BIO 3P3 EXAM WITH VERIFIED AND CORRECT ANSWERS.
When will diffusion be the fastest between compartments? - CORRECT
ANSWERS -when there is a large difference in # of molecules between them (flux is proportional
to change in conc)
Demyelinating neuropathy - Guillain Barre (disease of peripheral nerves) - CORRECT ANSWERS -
molecular mimicry between microbial & nerve antigens lead to immune stimulation that induces
aberrant autoimmune response targeting peripheral nerves & their spinal roots
antibody injures myelin or axonal membrane (remyelination is possible but axonal regeneration is
not)
result: APs conducted at different velocities so loss of synchrony of conduction in response to
stimulus
Measuring conduction velocity - CORRECT ANSWERS -apply shock through proximal (S2) or distal (S1)
stimulating electrode & measure AP
conduction vel. = distance from S1 to S2/(ts2 - ts1)
Duchenne Muscular Dystrophy (DMD) - CORRECT ANSWERS -point mutation or deletion of gene
for dystrophin protein (x-linked recessive)
dystrophin acts as shock absorbed during contraction
,Why is Ca2+ a good 2nd messenger? - CORRECT ANSWERS -small influxes of Ca2+ lead to rapid
& dramatic changes in intracellular [Ca2+]
Plasma membrane Ca2+ transports - CORRECT ANSWERS -PMCA, NCX exchanger, voltage-gated Ca2+
channels
Mitochondria Ca2+ transports - CORRECT ANSWERS -calcium uniporter (MCU) - brings Ca2+ into
matrix 2Na:1Ca exchanger - releases Ca2+ from matrix
Ca:2H exchanger
SR Ca2+ transports - CORRECT ANSWERS -Ca2+ channels (for release) SERCA (for reuptake)
SERCA vs. PMCA - CORRECT ANSWERS -- PMCA on plasma membrane, SERCA on SR membrane
- PMCA maintains low [Ca2+], SERCA restores low [Ca2+]
- PMCA has 4 genes, SERCA has 3
- both are high affinity but low capacity
Inhibitor of SERCA - CORRECT ANSWERS -phospholambin (PLN) - when phosphorylated, SERCA is
active
"ON" reactions - CORRECT ANSWERS -stimuli induce Ca2+ entry
, "OFF" reactions - CORRECT ANSWERS -Ca2+ is removed from cell or stored in SR & mitochondria
NCX - CORRECT ANSWERS -- 3Na in, 1 Ca2+ out (small inward current)
- activity depends on Na gradient to drive Ca movement & voltage gradient
- channel can reverse direction when Em > Er
- low affinity, high capacity
MCU - CORRECT ANSWERS -- low affinity, located at hot spots where [Ca] is high enough
- made up of 4 parts: uniporter + 3 regulators MICU 1 & 2:
mitochondrial Ca uptake proteins EMRE: essential MCU
regulator
at rest, EMRE recruits MICUs to keep MCU closed. Increase in [Ca] causes Ca2+ to bind to MICU &
open MCU
Low affinity mechanisms for transporting bulk amounts of Ca2+ (fast & urgent) - CORRECT
ANSWERS -exchangers, channels & uniporters
high affinity, fine-tuning transport of Ca - CORRECT ANSWERS -ATPases
mitochondrial dysregulation of Ca2+ homeostasis - CORRECT ANSWERS - forms ROS, stimulates
Kreb's cycle which increases e- flow through ETC and stimulates NOS (NO inhibits ETC complex
1 & 4 causing more ROS)
When will diffusion be the fastest between compartments? - CORRECT
ANSWERS -when there is a large difference in # of molecules between them (flux is proportional
to change in conc)
Demyelinating neuropathy - Guillain Barre (disease of peripheral nerves) - CORRECT ANSWERS -
molecular mimicry between microbial & nerve antigens lead to immune stimulation that induces
aberrant autoimmune response targeting peripheral nerves & their spinal roots
antibody injures myelin or axonal membrane (remyelination is possible but axonal regeneration is
not)
result: APs conducted at different velocities so loss of synchrony of conduction in response to
stimulus
Measuring conduction velocity - CORRECT ANSWERS -apply shock through proximal (S2) or distal (S1)
stimulating electrode & measure AP
conduction vel. = distance from S1 to S2/(ts2 - ts1)
Duchenne Muscular Dystrophy (DMD) - CORRECT ANSWERS -point mutation or deletion of gene
for dystrophin protein (x-linked recessive)
dystrophin acts as shock absorbed during contraction
,Why is Ca2+ a good 2nd messenger? - CORRECT ANSWERS -small influxes of Ca2+ lead to rapid
& dramatic changes in intracellular [Ca2+]
Plasma membrane Ca2+ transports - CORRECT ANSWERS -PMCA, NCX exchanger, voltage-gated Ca2+
channels
Mitochondria Ca2+ transports - CORRECT ANSWERS -calcium uniporter (MCU) - brings Ca2+ into
matrix 2Na:1Ca exchanger - releases Ca2+ from matrix
Ca:2H exchanger
SR Ca2+ transports - CORRECT ANSWERS -Ca2+ channels (for release) SERCA (for reuptake)
SERCA vs. PMCA - CORRECT ANSWERS -- PMCA on plasma membrane, SERCA on SR membrane
- PMCA maintains low [Ca2+], SERCA restores low [Ca2+]
- PMCA has 4 genes, SERCA has 3
- both are high affinity but low capacity
Inhibitor of SERCA - CORRECT ANSWERS -phospholambin (PLN) - when phosphorylated, SERCA is
active
"ON" reactions - CORRECT ANSWERS -stimuli induce Ca2+ entry
, "OFF" reactions - CORRECT ANSWERS -Ca2+ is removed from cell or stored in SR & mitochondria
NCX - CORRECT ANSWERS -- 3Na in, 1 Ca2+ out (small inward current)
- activity depends on Na gradient to drive Ca movement & voltage gradient
- channel can reverse direction when Em > Er
- low affinity, high capacity
MCU - CORRECT ANSWERS -- low affinity, located at hot spots where [Ca] is high enough
- made up of 4 parts: uniporter + 3 regulators MICU 1 & 2:
mitochondrial Ca uptake proteins EMRE: essential MCU
regulator
at rest, EMRE recruits MICUs to keep MCU closed. Increase in [Ca] causes Ca2+ to bind to MICU &
open MCU
Low affinity mechanisms for transporting bulk amounts of Ca2+ (fast & urgent) - CORRECT
ANSWERS -exchangers, channels & uniporters
high affinity, fine-tuning transport of Ca - CORRECT ANSWERS -ATPases
mitochondrial dysregulation of Ca2+ homeostasis - CORRECT ANSWERS - forms ROS, stimulates
Kreb's cycle which increases e- flow through ETC and stimulates NOS (NO inhibits ETC complex
1 & 4 causing more ROS)
