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1a) Who discovered the BBB?
1a) Paul Ehrlich
1b) What role do astrocytes play in forming the BBB?
1b)
surround capillaries in CNS
& secretes chemical that causes tightening
1c) why is there reason for leaky (weakened) areas in the BBB?
1c)
homeostasis
pituitary gland: endocrine and hormone reg
pineal glad: melatonin release
area postrema: toxicity monitor (vomitting)
2a-1) intermittent, low lvl depolarization (less neg) that creates small, short-lived changes in potential across axonal membrane—what are the changes called?
2a-1)
graded potentials
sub threshold events that aren’t strong enough to travel long distance
2a-2) Why was an AP not produced with low lvl depolarizing stimulation?
2a-2)
threshold potential not reached
need to depolarize (less neg) to open voltage-gated Na+ channels
2b-1) Then: more depolarizing stimulation is applied to giant squid axon and an AP is produced.
Why do the actions of the ion channels and movements across the axonal membrane cause the depolarization phase (the upsweep) of the AP and subsequent return to resting potential?
2b-1)
threshold reached to open voltage-gated Na+ channels (rapid)
upsweep (depolarization - less neg)
THEN: Na+ inactive & K+ channels open & flow
repolarization
delayed K+ close
hyperpolarization (more neg)
resting potential restored
3a) When neuron receives natural stimulation (from other neurons), why do APs first form at the axon hillock and not in the dedrites or the soma of a neuron?
3a)
@ axon hillock bc high density (voltage-gated Na+ channels)
EPSPs formed & detected here to determine if threshold reached
Not in dendrite or soma bc:
ligand-gated channels w little/no voltage-gated channels to start AP
3b) Why does the size of AP remain same as it travels down unmyelinated axon?
3b)
regenerative = continuous conduction bc of depolarizaiton (less neg) voltage-gated Na+ channels that trigger new AP
3c) If you place a stimulated electrode inside of a long axon midway b/w the soma of a neuron and the axon terminal (end foot) and provide sufficient stimulation to cause an AP, what direction would the AP travel?
3c)
both directions bc middle stimulated
surrounding tissues not in refractory pd
3d) How would the shape of an AP change if you were to treat the axon w/ a chemical that selectively blocked voltage-gated K+ channels w/out altering the activity of any other channels?
3d)
repolarization (reset) slowed bc depolarization (less neg) prolonged
AP would have:
slower down slope (repolarization)
or incomplete repolarization
wider shape (longer duration)
risk of Na+ channels not working and K+ channels causing neuron dysfunction bc of it