1.5 Phys Must Knows Flashcards
Name ligand receptors with tyrosine kinase activity?
*insulin, epidermal GF and fibroblast GF
what is JAK/STAT pathway?
JAK is a membrane transduction pathway
*in this case, the receptor doesn’t have an enzymatic subunit but it is closely related to phosphorylation of STAT
the degree of cell electronegativity is dictated by?
cell type and cell size
- large motor skelelal/cardiac muscle = -90mV
- small nerves/CNS/smooth muscle = -40 to -60mV
- RBCs= -10 to -20
Big point of opening K+ channels (equilibrium potential for K+)
open K channels, K leaves cell (EFFLUX)nand membrane charge races to -94 (which is equilibrium potential for K)
*this is where the chemical conc gradient from inside to outside is equal to and opposite of the electrical gradient which is 0mV on outside and now -94 inside
No efflux of moleules when their channels are open indicates?
electronegative equalibrium
(Ex: once cell membrane reaches -94 for K, it’s so negative that it’ll refuse to let K+ leave anymore – opposites attrack)
what is equilibirum potential for K+? for Na+?
K+ = -94 (will hyperpolarize; inhibitory) Na+ = +61 (will depolarize; excitatory)
Big point of opening Na+ channels (equilibrium potential for Na+)
Na INFLUXES (rushes inside cell) *as the membrane races towards +61 and the inside of the cell becomes more electropositive, it eventually REPELS any further + charge from entering
Big point about equilibrium potentials?
for any molecule, it only tells you what the membrane charge is going to race towards, does NOT mean it will get there
EPSP?
excitatory post-synaptic potentials are GRADED
- drives axon hillock closer to threshold (depolarize)
- makes nearuon more excitable
IPSP?
inhibitory post-synaptic potentials are GRADED
- drive axon hillock AWAY from threshold (hyperpolerize)
- makes neurons less excitalbe
Example of EPSP?
1) Ach binds onto receptor
2) Na+ pores OPEN (influx)
3) membrane depolarizes/excited/towards threshold
* ** can also be ligand that CLOSES K or CL
Example of IPSP?
1) ligand binds on post-synaptic membrane
2) causes K+ or Cl- channels to open
3) K+ = EFFLUX; Cl- = influx
4) membrane hyperpolarizes/UNexcited/away from threshold
describe depolarization, overshoot, repolarization, hyperpolarization and stimulation for A and G potentials?
- depolarization= line goes up towards negative
- oveshoot= line bypasses 0mV
- repolarization= line descends back to resting poten.
- hyperpolarization= line dips below resting, more -
- stimulation= NOT continuous, an event
Local anesthetic blocks?
*Ex of local?
blocks sodium channels, so dendrites and cell bodies unaffected
*lidocaine
two types of stimulus in action and graded potentials? What dependent on stimulus?
inhibitory= hyperpolarization (K+)
excitatory= depolarization (Na+)
**amplitude of GRADED potentials are modulated by stimulus strength
location of graded and action potentials?
graded= dendrites/cell body with ligand gates action= axon with voltage gates
temportal vs spatial summation?
which one has greater stimulation?
- temporal= over time with 1 stimulating force happening multiple times
- spatial summation= multple stimulating events coming from different places at same time great stimulation
mylinated vs unmyelinated nerves?
*Myelinated= nerve conduction velocity 5-50X greater, decreases energy requirment for conduction, better nerve generation, BUT takes more energy to form myelinated nerves, take longer to numb
characteristic of graded vs action potentials?
- action= all-or-not; MUST meet threshold, have refractory periods; NO Summation
- graded= opposite
Absolute refractory period (ARP) ENDS and relative refractory period (RRP) begins with?
opening of H gate
when does threshold vary for action potentials?
during refractory periods
Na+ channel gating: at rest? at threshold? reaching depolarization? membrane repolarization?
- at rest= m activation gate is closed; h inactivation gate open
- at threshold= m activation gate opens and Na+ flows in BEGINNING ARP
- depolarization= h gate closes
- repolarization= m gate closes and THEN h gate reopens (end ARP/begin RRP) *microsencond they are both closed**
K+ channel gating?
- at rest n gate is closed
- as membrane depolarizs to overshoot, n gate open allowing EFFLUX and repolarization
- when resting is restored the n gate closes
hypoatremia
a condition of low blood sodium (can be caused by water intoxication aka too much water)
*neural dysfunction, heart’kidney imparment, sluggish, negative storke test
what keep impulses from reversing on axon?
1) the absolute refractory period
What are the mylinating cells in PNS and CNS?
schwann cells= PNS
oligodendoglia cells= CNS
salatory conduction
when action potentials occur only at the nodes on myelinated axon
multiple sclerosis?
autoimmune attack on and degradation of myelin sheath
Bad bc 1) prevents regrowth of myelin 2) poor insulator 3) nerve disfuntion/motor loss
7 synaptic steps at terminal?
1) membrane depolarizes
2) Ca+ influx thru gated channels
3) Ca+ activation of calmodulin
4) calmodulin activation of protein kinase
5) protein kinase activation of synapsin to move synaptic vesicle to surface
6) exocytosis of synaptic vesicles
7) release of neurotransmitters
presynaptic inhibition? usually used?
- inhibition of an excitatory PS neuron=
- *inhibition of an inhibitory PS neuron=
(this is special circumstance)
PS inhibition nuerons usually release GABA neuromodulator at nerve terminal of PS; GABA then opens CL channels on PS which prevents neurotransmitter release from PS
- inhibition of an excitatory PS neuron= Postsynaptic INhibition
- *inhibition of an inhibitory PS neuron= Postsynaptic excitation
facilitation of neurons?
some neuropeptides can regulate long-term membrane permeability for select ions by “re-setting” resting membrane potentials
*if re-set to a potential that is near threshold, it is said to be facilitated and can generate action potentials/excitation more easily
defacilitation of neurons is?
harder to activate pathways
*probably “re-set” ion far away from threshold
1) metbolic alkalosis=
2) metabolic acidosis=
3) central hypoxia=
4) caffeine=
5) most aneathetics
1) increase excitability; seizures
2) increase excitability; coma
3) decrease excitability; unconsciousness
4) increase excitability
5) decrease excitability
agonists vs antagonists
Agonists= a ligand that can bind to another receptor & activate a similar cellular response but NOT to the same degree Antagonist= has affinity and can bind but has no acitvation cite so it WON'T produce cellular activity
