pre exam 3 (part 2) Flashcards

1
Q

action potential generation at the AIS

A
  • AIS has high density of voltage-gated ion channels

- if threshold potential reached, tons of Na+ let in from these

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2
Q

action potential propagation along the axon

A
  • # of action potentials must be conserved (same at AIS and at axon terminal)
  • voltage gated ion channels along the axon restore the action potential as it’s conducted
  • myelination increases speed of conduction
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3
Q

unmyelinated vs myelinated axons

A

unmyelinated

  • came first, common in autonomic parts of the brain
  • more Na+ and K+ channels because current is lost (and voltage must be conserved)

myelinated

  • myelinated by oligodendryoctes
  • Na+ and K+ channels only at nodes of ranvier
  • 4-10x faster

*15k miles of axons in the body!

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4
Q

demyelination

A
  • demyelination causes loss of action potentials in nerves and circuit disfunction
  • many diseases result from demyelination, MS is common (antibodies against myelin-making protein)
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5
Q

significance of Na+/K+ pump for membrane potential

A
  • expressed in every cell
  • pump is electrogenic–generates a negative electric potential in the cell (3 Na+ out, 2 K+ in)
  • negative potential from pump powers membrane transport (Na+ diffuses in when channels open based on concentration AND electrical gradient)
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6
Q

positive and negative feedback

A

positive

  • positive feedback loops move you away from a set point
  • few examples in bio, inherently unstable

negative

  • negative feedback loops move you toward the set point
  • allow control
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7
Q

significance of the hypothalamus and pituitary gland

A
  • major hubs of homeostatic control

- all the hormonal output is controlled by feedback loops

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8
Q

respiration feedback loop

A
  • lack of O2/increase in CO2
  • peripheral/central chemoreceptors sense
  • activate respiratory centers in medulla
  • activate breathing muscles
  • increase alveolar ventilation rate
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9
Q

blood pressure regulation loop

A
  • baroreceptors sense change in blood pressure
  • medulla responds (sympathetic or parasympathetic)
  • HR and SV change, altering blood flow
  • blood pressure is corrected to set point
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10
Q

role of thyroxine

A
  • thyroxine regulates metabolism in all cells

- sets the basal metabolic rate of the cell

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11
Q

hypothalamus/anterior pituitary relationship

A
  • anterior pituitary and 6 hormones that come out of it are regulated by releasing hormones from the hypothalamus
  • each pituitary hormone has a unique releasing or inhibiting hormone from the hypothalamus
  • hormones released by different cell types
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12
Q

regulation of thyroxine

A
  • 2 forms of thyroid hormones: thyroxine (T4) and triiodothyronine (T3)
  • low levels of T3/4 signal release of thyrotropin releasing hormone (TRH) from hypothalamus
  • causes release of thyroid stimulating hormone (TSH) from anterior pituitary
  • TSH binds to thyroid stimulating hormone receptor (TSHR), releasing T3 and T4
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13
Q

normal blood glucose levels

A

70-140 mg/dl

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14
Q

T3 vs T4

A
  • T3 (triiodothyronine) is more biologically active than T4 (thyroxine)
  • after transporters bring T3/4 into cell, T4 converted into T3
  • deiodinases D1 and D2 remove an iodine from T4 to make T3
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15
Q

function of T3 in the cell

A
  • T3 is a global transcription factor (increases metabolism in all cells)
  • binds to its hormone receptor element on DNA (TRE)
  • binding to different genes (some enhanced and some inhibited) has a net effect of increasing metabolism
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16
Q

enhancers vs repressors

A

enhancers increase gene transcription, repressors decrease gene transcription

17
Q

goiter formation

A

goiter: enlarged thyroid, low T3/T4 levels due to lack of iodine (normally we get it from salt)

  • T3/4 can’t be made without iodine
  • negative feedback loop lost: thyroid keeps trying to make more T3/4 due to low levels, but it’s all non-functional without the iodine
  • leads to cellular hypertrophy (swelling) and hyperplasia (more cells) as the thyroid attempts to make more T3/4
18
Q

growth hormone cascade

A
  • hypothalamus secretes releasing or inhibiting factors (primary hormone)
  • anterior pituitary releases growth hormone (secondary hormone)
  • liver and other tissues release insulin-like growth factor (IGF-1) (tertiary hormone)

***IGF-1 does most of the work in increasing growth!

19
Q

binding of IGF-1

A
  • like insulin, IGF-1 binds to tyrosine kinase receptors
  • receptors dimerize, autophosphorylate, and then can phosphorylate targets
  • activates kinases that cause global changes in gene transcription through phosphorylation
20
Q

impacts of IGF-1

A
  • promotes growth, cell proliferation, and survival (similar to insulin)
  • greatly impacts bone growth
  • excess can cause tumors or feedback issues
21
Q

what functions can kinases do? how is their activity undone?

A
  • regulate transcription
  • regulate cellular signaling
  • phosphatases dephosphorylate targets!