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Signalling and Men > BRUNO MARS > Flashcards

BRUNO MARS Flashcards

1
Q

(1) Organisation of peripheral nervous system

A
  • Somatic NS (skeletal muscle)
  • Enteric NS (Gut)

AUTONOMIC NERVOUS SYSTEM (all targets except skeletal muscle)

  • Sympathetic NS (fight or flight)
  • Parasympathetic NS (Rest & Digest)
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2
Q

(1) Different fibres within PNS

A

Afferent fibres: Carry sensory info to CNS

Efferent fibres: Carry signals from CNS to periphery

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3
Q

(1) Synaptic transmission

A

1) Synthesis
2) Storage
- Protect
- Package (concentrated)
3) Release
- Docking of vesicle
- Ca2+ entry
- Fusion (exocytosis)
- Recycling (endocytosis)
4) Activation
5) Inactivation

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4
Q

(1) Efferent pathways in ANS

A

1) Preganglionic neurones (arise in brain stem or lateral horn of spinal cord)
2) Postganglionic neurone (Nerve endings of Postgang neurones synapse with effector cells including smooth muscle, cardiac muscle, vascular muscule and exocrine glands)

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5
Q

(1) Ach is the neurotransmitter released from…..

A

All the parasympetic postganglionic neurones at neuroeffector junction

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6
Q

(1) NA is the neurotransmitter released from….

A

MOST postganglionic neurones of Sympathetic NS (except those innervating sweat glands: Ach)

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7
Q

(1) Cholinergic synapses

A

Cholinoreceptors bind Ach

2 types:

1) Nicotinic: Activated by ACh and nicotine
2) Muscarinic: Activated by ACh and muscarine

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8
Q

(1) Noradrenergic synapses

A

Adrenoreceptors bind NA

2 types:
Alpha
Beta

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9
Q

(1) Types of receptors using NA and Ach

A

nACHR: Ligand-gated ion channels (pentamer)

mACHR, all adrenocetptors are GPCRs.

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10
Q

(1) Organs innervated by PNS

A
  • Contriction of pupils
  • Constricts bronchi
  • Slow heart
  • Increases gut motility and secretion
  • Contracts bladder
  • Erects genitals
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11
Q

(1) Organs innervated by SNS

A
  • Dilates pupils
  • Contricts blood vessels
  • Dilates bronchi
  • Increases HR and contractibility
  • Slows gut motility
  • Stimulates adrenaline production
  • Stims renal renin secretion
  • Stims liver to export glucose and FFA
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12
Q

(2) Synthesis (in NMJ)

A

1) Choline acetyltransferase (ChAT) synthesises Ach from choline and Acetyl Coenzyme A (from Mito)

Reuptake of choline can be compet blocked by hemicholinium 3

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13
Q

(2) Storage (in NMJ)

A

2) uptake and storage of Ach in synaptic vesicles is inhibited by vesamicol

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14
Q

(2) Release (in NMJ)

A

3) Tetrodoxin (TTX) blocks voltage-gates Na+ channels (no action potential)

Voltage-gated Ca2+ channels blocked by conatoxins

Botulinum toxin blocks vesicle fusion

Dendrotoxins block voltage-gated K+ channes (more Ca2+ influx, more release)

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15
Q

(2) Activation (in NMJ)

A

4) Release of vesicle gives a quanta of transmitter

At NMJ, each quanta gives a miniature end plate potential (mEPP) using acti of nAChRs

mEPPs summate to give end plate potential (EPP) which if large enough can cause action potential and cause muscular contraction

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16
Q

(2) Inactivation (in NMJ)

A

5) Activation of nAChR at NMJ is terminated by AChE that breaks down Ach to acetate and choline

Drugs that inhibit AchE (anticholinesterases like nerve gases, neostigmine) increase conc and effects of Ach leading to muscle spasms

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17
Q

(2) Competitive non-depolarising blocks (antagonists)

A

1) Tubocurarine
2) Vecuronium / Rocuronium

REVERSED BY ANTICHOLINESTERASES (e.g. neostigmine)

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18
Q

(2) Depolarising blocker (agonist)

A

Suxamethonium

  • Used clinically for rapid onset of paralysis
  • short duration (broken down by plasmacholinesterases)
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19
Q

(2) Effect of depolarrising blockers

A

PHASE 1 BLOCK

1) Persistent activation of endplate nAChR by suxamethonium
2) Prolonged depolarisation of endplate
3) Inactivation of voltage-gated Na+ channels

PHASE 2 BLOCK

4) Desense of endplate of nAChR
5) Repolarisation of endplate
6) Receptor desense maintains blockade

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20
Q

(2) Effect of ganglion blockers

A

Reduced actions of both SNS and PNS

21
Q

(2) Ganglionic Non-depolarising blockers (antagonists)

A
  • k-bungarotoxin
  • trimethaphan (compet)
  • Hexamthonium (non-compet open channel blocker)
  • Tubocurarine (non-compet)
22
Q

(2) Ganglionic depolarising blockers (agonists)

A

Nicotine and lobeline
(nACh agonists)
-Repeatedly stim receptors to inactivate VG Na+ channels and desense nAChR

23
Q

(3) Synthesis of Adrenaline

A 
1) L-Tyrosine 
TYROSINE HYDROXYLASE
2) DOPA 
DOPA CARBOXYLASE
3) Dopamine
DOPAMINE-B-HYDROXYLASE
4) NA
PHENYLETHANOLAMIN N-METHYL TRANSFERASE
24
Q

(3) Adrenoceptor diveristy

A

A-adrenoceptors (1,2)
NA > A&raquo_space; Isoprenaline

B-adrenoceptors (1,2,3)
Isoprenaline > A > NA

25
Q

(3) Adrenorepctor actions

A

A1: contraction (vascular smooth muscle)
A2: Decrease NA release (adrenergic nerve terminals)
B1: Increase HR and force of contractions (cardiac muscle)
B2: Dilation/relaxation (Cardiac/skeletal muscle blood vessels, bronchial smooth muscle)
B3: Lipolysis (adipose tissue)

26
Q

(3) Adrenreceptor messengers

A

A1: Gaq = PIP2 –> PKC, Ca2+
A2: Gai = cAMP –> decrease VGCC
B1/2/3: Gas = cAMP, PKA

27
Q

(3) Drugs on presynaptic terminal (storage)

A

Reserpine: Inhibits NA uptake, depletes NA.
-Decrease in sympathetic function

a-methyl DOPA: Converted to a-methyl NA, replaces NA, less potent than NA at A1, activates A2 less NA released. Decreases HR and BP

28
Q

(3) Drugs on presynaptic terminal (release)

A

Bretylium: Taken up and stored in vesicles. Local aneasthetic action to block nerve conduction of noradrenergic neurones (long depletion of NA)

Clonidine: A2 agonist, less NA released

29
Q

(3) Alpha adrenoR antagonists

A

Prazosin: A1, decrease BP

Labetalol: A/B, decrease BP via A1

30
Q

(3) Beta adrenoR antagonists

A

Propranolol: B, decrease BP/HR

Atenolol: B1, decrease HR, BP and cardiac

Pindolol: partial agonist

31
Q

(3) Use of salbutamol

A

B2: smooth muscle relaxation in asthma

32
Q

(3) Tyramine

A

Stimulates NA release:

1) Competes with NA for U1
2) Displaces NA from vesicle

33
Q

(3) Amphetamine

A

Stimulates NA release

1) Competes with NA for U1
2) Displaces NA from vesicle
3) Inhibits MAO

34
Q

(4) Purinergic signalling

A

Inter-cellular signalling involving purine-based molcules

35
Q

(4) ATP as a transmitter

A

Targets postganglionic sympathetic neurones (e..g. blood vessels)

  • Cause fast depolarisation/contraction of smooth muscle cells
  • Uses the P2X receptor
36
Q

(4) Different purinergic receptors

A

P2X: Binds ATP
P2Y: Binds ATP/ADP/UTP
P0: Adenine
P1: Adenosine

37
Q

(4) Different ligand gated ion channels

A

Trimeric: ATP P2X
Tetrameric: Glutamate Rs, AMPA/NMDA
Pentameric: Nicotinic receptors, nAcHRs, GABAa

38
Q

(4) Where is ATP and ADP

A

They are key in platelet aggregation

39
Q

(4) Adenosine P1 receptors

A

They are all GPCRs
A1: Gai/o = Reduction of PNS, SNS
A2A: Gas = Inhibition of platlet aggragation, wound healing
A2B: Gas, Gaq = Relaxation of smooth muscle in intestine
A3: Gai = Enhancement of mediator release from mast cells

40
Q

(4) Adenosine receptor antagonists

A

Theophylline/aminophylline

41
Q

(4) Evidence in COPD on adenosine role

A

1) Elevated levels of Adrenosine in plasma and exhalaed breath condensate of patients with asthma and COPD
2) Aerosol adenosine exposure indcues bronchocontriction in patients with COPD but not in control
3) Non selective adenosine receptor antagonists improve lung funcion and symptions in asthma and COPD
4) Activation of adenosine receptors subtypes involved in COPD shown to elicit pro-inflam responses

42
Q

(4) Why hard to create agonists and antagonists for ATP P2 receptors

A

Similarity between ATP P2 receptors make it difficult.

43
Q

(5) 2 types of L-glutamate receptors

A

Ligand-gated ion channels: Ionotropic GluRs (Fast excitatory) (GLuR)
GPCRs: Metabotropic GluRs (mGLuR) (slow modulatory)

44
Q

(5) NMDA receptor

A

Tetramer: Glutamate binding site (GluN2), GLycine binding site (GluN1)
-Transmembrane pore blocked by Mg2+

45
Q

(5) Roles of glutamate receptors in mammalian brain

A

1) Mediate majority of fast exicitaory synaptic transmission in CNS
2) Implicated in host of neurodevelopmental, neurological and neurodegrerative conditons
3) Target of drugs of abuse like ketamine

46
Q

(5) Active synapse

A

Transmits information at hyperpolarised (resting) membrane potentials through AMPA receptors

47
Q

(5) Silent synapse

A

One that lacks AMPARs at synpase and does NOT transmit info at hyperpolarised (resting) membrane potentials due to Mg2+ block of the NMDA receptor.
-AMPA receptors stored in intracellular vesicles at extrasynaptic sites

48
Q

(5) Summary

A

Strength of synaptic transmission can be rapidly and bidirectionally regualted by AMPAR trafficking
-Trafficking may underlie learning and memory, also patholgical and psychiatric conditons

Signalling and Men (6 decks)

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