Page 191 - Anatomy and Physiology of Farm Animals, 8th Edition

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entrance of sodium (a positively charged channels open to allow the inward diffusion
of sodium, and another action potential
cation) shifts the membrane electrical
VetBooks.ir potential in a positive direction (depolari- results. Local flow of current occurs again,
and other action potentials are generated in
zation). The effect of ACh persists only
momentarily, since another enzyme, acetyl- other areas adjacent to the site of the first
cholinesterase, quickly degrades ACh. action potential. The process is repeated,
ACh is synthesized in the cytoplasm of and the overall effect is the propagation of
the presynaptic nerve endings and stored action potentials over the entire sarcolemma
in membrane‐bound synaptic vesicles in of the muscle fiber. This process is similar
the end of the nerve fiber (Fig. 9‐4). Each to that for propagation of action potentials
action potential reaching the end of the along the axon of a nerve cell (see Fig. 2‐16).
nerve stimulates the release of a set num- Since the T tubules are inward continu-
ber of vesicles and thus a set amount of ations of the sarcolemma, the action poten-
ACh. Continuous synthesis maintains a tial (or impulse) travels along these tubules
constant supply of vesicles so that ACh is throughout the muscle fiber (Fig. 9‐5).
not depleted, even with intense exercise. In certain sites where the T tubules pass
immediately adjacent to the sarcoplasmic
End‐Plate and Action Potentials. The reticulum, there is a structural link between
local depolarization of the sarcolemma a protein in the sarcolemma of the T tubule
at the neuromuscular junction is called (dihydropyridine receptor) and a mem-
an end‐plate potential. This change in brane protein channel in the sarcoplasmic
potential produces a local flow of current reticulum. When an action potential
that depolarizes adjacent areas on the occurs on the sarcolemma in the area of
sarcolemma. Normally, the depolarization the dihydropyridine receptor, the channel
of the adjacent sarcolemma is enough to in the sarcoplasmic reticulum becomes
reach the threshold potential of electrically permeable to Ca . The permeable change
2+
gated channels in these areas of the is possible because of the link between the
cell membrane. When this occurs, these two membrane proteins.

Cell membrane
1

2

3 4 Dihydropyridine
Ca 2+ Ca 2+ Sarcoplasmic receptor
reticulum

Actin filament with
calcium binding sites

Figure 9-5. The sources and role of calcium during excitation–contraction coupling in skeletal muscle. An
action potential is propagated along the T tubule (1). The action potential on the T tubule reaches a region
with dihydropyridine receptors (2). Calcium ions are released from the sarcoplasmic reticulum to bind with
regulatory proteins on actin filaments (3), and muscle contraction results. When calcium is released from its
binding sites and transported back into the sarcoplasmic reticulum, muscle relaxation occurs (4).