dynorphin –> 3 molecules of Leuk-enkephalin–> Dynorphin

Orphanin FQ–> nociceptin

46
Q

How are opioids synthesized and removed?

A

Synthesized by standard protein synthesis in cell body

Removed from trough/cleft by probable reuptake and enzymatic degradation by ENKEPHALINASE and AMINOPEPTIDASE (breaks aa off- thats all needs !)

47
Q

What receptors do opioids have? what are they?

A

mu receptors, kappa receptors, and delta receptors

metabotropic (serpentine)–> activate second messenger systems with ligand binding (Gi/Go proteins)

48
Q

What does activation of the mu opioid receptor cause? Leads to an increase in what?

A

ANALGESIA, RESPIRATORY DEPRESSION, EUPHORIA, constipation, sedation

Gi (decreased AC)–> leads to an increase in K+ efflux and hyperpolarization

49
Q

What does activation of the kappa opioid receptor produce?

A

ANALGESIA and DYSPHORIA mainly

50
Q

What does activation of the delta opioid receptor produce?

A

ANALGESIA

51
Q

What do the kappa and delta opioid receptors do in terms of ions?

A

decrease Calcium influx

Go= leads to decreased Calcium influx (from decreased IP3/DAG)

52
Q

What are identified endogenous cannabinoids?

A

anandamide and 2-arachidonylglycerol (2AG)

53
Q

What was first identified of endocannabinoids?

A

exogenous chemicals such as THC- tetrahydrocannabinol

54
Q

Where are endocannabinoids found?

A

broadly distributed in CNS

BASAL GANGLIA(mood and motor performance)

SPINAL CORD (modulation of nociception)

CORTEX (neuroprotection)

hippocampus (memory formation)

hypothalamus (control of body energy/hunger- munchies)

55
Q

How are endocannabinoids synthesized?

A

derived from membrane lipids (arachidonic acid)

occurs in PRESYNAPTIC TERMINAL

56
Q

What are the receptors of endocannabinoids?

A

CB1 and CB2

57
Q

Why is the CB1 important?

A

relevant for neurophysiology

found on PRESYNAPTIC terminals of EAA and GABA releasing synapses

reduces EAA and GABA release

Gi coupled protein

Anandamide and 2-AG equally effective!!!

58
Q

Why is CB2 receptor important? where is it located?

A

Associated with immune system (Action: anti-inflammatory!!)

located: microglia in barin, gut, immune system in general
* In brain, CB2R activation increases B-amyloid removal *

59
Q

Which NTs’ receptors are only metabotropic?

A

Opioids and endocannabinoids

60
Q

Which NTs’ receptors are only ionotropic?

A

Glycine

61
Q

Which Receptors are metabotropic?

A

nAChR, GABA-B, P1(A), P2Y, Mu,delta,kappa opioid, CB-1

62
Q

Which receptors are ionotropic?

A

nAChR, GABA-A, GlyR, P2X

Neuro test 2 (15 decks)

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