LO 1

Question 1

effector organs which interact with a1 adrenergic receptors

Answer 1

blood vessels, eye, GI tract

Question 2

is vascular tone controlled primarily by sympathetic or parasymp?

Answer 2

sympathetic

(sympathetic control of tone for BVs is the exception, the dominant control of tone for everything else is parasympathetic - calms down your body)

Question 3

Enzyme that makes ACh

Answer 3

acetyl coA + Choline ——-Choline acetyl transferase (ChAT) ———–> ACh

(all takes place in cytoplasm

Question 4

toxin that increases ACh release

toxin that decreases ACh release

Answer 4

toxin that increases ACh release
- Black widow spider toxin (BWST)

toxin that decreases ACh release
- botulinum toxin

Question 5

M1 and M3 receptors act on Gq proteins, where do they act?

Answer 5

M1: CNS, GI/gastric glands, symp postgang cells

M3: exocrine glands, smooth muscle

Question 6

M2 and M4 receptors act on Gq proteins, where do they act?

Answer 6

heart, lungs, CNS

Question 7

How is epinephrine produced?

Answer 7

NE is converted to E by phenylethanolamine N methyl transferase in the ADRENAL GLAND and certain CNS NEURONS

Question 8

What is the name of the transporter that takes up these NTs into the vesicle?

1. ACh
2. NE
3. E
4. GABA

Answer 8

1. ACh - VAT
2. Dopamine - VMAT (vesicular monoamine transporter)
3. NE - synth in the vesicle from Dopamine
4. E - made from NE
5. GABA - VGAT

*note: monoamines are DA and NE

Question 9

What is the name of the transporter that takes up these NTs into the presynaptic membrane?

1. ACh
2. Dopamine
3. NE
4. serotonin
5. GABA
6. Glutamine

Answer 9

1. ACh : choline transporter
2. Dopamine: DAT
3. NE: NET
4. serotonin: SERT
5. GABA: GABA transporter
6. Glutamine: Gt(n)/Gt(g)->astrocytes

Question 10

What is more common, direct acting or indirect acting adrenergic agonists for therapeutic agents?

Answer 10

direct - due to receptor subtype allowing selectivity

Question 11

characteristics of catecholamine (NE and E) absorption, distribution, duration of action

Answer 11

not effective orally
do not enter brain well
have short durations of action

Question 12

why are sympatholytics clinically limited?

Answer 12

due to their lack of specificity of action

- all adrenergic synapses are affected

Question 13

What type of adrenergic antagonists have the greatest clinical utility

Answer 13

adrenergic receptor blockers - due to their specificiy

Question 14

how are a2 receptors counterintuitive?

Answer 14

reduces sympathetic nervous system activity

ie: reduces NE release

Question 15

what adult structures do the metencephalon diff into?

Answer 15

pons, cerebellum

Question 16

third ventricle comes from which secondary structure?

Answer 16

diencephalon

Question 17

4th ventricle comes form which secondary structure?

Answer 17

metencephalon and myelencephalon

Question 18

the prosencephalic vesicle segments into how many vesicles?

Answer 18

3

• two telen
• 1 dien

Question 19

what structure releases Shh?

What structures releases BMP?

Answer 19

notochord: Shh signals overlying ectoderm to divide more rapidly

lateral ectoderm: BMP

Question 20

Shh is produced by more (pick one) ventral/dorsal structures

Answer 20

ventral

basal plate

Question 21

Diff between neural progenitors in the cerebral cortex vs spinal cord

Answer 21

cerebral cortex: inside out

spinal cord: pop developed based on dorsal ventral axis -

• ventral = motor
• dorsal = sensory

Question 22

sulcus limitans

Answer 22

when the neural tube develops a crease, which separates ventral from dorsal populations

Question 23

ventral and dorsal positions with regards to alar/basal plate

until which segment in the brain do you see this pattern?

Answer 23

ventral = basal plate (Shh)
dorsal = alar plate (BMP)

This pattern is seen up through the mesensephalon (though not as well preserved)

Question 24

what are rhombomeres and why are they imp?

Answer 24

rhombencephalon is made of 8 rhombomeres
neurons for CNs originate from rhombomeres

rhombomeres form the rhombocephalon due to diff expression of HOX genes, which forms the hindbrain in vertebrates.