Transcript Calcium-Dependent (-Derived) Action Potentials Two Types 1. Na+/Ca2+-dependent APs. • Present in axon terminals, cardiac myocytes and skeletal myocytes (for muscle fiber contraction). • Occurs in.

Calcium-Dependent (-Derived)
Action Potentials
Two Types
1. Na+/Ca2+-dependent APs.
• Present in axon terminals, cardiac myocytes
and skeletal myocytes (for muscle fiber
contraction).
• Occurs in response to neurotransmitter
release in the presynaptic axon.
Two Types (cont’d)
2. Ca2+-dependent AP (No Na+).
 Present in dendrites of Purkinje cells
(cerebellum) and in endocrine cells to trigger
hormone secretion.
 Characterized by small amplitude and long
duration.
A schematic diagram of the components in the cerebellar cortex studied here, with Purkinje
cells in blue and granular cells in green.
Cohen D , Yarom Y PNAS 1998;95:15032-15036
©1998 by National Academy of Sciences
Example of how an endocrine cell
(pancreatic β-cell) depolarizes its
membrane with Ca2+ to release
insulin.
The synthesis and release of
insulin is modulated by:
1. Glucose (most
important), AAs, FAs
and ketone bodies
stimulate release.
2. Glucagon and
somatostation inhibit
relases
3. α-Adrenergic
stimulation inhibits
release (most
important).
4. β-Adrenergic
stimulation promotes
release.
5. Elevated intracellular
Ca2+ promotes release.
Insulin secretion - Insulin secretion in beta cells is triggered
by rising blood glucose levels. Starting with the uptake of
glucose by the GLUT2 transporter, the glycolytic
phosphorylation of glucose causes a rise in the ATP:ADP
ratio. This rise inactivates the potassium channel that
depolarizes the membrane, causing the calcium channel to
open up allowing calcium ions to flow inward. The ensuing
rise in levels of calcium leads to the exocytotic release of
insulin from their storage granule.
Why are fibers of the conducting system autorhythmic?
If channels
How does the depolarization in
these cells affect cardiac muscle
cells?
Superimpose changes in the muscle
cell’s membrane potential on this
graph
Membrane potential of SA nodal cells
Ventricular AP
•Phase 4: resting
membrane potential near
the K+ equilibrium
potential.
•Phase 0: depolarizing
impulse activates fast Na+
channels and inactivates K+
channels.
•Phase 1: Transient
opening of K+ channels and
Na+ channels begin to
close.
•Phase 2: Ca2+ channels are
open, key difference
between nerve AP.
•Phase 3: repolarization,
Ca2+ inactivate and K+
channels open.
•Refractory period: Na+
channels are inactive until
membrane is repolarized.
Changes in ion concentrations in a cardiac muscle fiber following depolarization
What causes the muscle resting
membrane potential to change
initially?
What would be happening with
a skeletal muscle at this point?
Similarities
• Note that whatever cation generates the AP,
all APs share a similar structure and and all are
activated by membrane depolarization.
• Thus, the Na+, Na+/Ca2+ and Ca2+ APs all have a
similar pattern of depolarization – influx of
some cation.
• Repolarization all entail the inactivation of Na+
or Ca2+ channels together with K+ efflux.
Differences
Na+/K+
Ca2+
• Threshold lower; therefore,
depolarization sudden.
• AP decays with distance
(but, do you recall what
keeps it going over long
distances?).
• Depolarization: Na+
channels open nearly
simultaneously.
• Threshold higher and gradual;
therefore depolarization
gradual.
• AP does not attenuate over
distance – what keeps it
going? (syncytium, gap
junctions, highly branched
processes).
• Local, gradual, and transient
Ca2+ entry – allows for fine
control and adjustments.
Propagation of Electrical Signals in
Heart Muscle
• Heart muscle is syncytial