pre exam 3 (part 2) Flashcards
action potential generation at the AIS
- AIS has high density of voltage-gated ion channels
- if threshold potential reached, tons of Na+ let in from these
action potential propagation along the axon
- # 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
unmyelinated vs myelinated axons
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!
demyelination
- demyelination causes loss of action potentials in nerves and circuit disfunction
- many diseases result from demyelination, MS is common (antibodies against myelin-making protein)
significance of Na+/K+ pump for membrane potential
- 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)
positive and negative feedback
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
significance of the hypothalamus and pituitary gland
- major hubs of homeostatic control
- all the hormonal output is controlled by feedback loops
respiration feedback loop
- lack of O2/increase in CO2
- peripheral/central chemoreceptors sense
- activate respiratory centers in medulla
- activate breathing muscles
- increase alveolar ventilation rate
blood pressure regulation loop
- 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
role of thyroxine
- thyroxine regulates metabolism in all cells
- sets the basal metabolic rate of the cell
hypothalamus/anterior pituitary relationship
- 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
regulation of thyroxine
- 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
normal blood glucose levels
70-140 mg/dl
T3 vs T4
- 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
function of T3 in the cell
- 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
enhancers vs repressors
enhancers increase gene transcription, repressors decrease gene transcription
goiter formation
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
growth hormone cascade
- 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!
binding of IGF-1
- 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
impacts of IGF-1
- promotes growth, cell proliferation, and survival (similar to insulin)
- greatly impacts bone growth
- excess can cause tumors or feedback issues
what functions can kinases do? how is their activity undone?
- regulate transcription
- regulate cellular signaling
- phosphatases dephosphorylate targets!
