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Applications Animal Health > C2S Theme 6-8: Chemical & Electrical communication > Flashcards

C2S Theme 6-8: Chemical & Electrical communication Flashcards

1
Q

Compare & contrast the histology of smooth/ skeletal & cardiac muscle fibres

A

Smooth –> spindle/ round central nucleus/ GAP junctions
Skeletal –> spindle, multi peripheral nuclei, cross striations from sarcomeres
Cardiac –> Branching, single pale central nucleus, intercalated discs, cross striations

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2
Q

Describe the innervation of skeletal muscles

A

Somatic –> voluntary

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3
Q

Describe the innervation of cardiac muscles

A

Autonomic –> involuntary

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4
Q

Describe the innervation of smooth muscles

A

Depends if multiunit or visceral…

Multiunit= 1 nerve supplies muscle fibres, functionally independant, never contract spontaneously

Visceral= Bundles of nerve fibres with GAP junctions, contract spontaneously if stretched beyond their capacity

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5
Q

Pls give example of multiunit smooth muscle

A

blood vessel walls

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6
Q

Give example of visceral smooth muscle

A

GIT smooth muscle

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7
Q

Define the A band of the sarcomere

A

Section of myosin filaments that can overlap with actin (interdigitating even when extended)

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8
Q

Define the H band of the sarcomere

A

Section of myosin only!

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9
Q

Define the I band of the sarcomere

A

Actin only filaments (opposite of H)

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10
Q

Define the Z line of the sarcomere

A

Line connecting 2 adjacent sarcomeres. Part of actin.

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11
Q

Draw a sarcomere

A

Draw it

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12
Q

Describe Type I muscle fibres

A 
Skeletal muscle 
Red muscle cells 
Thin 
Inc mitochondria + myoglobin 
Dec myosin ATPase 
Slow & sustained contraction 
e.g. posture
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13
Q

Describe Type II muscle fibres

A 
Skeletal muscle 
White muscle fibres 
Thick
Less myoglobin 
Inc myosin ATPase 
Fast contraction
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14
Q

What are muscle spindles?

A

A bundle of specialised intramural fibres surrounded by a CT capsule that are embedded in the muscle belly and detect stretch to aid perception of stretch/ velocity/ acceleration

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15
Q

What are the 3 specialised cell junctions that aid the function of cardiac cells? What do these make up?

A

Fascia adherens
Macula adherens
Gap junctions

Make intercalated discs

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16
Q

Describe fascia adherens

A

Structure that anchors actin to the nearest sarcomere

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17
Q

Describe macula adherens

A

Desmosomes

Stop separation during muscle contractions

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18
Q

Describe gap junctions

A

Cell junction that enables action potentials to spread from cardiac muscle to cardiac muscle

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19
Q

What are purkinje fibres?

A

Bundles from the AV node of the heart that bifurcates to travel to the apex of the heart, connecting to cardiac muscles –> facilitating ventricular contraction

Conduct stimuli faster than cardiac muscle fibres

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20
Q

What are the 4 classifications of signalling cells

A

Paracrine
Autocrine
Endocrine
Synaptic

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21
Q

Define paracrine cells

A

Relating to a substance secreted by a cell with a localised effect on DIFFERENT neighbour cells
e.g. inflammation

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22
Q

Define autocrine cells

A

Effect on same cell (or neighbouring cell of same type) from which substance was secreted
e.g. cytokine binds to receptor on same cell

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23
Q

Define endocrine

A

Substance that travels to have effect distally

e.g. hormones

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24
Q

What are the 7 types of signals? (shit question soz)

A
  1. Hormones & ligand bonding
  2. Neurotransmitters
  3. External environmental factors
  4. Mechanical (stretch)
  5. Immunological
  6. Metabolic
  7. Dissolved gases
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25
Q

What are the 4 classes of hormones?

A

Peptides/Proteins, Amines, Steroids, Eicosanoids

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26
Q

What are ligands used for?

A

Conduits for receptor activation

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27
Q

What is a tropic hormone?

A

1ary function is regulation of hormone secreting cells/ other endocrine glands

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28
Q

What is an example of a tropic hormone

A

Thyroid stimulating hormone produced by anterior pituitary that causes release of thyroxine

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29
Q

What is a non-tropic hormone?

A

Exerts effect on non-endocrine target tissues

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30
Q

What is an example of non-tropic hormones?

A

Insulin on liver/ muscle/ adipose

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31
Q

What is the functional class of peptide hormones? (i.e solubility)

A

Water soluble (hydrophilic)

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32
Q

Describe how hydrophilic hormones bind to target

A
  1. 1st messenger (hormone binds to membrane)
  2. Activated receptor –> cascade –> enzyme activation
  3. Enzyme –> 2nd messenger
  4. 2nd messenger –> response
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33
Q

Why do hydrophilic/ lipophilic hormones bind to cells via different mechanisms?

A

Because hydrophilic hormones can’t cross cell membranes by themselves (lipophilic can), they must bind to external membrane receptors and initiate a catalytic enzyme cascade/ G protein coupled receptor that ultimately releases a 2nd messenger (e.g. cAMP) to elicit the response intracellularly!

Contrastingly, lipophilic hormones can diffuse through cell membranes and subsequently bind to intracellular receptors e.g. cytosol or nuclear receptors, activate gene transcription and exert their desired effect on protein synth.

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34
Q

What is the ultimate actions of cell surface receptors for hydrophilic hormones?

A

G protein coupled receptor or catalytic enzyme coupled receptor –> both activate a transduction cascade and stimulate paths leading to gene transcription

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35
Q

How are peptide hormones secreted?

A

Exocytosis

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36
Q

What is the “action” of peptide hormones

A

Ion channel changes

Second messenger systems

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37
Q

What are 3 examples of peptide hormones

A

Insulin
Glucagon
Angiotensin

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38
Q

Describe the hormone class and function of insulin

A

Peptide
“Store hormone”
Produced in pancreatic B cells
Dec liver gluconeogenesis, inc glycogen synthesis, inc fat retention –> acts on liver/ muscle/ adipose

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39
Q

Describe the hormone class and function of glucagon

A

Peptide
“Mobilise hormone”
Inc liver gluconeogenesis, blood glucose, triglyceride breakdown

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40
Q

Describe the hormone class and function of Angiotensin?

A

Peptide
Na+ & H20 retention
Vasoconstriction
NaCl reabsorption at proximal tubule (via Na+/H+ antiporter, and cAMP drop at GIT)
ADH & aldosterone release as part of RAAAAAAAS

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41
Q

How is the peptide hormone insulin regulated?

A

Pancreatic B cells monitor circulating metabolites (glucose levels) –> parasympathetic stimulation somehow idk

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42
Q

What are the two types of amine hormone;?

A 
Catecholamines (tyrosine derived) 
Thyroid hormones (iodinated forms of tyrosine derivatives)
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43
Q

List some areas of the bod that peptide hormones are produced

A

hypothalamus, pituitary, pancreas, parathyroid, kidneys, liver, heart, GI

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44
Q

Where are amine hormones produced?

A

Adrenal medulla

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45
Q

Describe the solubility of amine hormones

A

Catecholamines are water soluble

Thyroid hormones are iodenated forms of tyrosine derivatives –> lipid soluble

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46
Q

How are hydrophilic amine hormones transported

A

Free hormone bound to plasma proteins

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47
Q

How are amine hormones secreted ?

A

exocytosis

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48
Q

Where do amine hormones bind?

A

Cell surface

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49
Q

What is the “action” of amine hormones over the general target cell?

A

Activation of the 2nd messenger system

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50
Q

What are two examples of catecholamine hormones?

A

Adrenaline

Noradrenaline

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51
Q

Describe the action of adrenaline

A 
Produced in adrenal medulla 
Inc glucose & FAs in blood to inc energy 
Dilate BV 
Glycogenolysis 
Inc glucagon synthesis 
Inc lipolysis
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52
Q

Describe the action of noradrenaline

A

Constrict BV

inc skeletal muscle contraction and HR

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53
Q

Describe the solubility of thyroid hormones

A

Lipid soluble

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54
Q

How are thyroid hormones stored & transported?

A

Stores as thyroglobin in colloids –> cleaved to active T3, T4

Transported bound to plasma proteins

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55
Q

What is the target receptor and action of thyroid hormones?

A

Inside target cell

Direct effect on genes

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56
Q

What is the function of thyroid hormones?

A

Growth (e.g. bone maturation)
BMR (inc metabolic rate, O2 consumption, nutrients, heat production)
Metab (inc glucose use & mobilisation, inc lipolysis & protein catabolism)

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57
Q

What are the steroid hormones derived from?

A

Cholesterol

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58
Q

What are the 4 areas where cholesterol hormones are produced from (+ match w/ hormone)

A
  1. Adrenal cortex (cortisone, androgens, aldosterone)
  2. Ovaries (oestrogen, progesterone)
  3. Testes (testosterone)
  4. Placenta (oestrogen and progesterone)
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59
Q

What is the solubility of cholesterol hormones?

A

Lipophilic

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60
Q

Describe the storage and transport of cholesterol hormones

A

Bound to plasma proteins

Not really stored, only cholesterol precursor stored

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61
Q

How are cholesterol hormones secreted?

A

Via diffusion

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62
Q

What is the general target of cholesterol hormones?

A

Inside cell target

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63
Q

What are two examples of steroid hormones

A

Aldosterone and cortisol

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64
Q

What is the action of aldosterone

A

Reabsorb Na+ to inc BV

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65
Q

What is the action of cortisol

A

Defence against hypoglycaemia –> anti-inflammatory actions

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66
Q

Describe the two feedback mechanisms of cortisol

A
  • ve feedback (long feedback) at pituitary and hypothalamus

- ve feedback (short loop) straight to hypothalamus by ACTH

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67
Q

What are the 4 types of eicosanoid hormones

A
  1. Prostaglandins
  2. Prostacyclins
  3. Thromboxanes
  4. Leukotrines
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68
Q

Which cells produce eicosanoids

A

most cells except erythrocytes!!

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69
Q

What is the solubility of eicosanoids

A

water soluble

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70
Q

What is the general cell target of eicosanoids

A

Cell membrane

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71
Q

What is the general effect of eicosanoid after binding to target

A

Activation of 2nd messenger system, in particular the G protein coupled fam

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72
Q

What I the functions of prostaglandins

A

Vasodilators

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73
Q

What is the function of leukotrienes

A

Allergy
Vascular permeability
Neutrophil chemo-attractant

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74
Q

What is the funcito n of thromboxane

A

Platelet aggregation

Vasoconstriction

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75
Q

What determines the level and duration of hormone secretions

A

Feedback loops –> changes rate of production and secretion
Lifespan in blood –> metabolic inactivation, excretion, extent of plasma protein binding
Number & sensitivity of receptors (cause up and down regulation

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76
Q

What are 3 mechanisms by which endocrine disfunction might lead to disease ?

A

1/ increased or reduced activity of hormones

  1. inc removal from blood/ bad transport
  2. transduction failure (e.g. adequate hormone but cells don’t respond)
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77
Q

What are 4 mechanisms that might cause inc/dec activity of hormones

A
  1. Tumour (e.g. thyroid tumour inc T43, pituitary tumour inc cortisol [cushing’s disease])
  2. Immune (type 1 diabetes from dead pancreatic islet cells)
  3. Genetic (enzyme absence)
  4. Dietary deficiency
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78
Q

What are the 4 types of cell receptors for hormones

A
  1. Kinase linked
  2. G coupled protein receptor
  3. Ligand gated ion channel
  4. nuclear receptors
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79
Q

Describe how ligand gated ion channels work

A

an ion channel opens or closes in response to a binding ligand e.g. acetylcholine

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80
Q

How quick do ion channels work

A

milliseconds

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81
Q

What is an example of a ligand gated ion channel receptor ?

A

nicotinic ACh receptor

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82
Q

What is the difference between ionotropic and metabotropic ion channels?

A

Ionotropic = nicotinic

  • ion channel
  • opens Na+ channel for depolarisation –> skeletal muscle contraction

Metabotropic = muscarinic
- G protein activated –> opens K+ channel for membrane hyperpolarization

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83
Q

Order the speed of the 4 types of endocrine receptors

A

Fastest - slowest

Ligand gated ion channel (milliseconds) > G protein coupled > kinase linked > nuclear (mins-hrs)

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84
Q

Describe how G protein coupled receptors function

A
  1. ligand bonds to exterior GPCR
  2. GPCR undergoes conformational change where A subunit moves away from B, Y subunit (via dissociation).
  3. A binds to one receptor enabling B+Y bind to another.
  4. A subunit changes ion channels to change excitability (I think?!) –> releasing Ca++ –> cell effects
  5. B+Y dimer activates enzyme to produce a 2nd messenger that causes protein phosphorylation –> cell effects
  6. Hydrolysis reverts back to normal
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85
Q

Describe how the ligand epinephrine binds to GPCR to elicit tis functions

A
  1. Binds to GPCR (adrenergic receptor)
  2. conformational change of GPCR
  3. A subunit regulates functions of adenylyl cyclase (i.e takes ATP and makes it cAMP)
  4. cAMP is the 2nd messenger which can intracellularly exert effects

^ HR
dilate skeletal muscle BV
^ Blood glucose

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86
Q

Describe kinase linked receptors

A

They are cytokine receptors where the receptor is an enzyme. The cytokine binds to the enzyme –> protein phosphorylation –> gene transcription –> protein synth –> cell effects

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87
Q

Describe how intracellular (nuclear) receptors function

A

regulate expression of target genes by binding to specific DNA sequences

Either at cytoplasm (cortisol, aldosterone)
Nucleus (thyroid)

88
Q

Endocrine cells secrete stuff in response to…

A

ions, nutrients, neurotransmitters, other hormones

89
Q

What are the two types of feedback loops for hormones ?

A
  1. -ve feedback driven by physiological response
    - -> endocrine gland –> hormone –> target organ = physiological effects –> circulating component e.g. blood glucose –> causes -ve feedback to endocrine gland
  2. Endocrine axis driven
    - -> Hypothalamus neurons –> RELEASE HORMONE –> pituitary gland –> TROPIC HORMONE –> peripheral endocrine gland –> HORMONE –> target organ –> physiological effect.

Hard to explain in a flashy but at the (peripheral) HORMONE level –> short arm -ve feedback acts on pituitary gland and long arm -ve feedback acts on the original hypothalamus neutrons

90
Q

Briefly describe how hormones can act additively with e.g.

A

Both glucagon and adrenaline act on Gs proteins (a class of GPCR receptor) to form adenylyl cyclase –> which is turned into a lot of cAMP and activates SAME enzymes (with an additive effect cause its double)

91
Q

How does cholera toxin exert its effect and on which type of receptor

A

Toxin –> blocks the subunit of GPCR that usually activates adenylyl cyclase so the GPCR can no longer hydrolyse GTP (subunit of the GPCR) so there is no conformational change of the GPCR and nothing can bind!

92
Q

What is the role of nitric oxide signalling

A

signalling molecule in cardiovascular system –> role in controlling blood flow and pressure.

Acts on vascular endothelial cells –> vasodilation

93
Q

Which cells have resting membrane potentials?

A

all cells

94
Q

Name 4 features of action potentials

A
  1. unidirectional
  2. do not lose amplitude along an axon
  3. messages capable of being sent long distances
  4. message intensity sent via frequency of action potentials
95
Q

What is the refractory period ?

A

The short time interval when the axonal membrane is no longer receptive to stimulus

96
Q

What factors influence the velocity of transmission of information along a two-chain neuron network?

A 
Myelination 
larger axon (more ions)
97
Q

Which molecules cause the release of NOs

A

ACh, Bradykinin, adenine nucleutides

98
Q

Which intracellular mechanism causes the release of NO, and from which cells> ?

A

NO synthase is activated by (ACh, bradykinin, adenine) to produce NO which is released from endothelial cells

99
Q

State the steps by which NO is synthesised, released from endothelial cells

A
  1. ACh binds to Gq protein linked receptor on endothelial cell
  2. Ca++ released from ER
  3. NO synthase converts arginine to NO
  4. NO diffuses from endothelial cells
  5. Makes cGMP (2nd messenger)
  6. Acts on smooth muscle
  7. Short T1/2 and breakdown to nitrates/ nitrites stops effect
100
Q

What is a clinical use of NOs?

A

Viagra (Put me in the clinic)

–> blocks degradation of 2nd messenger cGMP so the NO signal is prolonged WOOOOOOO ;)

101
Q

What are 5 key aspects of hormone signalling via cell surface receptors

A
  1. Specficity (e.g. ligand bonding)
  2. Amplification (e.g. because 1st messenger is short lived, 2nd intracellular messenger amplifies effect)
  3. Integration (e.g. pathways that provide reciprocal response to signals
  4. Rapid decay (e.g. allows short term/ reversibility)
  5. Desensitisation (e.g. achieved by feedback loop to reduce effect when appropriate)
102
Q

Where is K+ higher (ICF/ECF)

A

ICF

103
Q

Where is Na+ higher (ICF/ECF)

A

ECF

104
Q

Where is Cl- higher (ICF/ECF)

A

ECF

105
Q

What type of gradient drives K+ out of cell?

A

conc gradient

106
Q

What type pf gradient pulls K+ back into cell?

A

electrical conc/ membrane potential formed by cell becoming more -ve as K+ leaves via ion channels

107
Q

Via what transport system does K+ leave cell?

A

Ion channels via diffusion down conc gradient

108
Q

Via what transport system does Na+ enter cell?

A

Voltage gated ion channels (threshold -50mv )

109
Q

What stops the cell reaching its threshold value for K+ (which is ~-90mV) whilst all dat K+ is leaving down its conc gradient??

A

Small amounts of Na+ are brought into cell to stop ICF from becoming too -ve. They come in via the Na+/K+ ATP-ase pump, which maintains the RMP

110
Q

Which membranes can facilitate AP production?

A

Excitable membranes e.g. of nerves/ muscle cells (sarcolemma)

111
Q

What does the membrane potential change from during production of an AP?

A

-70mV > -50mV (reaches threshold here) > +30mV (polarisation) > ~-80mV (hyper polarisation) > -70mV (RMP)

112
Q

What is important about the conformational channel change at the peak of polarisation?

A

Na+ channels close so no more can enter!
K+ channels open so that RMP can be reinstated
Na+/K+ ATPase channel pumps 2Na+ out for every 2K+

113
Q

Why does hyper polarisation occur?

A

K+ are open so more K+ leaves cell than necessary (making cell more -ve and further from threshold) (i.e value below -70mV)

114
Q

What is the absolute refractory period?

A

time when Na+ permeability changes

115
Q

What is the relative refractory period?

A

Time when K+ permeability changes

116
Q

What are the 3 types of graded potentials

A
  1. Synaptic
  2. Receptor
  3. Pacemaker
117
Q

What determines the effect of neurotransmitters at a post synaptic membrane?

A

Synapse –> excitatory or inhibitory!

Strength of AP

118
Q

How does an excitatory membrane do its thang ?

A

INC permeability to na+, K+ :D
Na+ flows down conch gradient + electrical gradient –> NET +ve ions into post synaptic cell –> brings membrane potential closer to threshold

119
Q

How do an inhibitory membrane work!? ?! !? ! ?!?

A

INC permeability to K+ or Cl- :(
So lessens likelihood of reaching threshold
Closer to hyperpolarisation

120
Q

Name 4x types of neurotransmitters pls

A

ACh,
Catecholamines
glycine
GABA

121
Q

Tell me about ACh

A

Neurot. from neuromuscular junction @ skeletal muscles

  1. Synthesised as postsynaptic axon when acetyl CoA –> acetyl choline via choline acetyltransferase)
  2. released quantally (in little packages) when enough AP affects snare proteins and allows exocytosis from presynaptic terminal
  3. AChE hydrolyses ACh to dec conc
122
Q

Tell me about adrenaline & noradrenaline

A

Neurot. from sympathetic junctions @ smooth muscles (also act as hormones in blood)
Noradrenline acts of forebrain (influencing attention etc) adrenaline not really known

123
Q

Why do APS have no effect at post synaptic neuron body (until axon hillock)? What type of AP are they?

A

Graded potential –> no polarisation effect because axon body has min ion channels

Axon hillock has plenty of voltage gated ion channels so can reach threshold

124
Q

Does ACh acting on a nicotinic receptor elicit an excitatory or inhibitory response

A

Excitatory –> increases Na+ permeability so brings membrane closer to threshold

125
Q

Does ACh acting on a muscarinic M1 receptor elicit an excitatory or inhibitory response

A

Excitatory –> Dec K+ permeability so brings membrane closer to threshold (i.e less K+ leaving = ICF more +ve and closer to -50mV)

126
Q

Does ACh acting on a muscarinic M2 receptor elicit an excitatory or inhibitory response

A

Inhibitory –> Inc K+ permeability so brings membrane further from threshold (i.e cell becomes more +ve)

127
Q

How can neurotransmitter ACh elicity an excitatory OR inhibitory effect at the neuron?

A

Depends on the type of the receptor at the post synaptic membrane!

Nicotinic/ Muscarinic (M1 vs. M2)

128
Q

What is the effect of botulinum toxins and Sarin?

A

Botulinum –> protease toxin that interferes with snare proteins that usually let vesicles travel to synaptic cleft. NO neurotransmission!

Sarin –> similar to OPs, AChE inhibition so can’t mop up neurotransmitter in synaptic cleft.

129
Q

Where does ACh bind to its receptors in skeletal muscles innervated by a nerve fibre?

A

Motor end plate

130
Q

How does AP travel into sarcoplasm of muscle cell

A

T tubule (continuation of the sarcolemma into the sarcoplasm)

131
Q

Outline the role of Ca++ in muscle contraction

A
  1. muscle AP propagated along sarcolemma into sarcoplasm via T tubule
  2. Ca++ released from SR
  3. Ca++ binds to troponin to remove blocking action of tropomyosin
  4. Cross bridge forms and moves to slide actin over mysosin
  5. Ca++ leaving troponin restores tropomyosin blocking actin w/ Ca++ sequestration
132
Q

Describe how APs etc change cause muscle relaxation

A
  1. AP stops

2. ca++ requested from sarcoplasm –> net movement into sarcoplasmic reticulum via Ca++ ATPase pump

133
Q

What are the 3 roles of ATP in muscle contraction and relaxation????

A
  1. energy for movement of cross bridge (actin sliding over myosin)
  2. binds to myosin head to break cross bridge
  3. Drives Ca++ ATPase pump that sequests Ca++ to aid process of relaxation .. so even to relax uses energy!
134
Q

What happens when muscle runs out of ATP

A

can’t relax –> rigor mortis

135
Q

What are the 3 modes of energy metabolism in skeletal muscle contraction?

A
  1. (initial 10sec) stores of creatinine phosphate that is broken by CK to form ATP
  2. Glycolysis –> break down glycogen into glucose –> glycolysis –> TCA (aerobic)
    Oxygen deprivation –> anaerobic glycolysis –> lactic acid builds up and is slowly converted back to glucose via the liver (aerobic TCA continues in background)
  3. B-oxidation –> FA’s broken into Acetyl CoA which goes through TCA to produce ATP
136
Q

What is the difference between Golgi tendon organs and Muscle spindles?

A

Muscle spindles are embedded deep in muscles to detect stretch, Golgi tendon organs are present in tendons to report tension.

137
Q

Describe the nerve supply of a muscle spindle

A

Y motor neuron = efferent neuron innervating intrafusal fibres
A motor neuron = innervating extrafusal fibres

138
Q

How does a muscle spindle detect stretch and describe the activation of the neurons

A

Co activation of Y and A neurons.

The more or the faster the muscle is stretched, the greater the rate of neuron firing

139
Q

Describe what occurs between the neurotransmitter and the post synaptic membrane to elicit an EXCITATORY response

A

Binding of ligand –> inc permeability to Na+, Ca+ –> E.g. Na+ flows down conc gradient –> NET +ve ions into post synaptic cell –> brings membrane potential closer to threshold (At axon hillock so can reach threshold!)

140
Q

Describe what occurs between the neurotransmitter and the post synaptic membrane to elicit an INHIBITORY response

A

Binding of ligand –> inc permeability to K+, Cl- –> lessens likelihood of reaching threshold b/c neurotransmitter binding causes membrane to become more -ve so is further from threshold

141
Q

Name 4 types of neurotransmitters

A
  1. ACh
  2. Noradrenaline/Adr
  3. GABA
  4. Glycine
142
Q

Tell me a lil about ACh

A

Acts at neuromuscular junction at skeletal muscle
NT for pre-ganglionic fibres of ANS
Synthesised at presynaptic axon
Acts on both nicotinic & muscurinic
Formed via acetyl CoA –> choline via choline acetyltransferase
Released quantally in vesicles
Released when voltage gated Ca++ enter presynaptic terminal, changes snare proteins to enable vesicle release via exocytosis
AChE hydrolysed via acetylcholinesterase to clean up cleft

143
Q

Tell me a lil bit about noradrenaline

A

Acts at neuromuscular junctions of smooth muscles
Synthesized by tyrosine –> LDOPA –> dopamine (@ nerve) –> NA (@ vesicle) +/- –> Adr (@ adrenal gland if needed!)
NT for post-ganglionic fibres of ANS
Turned into Adr when sympathetic nerves stimulate the adrenal medulla for production

144
Q

Tell me a tiny bit about Glycine & GABA

A

They inhibit generation of APs at CNS by opening Cl- channels

145
Q

What is the response of a Nicotinic EPSP post synaptic membrane?

A

INC Na+ permeability to move membrane closer to threshold

146
Q

What is the response of a Muscurinic EPSP to the bonding of ACh?

A

M1- DEC K+ permeability, membrane moves closer to threshold e.g. GLAND

147
Q

What is the response of a Muscurinic IPSP to the bonding of ACh?

A

M2- INC K+ permeability, membrane further from threshold e.g. CARDIAC

148
Q

What is the effect of botulinum toxins?

A

Protease toxin interferes with snare proteins that usually let vesicles travel to synaptic cleft. Vesicles can’t migrate to the cleft –> NO transmission of AP

149
Q

What is the effect of sarin?

A

Opposite of Botulinum.

Inhibits AChE, similar to action of OPs

150
Q

What occurs at synapses during skeletal muscle relaxation?

A
  1. AP stops
  2. Ca++ ATPase pumps back to SR
  3. AChE mops up @ cleft
151
Q

What are the 2 sources of ATP for muscles

A
  1. Creatinine phosphate
  2. Glycolysis + TCA
  3. B oxidation
152
Q

Where is the very initial energy derived from for skeletal muscle contraction?

A

Creatinine phosphate that is broken via CK

153
Q

What is the 2nd type of energy metabolism recruited for skeletal muscles during early exercise

A

Glycolysis (aerobic, set amount stored in muscles, then received from blood) then glycolysis (anaerobic, lactic acid converted back to glucose via liver). Can occur concurrently, one is for long term sustainability & the other short term
Also B-oxidation at the same time? IDK

154
Q

Describe the process of B oxidation

A

FAs –> Acetyl CoA –> TCA (dependant on O2)

155
Q

What is the difference in how contraction of cardiac muscle is facilitated compared to skeletal muscle?!

A
  • Contraction not initiated by neuronal input, only influenced by
  • Cells are electrically coupled (pacemaker cells are self excitatory)
  • Long APs
156
Q

Describe excitation- contraction coupling in Cardiac fibres

A

AP spreads along plasma membrane down T tubules, opens voltage gated ion Ca++ channels in T tubules, Ca++ comes in from extracellular environment (no SR) –> facilitates cross bridge cycling

157
Q

How does Ca++ enable contraction of smooth muscle cells

A

changes the shape of myosin (there is no troponin to bind to!), allowing actin to bind

158
Q

Describe the excitation- contraction coupling in smooth muscles

A

^ cytosolic Ca++ > Ca++ binds to calmodulin in cytosol > Ca++ calmodulin complex binds to myosin kinase > Myosin kinase uses ATP to phosphorylate myosin cross bridges > Phosphorylated cross bridges bind to actin filaments > cross-bridge cycling production tension & shortening

159
Q

What are Golgi tendon organs?

A

Situated at muscle-tendon junctions to detect tendon tension as a result of muscle contraction

160
Q

What are muscle spindles vs Golgi tendon organs?

A

detect muscle stretch, GTOs detect tendon tension

161
Q

How do GTOs enable reflexes and the control of muscle activity

A

INC tension stimulates sensory receptor –> GTO stretch releases AP –> EXCITATION, signal travels from local reflex circuitry (sensory neurons) –> AP to SC, sensory neurons synapse directly with A motor neurons –> conduct AP back to muscle, causing it to contract and resist being stretched **Control via -ve feedback by means of local spinal reflexes

162
Q

What does the antagonist muscle do in the situation of a stretch reflex to allow the reflex to occur?

A

Reciprocal innervation allows the relaxation of the antagonist muscle

Interneuron is present to convert the signal from A receptors to inhibitory message for the relaxation of the antagonist muscle in the stretch reflex.

163
Q

How does selectivity for molecular targets lead to specific drug action

A

As determined by receptor/ molecular targets (e.g. full/ partial agonist, antagonist)

164
Q

What is the EC50?

A

Potency of the drug i.e how much you need, measured by the ability to shift the agonist on the curve thing

165
Q

What is the Emax?

A

efficacy of the drug= ability to switch on a response

166
Q

What is drug affinity?

A

Likelihood to bind to target

167
Q

What is the action of a drug agonist?

A

Mimic endogenous molecules that would produce that effect

168
Q

What is the action of a drug antagonist

A

Inhibits endogenous (agonist) molecules by binding competitively –> agonist must be present in the system!

169
Q

What is drug clearance?

A

Irreversible removal

170
Q

What are the main adrenergic NT’s?

A

Adr, NA, dopamine

171
Q

What are the main cholinergic NT’s?

A

Ach

172
Q

What are metabotropic receptors?

A

Muscarinic receptors

173
Q

How do muscarinic receptors convert NT’s to produce a response

A

Activation of 2nd messengers

174
Q

On what tissues are muscarinic receptors??

A

Smooth muscle & glands

175
Q

Why can amplification occur in muscarinic receptors?

A

Amplification can occur with 2nd messengers facilitated intracellular cascades. This ‘magnification’ enables the signals to be more systemic/wide spread but a lil slower

176
Q

What are ionotropic receptors?

A

nicotinic

177
Q

How does a nicotinic receptor interact with a NT to produce an intracellular response

A

Ligand binds to open ion channels

Excitatory/ inhibitory depends on ion coming in

178
Q

Where are the 2 types of nicotinic receptors found?

A 
Skeletal muscle (Nm) 
Neural/ Ganglia (Nn)
179
Q

Name 2 nicotinic agonists

A

ACh, Nicotine

180
Q

Name 2 nicotinic antagonists

A

d-tubocurarine (neuromuscular blocker)

Hexamethonium (ganglia blocker)

181
Q

What are the muscurinic receptors?

A

5x GPCRs

e.g. M3, M2

182
Q

Where are M3 receptors found

A

Smooth muscle & glands

183
Q

Where are M2 receptors found

A

Cardiac muscle

184
Q

Name 2 muscurinic agonists

A

Pilocarpine (tx glaucoma)

Carbachol (tx GIT paralysis)

185
Q

Name 2 muscurinic antagonists

A

Atropine (dec secretions, inc HR and cause bronchodilation)

Hyoscine (treatment of motion sickness)

186
Q

Where are A1 adrenoceptors found?

A

Blood vessels, GIT, pupils

187
Q

Where are A2 adrenoceptors found?

A

nerves

188
Q

Where are B1 adrenoceptors found?

A

Heart, kidney, liver

189
Q

Where are B2 adrenoceptors found?

A

Skeletal BV, bronchi

190
Q

How does activation of A1 receptors activate organs?

A

BV constrict
GIT constrict
pupil constrict

191
Q

Name 4 A1 receptor agonists

A

Phenylephrine
NA
DA
Epinephrine

192
Q

Name 2 A1 antagonists

A

Phentolamine

Prazosin

193
Q

How does activation of A2 receptors activate its target organs?

A

Inihibition of NT release from nerves

194
Q

Name 5 A2 receptor agonists

A

Clonidine, Xylozine, NA, DA, epinephrine

195
Q

Name 2 A2 receptor antagonists

A

Phentolamine

Yonimbine

196
Q

How does activation of B1 receptors activate its target organs?

A

Heart - INC HR, INC CO
Kidney- Renin
Liver - Glycolysis

197
Q

Name 2 B1 agonists

A

Isoprenaline

Dobutamine

198
Q

Name 2 B1 antagonists

A

Propanolol

199
Q

How does activation of B2 receptors activate its target organs?

A

Skeletal BV dilate

Bronchi dilate

200
Q

Name a B2 agonist

A

Salbutamol

201
Q

which receptor is NA most efficient at acting on?

A

A1 > B1 ~ A2&raquo_space; B2

202
Q

Which receptor does NA have worst affinity for?

A

B2

203
Q

Which receptor does Adr have highest affinity for?

A

B2 ~ B1 ~ A1 > A2

204
Q

Which receptor does Adr have worst affinity for?

A

A2

205
Q

Which G protein does A1 activate?

A

Ga

206
Q

Which G protein does A2 activate ?

A

Gi

207
Q

Which G protein does B1 activate ?

A

Gs

208
Q

Which G protein does B2 activate ?

A

Gs

209
Q

Describe the ligand bonding/2nd messenger/ enzyme cascade of A1 adrenoceptors

A

A1 –> Ga –> Phospholipase enzyme –> IP3, DAG

210
Q

Describe the ligand bonding/2nd messenger/ enzyme cascade of A2 adrenoceptors

A

A2 –> Gi –> Adenylyl cyclase –> DEC cAMP

211
Q

Describe the ligand bonding/2nd messenger/ enzyme cascade of B1 adrenoceptors

A

B1 –> Gs –> Adenylyl cyclase –> INC cAMP

212
Q

Describe the ligand bonding/2nd messenger/ enzyme cascade of B2 adrenoceptors

A

B2 –> Gs –> Adenylyl cyclase –> DEC cAMP

213
Q

What are the 4 types of cholinergic receptors (we know)

A

Muscurinic –> M2, M3

Nicotinic –> Nm, Nn

214
Q

Describe how ligand bonding causes a decrease in HR in M2 receptors

A

Ligand bonds to GPCR Gi –> Gi acts via adenylyl cyclase enzyme –> DEC cAMP, DEC K+ channels (NET inhibitory) –> DEC HR

215
Q

Describe how ligand bonding causes stimulation of smooth muscles and glands in M3 receptors

A

Ligand bonds to GPCR Gq –> Gq acts via phospholipase C enzyme –> INC IP3 (INC Ca2+ for INC GIT contraction & secret) & INC DAG (protein kinase C)

Applications Animal Health (9 decks)

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