Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro Exam 2 > Neurotransmitter Systems - Terminology > Flashcards

Neurotransmitter Systems - Terminology Flashcards

1
Q

Where is the Raphe Nucleus located?

A

Positioned midline in brainstem throughout midbrain, pons, and medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What neurons are found in Raphe Nucleus?

A

Serotonergic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 5 Monoamines and what is the definition of a monoamine?

A

Epinephrine (adrenaline)

Norepinephrine (noradrenaline)

Dopamine

Serotonine

Histamine

Definition: class of neurotransmitters that are created by modifying single amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where do you find norepinephrine in the brain?

A

Locus ceruleus

other pontine/medullary areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the role of norepinephrine?

A

Wakefulness/alertness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where do you find epinephrine?

A

Medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the role of epinephrine?

A

Modulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are norepi and epi made?

A

Derived from Tyrosine (along with dopamine)

Tyrosine –> Dopamine –> Norepi –> Epi

Tyrosine Hydroxylase conversion of tyrosine to DOPA is rate limiting step

then moved into vessicles

NE created

Neurosn that have Phenolethanolamine N methyl transferase (PNMT) convert NE to Epi after NE leaves the vesicles

Epi moved back into vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are Epi and norepi transported into the vesicles and what inhibits this process?

A

VMAT1 and VMAT2 move them into vesicles and Reserpine inhibits this process (leads to synaptic failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is epinephrine and norepinephrines action limited?

A
  • Reuptake
  • Enzymatic degreadation
  • Monoamine oxidase
    • outersurface of mitochondria
    • Metabolites released into ECF
  • Catechol-O-methyl Transferase
    • Glial cells/ post synaptic membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do Epinephrine and Norepinephrine bind to?

A

Two general classes of receptors (with multiple subtypes)

Alpha - adrenergic

Beta - adrenergic

Both are serpentine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where do you find Dopamine?

A

Cortex

Basal ganglia (motor control)

hypothalamus and limbic system (endocrine and emotional control)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you make Dopamine?

A

Tyrosine –> Dopamine

Tyrosine Hydroxylase conversion of tyrosine to DOPA is rate limiting step

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you limit Dopamines action?

A

Reuptake and Catabolism by MAO and COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does Dopamine bind to?

A

5 receptor types with multiple subtypes

Metabotropic (serpentine) receptors connected to G proteins

D1 and D5 (aka D1 like): increase cAMP

D2: decrease cAMP –> increases gK (=potassium efflex)

D3 and D4: decrease cAMP (aka D2 like)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where do you find Serotonin (5HT)?

A

Hypothalamus and limbic system (mood), Cerebellum (modification of motor activity) and brainstem Raphe nuclei (modification of motor and sensory activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you make Seratonin (5HT)?

A

Derived from Typtophan

Tryptophan hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do you limit Serotonin (5HT) action?

A

Reuptake

Catabolism by MAO and COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the SErotonin (5HT) Receptors?

A

7 receptors with multipule subtypes

Serpentine receptors

5HT 1, 2, 4, 5, 6

once ionotropic receptor: 5HT3 (Na influx)

Interesting Notes: 5HT2c: knock out mice are obese and seizure prone

5HT3: arae postrema (vomiting)

5HT6: anti-depressant effect

5HT7: limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where do you find Histamine?

A

Tuberomammillary nucleus of hypothalamus (wakefulness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you make Histamine?

A

Derived from Histidine

Histidine decarboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do you limit Histamines action?

A

Reuptake

Catabolism by diamine oxidase and COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the Histamine receptors?

A

3 receptor subtypes

Serpentine receptors: H1: PLC activaton

H2: increase cAMP (associated with Gastric acid release)

H3: presynaptic, decrease in histamine release

More H1 and H3 in brain than H2

H1 invovled in wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the two inhibitory amino acids?

A
  1. GABA ( gamma - amino butyric acid)
  2. Glycine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is GABA located in the CNS?

A

Major inhibitory amino acid neurotransmitter in CNS

  • Widely distributed throughout higher levels of CNS
  • Cortex
  • Cerebellum
  • Basal Ganglia
  • The list goes on and on
  • Spinal cord has the least GABA of all
26
Q

What are the roles of GABA and what is it critical in?

A

Too many roles to name

Critical in:

Consciousness

Motor Control

VIsion (retina)

27
Q

How is GABA synthesized?

A

Synthesis: From Glutamate

Important enzyme: Glutamate decarboxylase (GAD)

Transported into vesicles by Vesicular GABA transporter protein (VGAT)

Removed from Synapse via GAT (GABA Transporter)

Two Forms: GAT1 - on the presynaptic terminal

GAT 2 - on glial cells surrounding the synapse

28
Q

What happens when GAT1 (on presynaptic terminal) takes GABA up?

A

The GABA is repackaged into vesicles as is

29
Q

What happens if GAT2 (on the astrocytes) take GABA up?

A

The GABA is converted to glutamine and released to the ECF. where it will be taken up by the presynaptic terminal and recycled into GABA

30
Q

What are GABAA Receptors?

A

Ionotropic (CI conductance)

Activation produces ipsp in adult neurons

multiple binding sites modulate:

Benzodiazepine site

Ethanol

Certain Steroids

These all potentiate

31
Q

The large number of extra-synaptic GABAA receptors are believed to be the site of action for?

A

a number of general anesthetics, including propofol

32
Q

What are GABAB Receptors?

A

Metabotropic

Gi/G0 protein coupled

Activate a K+ channel (GIRK)

close down (inhibit) a Ca++ channel

located pre and post synaptically

presynaptic: regulate NT release

Postsynaptic: inhibition of post synaptic cell

33
Q

Where is Glycine found?

A

Spinal cord (Major)

Brainstem (medulla)

Much less in higher areas of CNS

34
Q

What is the function of Glycine?

A

Mediates many spinal inhibitions

35
Q

What is the production of Glycine?

A

Unmodified amino acids

36
Q

How do you remove Glycine from teh Synapse?

A

GAT proteins (same as GABA)

Recylcing

37
Q

What are Glycine Receptors and what blocks it?

A

Ionotropic (chloride)

influx of chloride leads to ipsp

ethanol and general anesthetics bind to it and potentiate

Strychine binds to it and blocks it

38
Q

Synthesis and Vesicular storage of purines (ATP, ADP, Adenosine)

A

ATP by mitochondria (presynaptic terminal have lots of mitochondria)

Stored in Vesicles (VNUT protein)

Released

ATP –> ADP –> Adenosine occurs in synaptic trough

39
Q

Where are purines (ATP, ADP, Adenosine) found in the CNS?

A

Virtually everywhere in the CNS

Especially cortex, cerebellum, hippocampus, and basal ganglia

40
Q

What are the two major classes of receptors for purines (ATP, ADP, Adenosine)?

A
  • P1 (aka A receptors)
  • ligand - adenosine
  • Post-synaptic locations
    • sleep induction
    • general inhibition of neural function
  • Pre-synaptic locations
    • inhibition of neurotransmitter release
  • P2 receptors
    • ​P2X receptors
      • ionotropic
      • ligand: ATP
      • many subtypes
    • P2Y
      • Metabotropic
      • Ligand: ATP, ADP, UTP, UDP
      • Gi/Gq coupled
    • functions= learning and memory (co release iwth EAA) and modification of locomotor pathway
41
Q

What are peptide transmitters?

A

These neurotransmitters are peptides made in teh soma and transported down the axon via fast axonal transport

42
Q

What are the four peptide transmitters?

A
  • The opioids (only one talked about in this lecture)
  • The tachykinins including substance P
  • Cholecystokinin
  • Somatostatin
43
Q

The opiods are a family of peptides that include

A

The endorphins, enkephalins, dynorphins, Nociceptin

44
Q

Where are the opiods located?

A

Basal ganglia, Hypothalamus, Multiple Pontine and medullary sites

45
Q

What are the general functions of Opiods?

A

Modification of nociceptive inputs

Mood/affect

46
Q

What are the four precursor molecules of opioids?

A
  • Proopiomelanocortinin (POMC - precursor molecule to ACTH)
    • B-endorphins
  • Pro-enkephalin
    • ​TYR-GLY-GLY-PHE-X
    • MET- ENKEPHALIN
    • MET-ENKEPHALIN
  • Pro-dynorphin
    • ​3 molecules of Leu-enkephalin
    • Dynorphin
  • Orphanin FQ –> Nociceptin
47
Q

How are opiods synthesized?

A

Standard protein synthesis in the cell body

48
Q

How are Opioids removed from the trough/cleft?

A
  • Probable reuptake
  • Enzymatic Destruction
    • Enkephalinase
    • Aminopeptidiase
49
Q

What happens when Opioid receptor, Mu ( μ)- Receptors (metobotropic receptor) get activated?

A
  • Analgesia
  • Respiratory depression
  • Euphoria
  • Constipation
  • Sedation
50
Q

What is produced with Kappa (k) recepor (serpentine) opiods receptor?

A

Produces analgesia

Dysphoria

Diuresis

Miosis

51
Q

What is produced with activation of Delta receptor (serpentine) opioid receptor?

A

produces analgesia when activated

52
Q

Opioid Receptors

A

All opioid receptors are metabotropic (Serpentine) and activate second messenger systems with ligand binding

All connect to Gi/Go proteins

Mu receptor - leads to an increase in potassium efflux and hyperpolarization

Delta and Kappa - decrease in calcium influx

53
Q

What are the two endocannabinoids?

A

Anandamide and 2-Arachidonylglycerol (2AG)

54
Q

Where are endocannabinoids distributed 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
55
Q

What is the synthesis of endocannabinoids?

A

Derived from membrane lipids (arachidonic acid) and occurs in presynaptic terminal

56
Q

What are Anandamide and 2-AG derived from?

A

Anandamide derived from NAPE

2-AG derived from PIP2

Notes: 2-AG is major source for arachidonic acid in certain tissues especially the brain and pharmacologic manipulation of 2-AG production has wide reaching effects beyond those of endocannabinoid system

57
Q

Cannabinoid Receptor #1

A

Neuronal location

Activation associated with the psychoactive responses to the cannabinoids

472 AA peptide coupled to G proteins

located on chromosome 6

polymorphisms linked to occurance of obesity, ADHD, schizophrenia, and depression in Parkinsons disease

can form a heterodimer with other NT receptors including dopamine and orexin

58
Q

Where are CB1 distributed in the CNS?

A

Uniform distribution: striatum, Thalamus, Hypothalamus, Cerebellum, Lower brain stem

Non- Uniform: Cortex, Amygdala, hippocampus

59
Q

What is the synaptic location of Cannabinoid receptors?

A

Synaptic location: largely presynaptic

generally away from active zone (where vesicles are)

Greater density at inhibitory synapse

Binds AEA and 2-AG with high affinity

60
Q

The cannabinoid receptors CB2

A

Neuronal location (dendrites and within soma) also reported, usually associated with nerve injury

Highly inducible in response to injury or inflammation

binds to 2-AG better than AEA

61
Q

Degradation of Anandamide and 2-AG

A
  • two differnet paths: hydrolysis or oxidation
  • Hydrolysis - prevelant in neurons
  • Anandamide and 2-AG are degraded via two separate pathways
  • Anandamide (AEA)
    • Fatty acid Amide Hydrolase (FAAH)
  • 2-AG
    • Mono-acyl glycerol lipase (MAGL)
  • Oxidation via cyclooxygenase and lipoxygenase pathway (both AEA and 2-AG

Neuro Exam 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions