respiration

Question 1

why do we need to respire?

Answer 1

get O2, remove CO2, maintain blood pH, match metabolism, temperature regulation

Question 2

respiration is controlled by what part of NS?

Answer 2

autonomic NS

Question 3

is expiration passive or active?

Answer 3

passive

Question 4

diaphragm
ins/exp?, innervation?

Answer 4

inspiration
phrenic nerve

Question 5

external intercostals
ins/exp?, innervation?

Answer 5

inspiration
thoracic intercostal nerves

Question 6

genioglossus
ins/exp?, innervation?

Answer 6

inspiration
hypoglossal nerve

Question 7

laryngeal aBductor muscles
ins/exp?, innervation?

Answer 7

inspiration
recurrent laryngeal nerve

Question 8

laryngeal aDductor muscles
ins/exp?, innervation?

Answer 8

expiration

Question 9

3 phase event - inspiration

Answer 9

Phrenic nerve activation increases = diaphragm contracts (down)
This causes intrapleural pressure to decrease (bigger cavity)
Tracheal dilation via firing of recurrent laryngeal nerve
Intra-alveolar pressure increase (air in)

Question 10

3 phase event - post inspiration

Answer 10

Phrenic nerve activation decreases = diaphragm relaxes (up)
This causes intrapleural pressure to increase (smaller cavity)
Radius of airway constricts -> via decreased firing of recurrent laryngeal nerve (traps O2 in = better diffusion)
Intra-alveolar pressure remains high b/c cavity is smaller

Question 11

3 phase event - late expiration

Answer 11

Diaphragm remains relaxed
Recurrent laryngeal nerve relaxes = airways dilate
Intrapleural pressure increased (cavity is smaller)
Intra-alveolar pressure decrease (empties)

Question 12

ventral respiratory group (vrg)

Answer 12

potential source of respiratory rhythm
projects to hypoglossal nerve from ventral surface of medulla

Question 13

pre-botzinger complex

Answer 13

potentially the respiratory rhythm generator
because:
firing pattern matches inspiration pattern
when dead: erratic, less frequent breathing that eventually ceases completely

Question 14

pre-botC neurons
chemical markers

Answer 14

Glutamatergic (subset that’s glycinergic)
NK1-receptor expressing
SST expressing (usually inhibitory neuropeptide)
Dbx-1 expressing (transcription factor- traces where neurons come from)

Question 15

Nk1-R

Answer 15

expressed on pre-botC neurons
Ligand = Substance P
GPCR
NK1-R & Substance P internalised after binding

Question 16

saporin (SAP)

Answer 16

inhibits ribosomes = cell death

Question 17

SAP + Sub P

Answer 17

internalised via Nk1-R
= cell death after a couple of days
resulted in:
gaps of apnea, and random bursts of activity
proving pre-botC needed for resp rhythm

Question 18

SST promoter delivery:

Answer 18

Drives expression of EGFP and allatostatin receptor = infected
This inhibits pre-BotC
In awake: apnea (breathing stopped)
In Anaesthetised: apnea, but recovery after 60 min mechanical ventilation (allatostatin unbinds)

Question 19

properties of pre-botC pre-inspiratory neurons

Answer 19

functionally: excitatory, inhibitory, rhythmogenic
Chemically: somatostatinergic, nk1 expressing, glycinergic, glutamatergic

Question 20

what happens when ca2+ current blocked in prebotc neurons

Answer 20

smaller intrinsic bursts

Question 21

what happens when ca2+ and Na+ blocked in prebotc?

Answer 21

complete loss of intrinsic bursting

Question 22

how many little bursts = big burst in pre-botC

Answer 22

9 cells activated

Question 23

MSA
multiple system atrophy

Answer 23

dysrhythmic breathing
less cells

Question 24

SCA3

Answer 24

normal amount of cells
no breathing issues with this disease

Question 25

add agonist to inhibitory u-opiod receptor

Answer 25

membrane potential down erratic respiration

Question 26

RTN / PFRG

Answer 26

rhythm generator for active expiration

Question 27

PiCo

Answer 27

post inspiratory complex - post inspiratory rhythm generator - Burst just after pre-botC

Question 28

two rhythm generator model

Answer 28

1. inspiration: prebotC 2. expiration: RTN/pFRG

Question 29

3 rhythm generators

Answer 29

Inspiration: pre-botC Post Inspiration: PiCo Expiration: lateral parafacial nucleus rtn / pfrg

Question 30

GABA injection into pontine respiratory group

Answer 30

increase respiratory frequency expiratory shortened

Question 31

inject glutamate into pontine respiratory group -> what neuronal subtype would increase activity?

Answer 31

post-inspiratory

Question 32

hering-bruer reflex & cough reflex

Answer 32

stop over inflation of lungs activated by pulmonary stretch receptors

Question 33

activation of PSRs will result in what?

Answer 33

Slowing of respiratory rhythm Prolongation of expiration Inhibition of inspiration

Question 34

PSR activation -> effect on post inspiratory website

Answer 34

excitation

Question 35

PSR activation -> inspiratory neurons

Answer 35

inhibit

Question 36

PSR activation -> aug E neurons

Answer 36

inhibit

Question 37

what do pulmonary stretch receptors

Answer 37

decrease respiration frequency increase expiration time

Question 38

peripheral chemoreceptors

Answer 38

carotic body, aortic body, baroreceptor fibres, glossopharyngeal nerve

Question 39

carotid travels via what spinal nerve to NTS?

Answer 39

IX (9)

Question 40

aortic travels via what spinal nerve to NTS?

Answer 40

X (10)

Question 41

difference between Type I and Type II cells near blood vessels

Answer 41

Type !: - Closer to detect changes - Chemosensing glomus cell - Respond to LOW O2 and HIGH CO2 Type II: - Glial Like ensheathing

Question 42

increased phrenic nerve activity and amplitude results in what

Answer 42

greater respiration

Question 43

hypoaxemia results in?

Answer 43

increased sympathetic activity and increased respiration

Question 44

what does a tonic receptor mean?

Answer 44

always sending in a certain phase, so when this is disrupted even a little bit, has a big affect

Question 45

peripheral chemoreceptors respond to

Answer 45

low O2 in blood, high CO2 in blood, low pH in blood

Question 46

central chemoreceptors respond to

Answer 46

high CO2 in CSF

Question 47

locomotor respiratory coupling

Answer 47

Stimulate forelimb = increased respiration Stimulate forelimb = shortening of Post-I phase Inhibition of Post-I neurons & Excitation of Aud-E neurons Brings E2 phase forward

Question 48

GABAa agonist injected in PRG

Answer 48

Goes at own rhythm Therefore phase mediated through PRG

Question 49

how is locomotor respiratory coupling resetting produced?

Answer 49

Feedback from somatic afferents resetting of rhythm mediated through the PRG mediated via substance P in the Bötzinger Complex