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Neuroanatomy > NTs and receptors > Flashcards

NTs and receptors Flashcards

1
Q

what are the two classes of NTs?

A
  1. small molecule NTs - Ach, glutamate, A.A, purines, biogenic amines
  2. Peptide NTs - >100, usually 3-30 aa
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2
Q

which one is the first NT to be identified and which one is the major excitatory NT in the CNS?

A
  1. first NT to be identified - Ach

2. glutamate

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3
Q

what is the difference b/w excitatory and inhibitory A.A NTs?

A

excitatory - 2 negative charges atphysiological pH

inhibitory - 1 negative charges at physiological pH

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4
Q 
Glycine despite being inhibitory NT, it is co-agonist for NMDA class of Glutamate receptors 
True or False
A

True

co transporters are usually a combination of +ve and -ve

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5
Q

name the following

  1. what is GABA synthesised from?
  2. it is loaded into synaptic vesicles via what?
  3. it is cleared by what?
A
  1. Synthesised from Glutamate by glutamic acid decarboxylase (GAD)
  2. Loaded into synaptic vesicles by VIAAT
  3. Cleared by GATs (GABA transporter 1) – Na+-dependent co-transporters
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6
Q

what are the two types of GABA receptors?

A
  1. GABAA ionotropic – Cl- channels

2. GABAB metabotropic- activate K+ channels or inhibit Ca2+ channels

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7
Q

where are GABAaR agonists used?

A

GABAA R agonists widely used sedatives, anxiolytics, anti-convulsants, anaesthetics

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8
Q

what is the difference b/w barbiturates and benzodiazepine?

A
  • barbiturates activates GABAa

- benzodiazepine enhances GABAa

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9
Q

give an example of barbiturates and benzodiazepine

A

barbiturates - pentobarbital benzodiazepine - diazepam

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10
Q

give an example where GABAa inhibitor is used?

A

Inhibitors (e.g. picrotoxin, PTZ) used experimentally as convulsants – animal models of epilepsy

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11
Q

give examples of GABAaR antagonists and where it is used?

A
  1. bicucilline - in the labs

2. flumazenil - used clinically for BZD (benzodiazepine) overdose

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12
Q

give examples of GABAbR agonists and where it is used?

A

Baclofen – spasticity - to make the muscles more relaxed

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13
Q

give examples of GABA reuptake inhibitors (GRI) and where it is used?

A

tiagabine/ Gabitril – anxiety, epilepsy

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14
Q

give examples of GABA analogues and where it is used?

A

GABA analogues e.g. gabapentin – seizures & neuropathic pain

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15
Q

name the conditions that result due to less or more inhibition

A

less inhibition - arousal, epilepsy, death

more inhibition - sleep, coma, death

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16
Q

GABA is excitatory in early development - True or False justify

A

True
embryo - High NKCC1 -> High [Cl-]I -> GABA -> Cl-efflux Depolarising
adults - High KCC1 -> Low [Cl]I -> GABA -> Cl-influx Hyperpolarising

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17
Q

which is the main inhibitory NT in spinal cord and brainstem?

A

glycine

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18
Q

where is glycine

  1. synthesised from
  2. loaded into synaptic vesicles via what
  3. how is it cleared?
A
  1. Gly synthesised from Ser by serine hydroxyl-methyltransferase
  2. Loaded into synaptic vesicles by VIAAT
  3. Cleared by specific GlyT – mutations give hyperglycinemia (lethargy, seizures, MR)
19
Q

what can the mutation in glycine transporter result in?

A

mutations give hyperglycinemia (lethargy, seizures, mental retardation)

20
Q

what type of receptors are glycine?

A

ionotropic, Cl- channels

21
Q

name a substance that inhibits glycine and what can that result into?

A

inhibited by strychnine – induces seizures

22
Q

what are the characteristics of purines?

A
  • ATP excitatory NT in CNS & PNS – MNs, sensory and autonomic ganglia
  • ATP rapidly catabolised to adenosine
  • Ionotropic receptors for ATP (P2X), metabotropic receptors for ATP (P2Y) and adenosine (P1)
23
Q

Adenosine is a NT

True or False

A

False, it does not meet the criteria of NT (able to pack into vesicles and release upon Ca2+ activation)

24
Q

what is the function of purinergic receptors?

A
  • Modulators:- neuroprotective agents?- chronic pain?

- Non-CNS functions, e.g. P2Y12 inhibitors anti-platelet agents

25
Q

name a few biogenic amines

A

Catecholamines – dopamine, norepinephrine/noradrenaline, epinephrine/adrenaline
Imidazoleamine - histamine
Indoleamine – serotonin (5-hydroxytryptamine)

26
Q

outline the catecholamine biosynthesis

A

L-tyrosine -> L-DOPA -> DOPAMINE -> L-Noradrenaline -> L-adrenaline

27
Q

what is the function of dopamine and what diseases are related to them?

A
  1. movement - PD
  2. Motivation, reward & enforcement - drug addiction
  3. cognition and emotion
28
Q

what are the dopaminergic pathways?

A
  1. SN to striatum – initiation of movement
  2. VTA-Nac – reward pathway – addictive behaviour
  3. VTA – MCP – limbic – cingulate gyrus – cognitive, emotion and motivation
29
Q

in which disease is MAO-B and COMT inhibitors used?

A
  • MAO-B and COMT catabolise dopamine
  • MAO-B inhibitors (Selegiline & Rasagiline) used early PD
  • COMT inhibitors (e.g. Entacapone & Tolcapone) used with Levodopa in PD
30
Q

what type of receptors are dopamine receptors and what are its classes?

A

All metabotropic i.e. G protein coupled

2 classes:- D1-like via Gs- D2-like via Gi

31
Q

which substance inhibits the removal of dopamine by DAT?

A

cocaine

32
Q

how dopamine receptors subtypes are present?

A
  • D1-D5

- D2/3/4 – targeted by anti-psychotics

33
Q

what is major source and function of NA?

A 
major source - locus coeruleus 
function - sleep, wakefulness and attention
34
Q

where is adrenaline produced?

A
  • mainly medullary epinephrine neurons in the medulla
35
Q

adrenergic beta blockers are used to terra what?

A

β-blockers, e.g. propranolol used to treat cardiac arrhythmias & migraines

36
Q

what is the function of histamine?

A

has role in attention and arousal

37
Q

what are the features of histamine?

A
  • Lots of peripheral effects e.g. allergies
  • Located in tuberomammillary nucleus (in the hypothalamus)
  • 3 classes – H1-3
    CNS relevance – can cross - the BBB – could be effective sedatives
  • Promethazine - may cause drowsiness (beyond a sedative for him)
38
Q

what are the function of serotonin? (5-HT)

A
  • function - Mood, sleep, wakefulness, nausea, appe
39
Q

what is the clinical significance of 5-HT?

A
  • loss of 5-HT in depression
  • therefore, targets for anti-depressants and anxiolytics to increase it
  • since 5-HT is cleared by SERT - drugs like SSRI - fluoxetine/prozac target them
40
Q

why are the down sides of too much 5-HT?

A

XS serotonergic agonism → serotonin syndrome, range from mild (shivering & diarrhea) to severe (rigidity, fever & seizures)
non-CNS - constipation

41
Q

all of the 7 5-HT are metabotropic except one, name it

A

5-HT3 - inotropic

42
Q

how are the 5-HT agonists and antagonists targeted in diseases?

A

5-HT agonists - migraine

5-HT antagonists - nausea/vomiting (chemotherapy), withdrawn diet pill (fen-phen)

43
Q

outline the role of peptide NTs in diseases and its function

A
  1. Pain – substance P & opioid peptides
  2. Stress responses – CRH/CRF
  3. Food intake – NPY, melanocortins
  4. Pituitary peptides – vasopressin, oxytocin
  5. Hypothalamic-releasing peptides – LHRH
44
Q

what is the significance of HPA axis?

A
  • Mediates stressresponses

- dysfunction - associated with psychiatric disorders

Neuroanatomy (16 decks)

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