Early Ca²+ release S LCS Ca²+ oscillator (SR load dependent) Potential causes: t-tubule loss reduced AP notch B-AR desensitization I SERCA activity RyR desensitization Inward TINCX ca Vmoscillator dv dt Vm Increasing SR load: 1B-AR activation LTCC activity † Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward Incx Fig. 5. Flow diagram for two interacting positive-feedback mechanisms that can drive Vm and Ca2+ oscillations during EADs. The red inner cycle represents the well-established Vm oscillator, wherein an increase in dv/dt (caused by a relative increase in depolarizing currents compared to repola- rizing currents, e.g., text in orange box at Lower Right) leads to voltage- dependent reactivation of Icar which in turn causes further depolarization. The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator mechanism for EAD initiation. Reduced early Ca²+ release and/or increased SR load increases LCS production, and the resulting increase in inward INCX tends to depolarize the membrane which then feeds onto Ica to trigger additional LCS. Green arrows indicate possible factors contributing to EAD initiation. ß-AR, beta-adrenoreceptor.
Early Ca²+ release S LCS Ca²+ oscillator (SR load dependent) Potential causes: t-tubule loss reduced AP notch B-AR desensitization I SERCA activity RyR desensitization Inward TINCX ca Vmoscillator dv dt Vm Increasing SR load: 1B-AR activation LTCC activity † Stimulus rate fintracellular Na Repol. reserve Potential causes: K* current density Late Na' currents Ica reactivation Inward Incx Fig. 5. Flow diagram for two interacting positive-feedback mechanisms that can drive Vm and Ca2+ oscillations during EADs. The red inner cycle represents the well-established Vm oscillator, wherein an increase in dv/dt (caused by a relative increase in depolarizing currents compared to repola- rizing currents, e.g., text in orange box at Lower Right) leads to voltage- dependent reactivation of Icar which in turn causes further depolarization. The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator mechanism for EAD initiation. Reduced early Ca²+ release and/or increased SR load increases LCS production, and the resulting increase in inward INCX tends to depolarize the membrane which then feeds onto Ica to trigger additional LCS. Green arrows indicate possible factors contributing to EAD initiation. ß-AR, beta-adrenoreceptor.
Chapter27: Medications That Affect The Nervous System
Section: Chapter Questions
Problem 21RQ
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Question
Recreate this diagram into a simpler one
Transcribed Image Text:Early Ca²+
release
A 2. A.
V
Potential causes:
t-tubule loss
uced AP notch
B-AR desensitization
SERCA activity
RyR desensitization
Ca2+ oscillator
(SR load dependent)
LCS
Ica Vmo
Inward
INCX
moscillator
dV
dt
27
三、
Increasing SR load:
1B-AR activation
LTCC activity
Stimulus rate
fintracellular Na
Repol.
reserve
Potential causes:
K* current density
Late Na' currents
Ica reactivation
Inward INCX
Fig. 5. Flow diagram for two interacting positive-feedback mechanisms
that can drive Vm and Ca2+ oscillations during EADs. The red inner cycle
represents the well-established Vm oscillator, wherein an increase in dv/dt
(caused by a relative increase in depolarizing currents compared to repola-
rizing currents, e.g., text in orange box at Lower Right) leads to voltage-
dependent reactivation of Ica, which in turn causes further depolarization.
The blue outer cycle represents the stochastic LCS-mediated Ca²+ oscillator
mechanism for EAD initiation. Reduced early Ca2+ release and/or increased
SR load increases LCS production, and the resulting increase in inward INCX
tends to depolarize the membrane which then feeds onto Ica to trigger
additional LCS. Green arrows indicate possible factors contributing to
EAD initiation. ß-AR, beta-adrenoreceptor.
V
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