Brainscape's Knowledge GenomeTM

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


See full index

PHPY 301 > 12. Lecture 26, 27 > Flashcards

12. Lecture 26, 27 Flashcards

1
Q

What are osmoreceptors?

A

Neurons able to sense changes in plasma osmolality
Located in the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO)
Elevated osmolality activates mechanosensitive cation channels in the neuronal membranes and causes depolarization and increased frequency of AP, hypo-osmolality decreases frequency

Slide 1-2 lecture 26

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

Where do osmosensitive neurons project to?

A

Project to large diameter neurons (magnocellular neurons) in the supraoptic (SON) and paraventricular nuclei (PVN) of anterior hypothalamus

Magnocellular neurons synthesize arginine vasopressin (AVP), that is transported along their axons to nerve terminals in the posterior line of pituitary
AVP enters general circulation

Slide 1-2 lecture 26

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

How does osmosensation turn to systemic osmoregulation?

A

Hyperosmolality triggers 2 parallel feedback control mechanisms that have a common endpoint: increase in whole body free water

AVP osmoreceptors in the hypothalamus trigger magnocellular neurons to release AVP, results in increase in reabsorption of water in the kidneys (reduced excretion of water)
Thirst osmoreceptors also trigger appetite for water

Reduction in osmolality
Increase in whole body free water

Slide 3 lecture 26

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

Study kidney breakdown slides 5-6 lecture 26

A

Okay

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

What makes collecting duct permeable to water?

A

Vasopressin makes collecting duct permeable to water

Permeability of last portion of tubules can vary greatly due to physiological conditions
Major determinant of controlled permeability is the peptide hormones arginine vasopressin (antidiuretic hormone; ADH)

Slide 7-8 lecture 26

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

What are the 4 steps of insertion fo water into the apical membrane?

A
  1. Vasopressin binds to membrane receptor
  2. Receptor activates cAMP second messenger system
  3. Cell inserts AQP2 water pores into apical membrane
  4. Water is absorbed by osmosis in the blood

Slide 9 lecture 26

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

Where are the 2 places AQP2 water pores are found?

How does vasopressin affect these pores?

A

AQP2 is found:
On the apical membrane facing the tubule
In the membrane of cytoplasmic storage vesicles

When vasopressin levels/water permeability levels low, collecting duct has few water pores but stores them in cytoplasmic storage vesicles
When vasopressin arrives at collecting duct it binds to its V2 receptors on the basolateral side of cell, exocytosis inserts AQP2 water pores into apical membrane

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

What is the short term regulation of water permeability?

A

AVP via cAMP causes water channel containing vesicles from a subapical pool to fuse with the membrane

Number of channels and water permeability sharply increase

Slide 11 lecture 26

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

What is the long term regulation of water permeability?

A

AVP by enhancing transcription of the AQP2 gene increases the abundance of AQP2 protein

Slide 11 lecture 26

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

Study the steps in these two scenarios:
If we were so overhydrated we had no ADH
If we were so dehydrated we had maximal ADH

Slide 12 lecture 26

A

Okay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does vasopressin do to urea?

A

Vasopressin increases urea reabsorption
Vasopressin increases permeability of the inner medullary portion of the collecting duct to urea by increasing the activity of apical UT-A1 urea transporters
Results in increase reabsorption and high interstitial urea

Slide 13 lecture 26

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

Study the graphs of no vasopressin and max vasopressin effect on slide 14 lecture 26

A

Okay

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

What is central (neurogenic) diabetes insipidus?

A

Inability to produce or release ADH from posterior pituitary
Distal tubular segments cannot reabsorb water in absence of ADH

Results in formation of large volume of dilute urine, thirst mechanisms are activated when excessive water is lost

Can be caused by brain tumour, trauma, infection, brain surgery
Treat with vasopressin analog desmopressin (DDAVP)

Slide 15 lecture 26

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

What is primary (psychogenic) polydipsia?

A

Compulsive water drinking
Synthesis, secretion, nephron sensitivity to ADH and osmoreceptor response all intact

Seen in some patients with severe mental illness
Water intoxication

Slides 16-17 lecture 26

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

What is regulatory volume increase (RVI)?

A

A hyperosmolal extracellular solution exerts an osmotic force that draws water out of a cell
The cell continues to shrink until the osmolality inside and out becomes the same
Many types of cells respond to this shrinkage by activating different types of solute uptake processes to increase cell solute and water content in a response known as RVI

Slide 1 lecture 27

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

What is regulatory volume decrease (RVD)?

A

A hypo-osmolal extracellular solution exerts a lesser osmotic force so that water moves into a cell
The cell continues to swell until the osmolality inside and out becomes the same
Many types of cells respond to this swelling by activating different types of solute efflux processes to decrease cell solute and water content in a response known as RVD

Slide 2 lecture 27

17
Q

What are osmosensitive neurons?

A

Unlike other cell types that regulate their volume when exposed to osmotic stress, osmosensitive neurons display passive changes in volume varying as an inverse function of extracellular fluid osmolality and can be maintained without adaptation during long lasting perturbations

Cells exposed to hypotonic conditions show an increase in volume and decrease in intracellular ionic strength

Slide 3-4 lecture 27

18
Q

What is the osmotic control of vasopressin release?

A

Changes in osmolality cause inversely proportional changes in cell volume
Hypertonicity evoked shrinkage activates nonselective cation channels leading to depolarization and an increase in the action potential firing rate and vasopressin release from axon terminals in the neurohypophysis
Increased VP levels in blood enhance water reabsorption by the kidney (antidiuresis) to restore extracellular fluid osmolality

Slide 5 lecture 27

19
Q

What is osmosensory transduction?

A

Mechanical process
Intrinsic osmosensitivity reflects a mechanical regulation of nonselective action channels during volume changes rather than an effect caused by changes in solute concentration or ionic strength
Volume changes by negative pressure (shrinking) or positive (swelling) through patch pipette have direct effects on magnocellular neurosecretory cells (MNCs)

Slide 6 lecture 27

20
Q

What do suction-evoked shrinkage activate?

What about inflation evoked swelling?

A

Activates nonselective cation channels (upper schematic) which causes a reversible membrane depolarization and an increased AP firing rate

Inflation evoked inhibits the cation channels that are open under basal conditions leading to hyperpolarization and a decrease in firing rate

Slide 6 lecture 27

21
Q

How does stretch activated (hypotonic and hypertonic) cationic channels transduce osmoreception?

A

Resting osmotic conditions, portion of stretch inactivated cationic channels is active and allows influx of positive charge

Hypotonic stim provokes cell swell and inhibits channel activity, hyperpolarize cell

Hypertonic stim provokes cell shrink and activated increased number of channels creates charge influx and depolarizes membrane

Slide 7 lecture 27

22
Q

What is local response?
What is synaptic response?
What is combined response?

A

Local response- opening of stretch inactivated cationic channels on MNCs in response to cell shrink (caused by increase in ECF osmolality causing depolarization)
Synaptic response- activation of primary osmosensitive neurons in the OVLT and SFO causes an increase in excitatory post synaptic potentials in MNCs

Combined response- both effects contribute to an increase in MNC firing and therefore an increase in the release of vasopressin

Slide 8 lecture 27

23
Q

What is the transient receptor potential channel subfamily V member 1 (TRPV1 channel)?

A

Transduces the sensation of painful heat and mediates pain-producing actions of capsaicin

Membrane currents are enhanced by a reduction in pH, a characteristic of the chemical milieu of inflammation

A variety of TRP channels is thought to underlie the perception of a wide range of temps

Slide 9 lecture 27

24
Q

How are nociceptive signals transduced?

A

Noxious stimuli depolarize free nociceptor endings and generate APs that are propagated centrally

The membrane of the nociceptor contains unique receptors that subserve the transduction of the thermal, mechanical, or chemical energy of noxious stimuli into a depolarizing electrical potential

Slide 10 lecture 27

25
Q

Study osmosensory channel expression of TRPV1 channels of slide 11 lecture 27

A

Okay

26
Q

How do components of the cytoskeleton contribute to osmosensory neurons?

A

Osmosensory neurons feature a unique cytoskeleton
Elements of the cytoskeleton including actin filaments (F actin) and microtubules participate in the transmission and distribution of forces applied to the osmoreceptor cell surface

The microtubules are positioned in a wide variety of angles relative to eachother creating complex dense and interweaves 3D scaffold
MNCs feature thin but dense layer of actin

Slide 12

27
Q

How to microtubules interact with TRPV1 channels?

A

Interact on surface of osmoreceptors
Microtubules extend all the way to the surface of where they come in close contact with the plasma membrane
At rest, many TRPV1 channels are bound to microtubules, few are activated because of lack of sufficient pushing force

Slide 13

28
Q

How is thirst created?

A

A 1% increase in osmolality is detected as the sensation of thirst
Irritability and lethargy are observed in the yellow range, and more severe effects become evident at larger deviations

Slide 14

29
Q

What is used for motivational drive of water intake?

A

The dynamic regulation of neurons in the median preoptic nucleus (MNPO) by OVLT and SFO neurons is critical for drive for water intake

Glutamatergic neurons in the MNPO have been shown to receive thirst promoting signals from OVLT neurons and SFO glutamatergic neurons which increases during rate of MNPO neurons in proportion with systemic water deficits

Slide 15

30
Q

How does drinking immediately quench thirst?

A

Drinking quenches thirst in anticipation of water absorption
The activity of MNPO neurons is regulated by inputs from the periphery that signal predictive information about impending changes in ECF osmolality expected to arise from fluid ingestion
GABA containing MNPO neurons increase activity in response to activation of sensory receptors in the oropharynx as a result of fluid ingestion

Slide 16-18

PHPY 301 (13 decks)

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