Control and Coordination in Mammals – A-Level Biology 9700
Control and Coordination in Mammals
Objective
Describe the roles of the neuromuscular junction, the T‑tubule system and the sarcoplasmic reticulum in stimulating contraction in striated muscle.
1. Neuromuscular Junction (NMJ)
The NMJ is the synapse between a motor neuron and a skeletal muscle fibre. It initiates the cascade that leads to contraction.
Neurotransmitter release: Acetylcholine (ACh) is released from the presynaptic terminal into the synaptic cleft.
Receptor activation: ACh binds to nicotinic acetylcholine receptors (nAChRs) on the sarcolemma, opening ion channels.
Depolarisation: Na⁺ influx generates an action potential that propagates along the sarcolemma.
Propagation to T‑tubules: The action potential travels into the T‑tubule system, ensuring rapid and uniform excitation of the fibre.
2. T‑Tubule System
T‑tubules are invaginations of the sarcolemma that penetrate deep into the muscle fibre.
Electrical coupling: They transmit the action potential from the surface to the interior of the fibre.
Mechanical coupling: T‑tubules are closely associated with the sarcoplasmic reticulum via the triad structure.
Triggering calcium release: The depolarisation of T‑tubules activates voltage‑sensitive dihydropyridine receptors (DHPRs), which mechanically interact with ryanodine receptors (RyRs) on the sarcoplasmic reticulum.
3. Sarcoplasmic Reticulum (SR)
The SR is a specialised endoplasmic reticulum that stores Ca²⁺.
Calcium storage: The SR maintains a high Ca²⁺ concentration (\overline{1} mM) compared with the cytosol (\overline{100} nM).
Release mechanism: Activation of RyRs by DHPRs opens Ca²⁺ channels, releasing Ca²⁺ into the cytosol.
Reuptake: Ca²⁺ is actively pumped back into the SR by the sarco(endo)plasmic reticulum Ca²⁺‑ATPase (SERCA), allowing relaxation.
4. Sequence of Events Leading to Contraction
Motor neuron fires an action potential.
Acetylcholine is released at the NMJ.
Na⁺ influx depolarises the sarcolemma, generating an action potential.
Action potential travels into T‑tubules.
DHPRs sense depolarisation and mechanically activate RyRs.
Ca²⁺ is released from the SR into the cytosol.
Ca²⁺ binds to troponin C, causing tropomyosin to move and expose myosin‑binding sites on actin.
Cross‑bridge cycling between actin and myosin produces contraction.
Ca²⁺ is pumped back into the SR by SERCA, leading to relaxation.
5. Summary Table of Key Components
Component
Primary Role
Key Molecules/Structures
Neuromuscular Junction
Initiates electrical signal
ACh, nAChR, Na⁺ channels
T‑Tubule System
Propagates action potential inward
DHPR, triad, T‑tubule membrane
Sarcoplasmic Reticulum
Stores and releases Ca²⁺
RyR, SERCA, Ca²⁺
Cross‑Bridge Machinery
Generates force
Actin, myosin, troponin, tropomyosin
6. Suggested Diagram
Suggested diagram: A cross‑section of a skeletal muscle fibre showing the neuromuscular junction, T‑tubules, sarcoplasmic reticulum, and the triad structure. Label the key components and indicate the flow of Ca²⁺ during contraction.
7. Key Equations
The change in intracellular Ca²⁺ concentration during contraction can be approximated by:
where \$J{\text{release}}\$ is the flux of Ca²⁺ from the SR, \$J{\text{uptake}}\$ is the flux back into the SR, and \$V_{\text{cell}}\$ is the cytosolic volume.
8. Assessment Questions
Explain how the T‑tubule system ensures that the action potential reaches all parts of the muscle fibre.
Describe the role of the sarcoplasmic reticulum in both contraction and relaxation.
Illustrate the sequence of molecular events from acetylcholine release to cross‑bridge cycling.