Control and Coordination in Mammals – Cholinergic Synapse
Control and Coordination in Mammals
Cholinergic Synapse – Structure
A cholinergic synapse is a specialised junction between a motor neuron and a skeletal muscle fibre that uses the neurotransmitter acetylcholine (ACh). The main structural components are:
Presynaptic terminal – contains synaptic vesicles loaded with ACh, mitochondria, and voltage‑gated calcium channels.
Synaptic cleft – a narrow extracellular space (\overline{20} nm) filled with extracellular fluid and enzymes such as acetylcholinesterase.
Postsynaptic membrane (motor end‑plate) – highly folded plasma membrane rich in nicotinic ACh receptors (nAChRs) and associated ion channels.
Functional Sequence of a Cholinergic Synapse
Action potential arrives at the presynaptic terminal and depolarises the membrane.
Depolarisation opens voltage‑gated Ca²⁺ channels, allowing an influx of calcium ions.
Elevated intracellular Ca²⁺ triggers fusion of ACh‑containing vesicles with the presynaptic membrane (exocytosis).
ACh is released into the synaptic cleft and diffuses across the gap.
ACh binds to nicotinic receptors on the postsynaptic membrane, causing the receptor‑associated Na⁺/K⁺ channel to open.
Na⁺ influx depolarises the muscle fibre, generating an end‑plate potential (EPP).
If the EPP reaches threshold, voltage‑gated Na⁺ channels open, producing an action potential that propagates along the muscle fibre.
ACh is rapidly hydrolysed by acetylcholinesterase into choline and acetate, terminating the signal.
Choline is taken back into the presynaptic terminal for re‑synthesis of ACh.
Role of Calcium Ions (Ca²⁺)
Calcium ions are the key trigger for neurotransmitter release. Their role can be summarised as follows:
Entry point – Voltage‑gated Ca²⁺ channels open only when the presynaptic membrane is depolarised.
Concentration gradient – Intracellular [Ca²⁺] rises from \overline{0}.1 µM to >10 µM, creating a steep gradient that drives Ca²⁺ into the cytosol.
Trigger for vesicle fusion – Ca²⁺ binds to synaptotagmin, a calcium‑sensor protein that interacts with the SNARE complex, pulling the vesicle membrane into close apposition with the presynaptic membrane.
Temporal precision – The rapid rise and fall of Ca²⁺ concentration ensure that ACh release is tightly coupled to each action potential, allowing high‑frequency signalling.
Summary Table of Key Features
Component
Location
Primary Function
Key Molecules
Voltage‑gated Ca²⁺ channels
Presynaptic terminal membrane
Allow Ca²⁺ influx on depolarisation
Ca \cdot 1.1, Ca \cdot 2.1
Synaptic vesicles
Presynaptic terminal cytoplasm
Store and release ACh
ACh, synaptophysin
Nicotinic ACh receptors (nAChR)
Postsynaptic motor end‑plate
Ligand‑gated Na⁺/K⁺ channels
α1, β1, δ, ε subunits
Acetylcholinesterase (AChE)
Synaptic cleft (basement membrane)
Hydrolyses ACh to terminate signal
ACh, choline, acetate
Suggested diagram: A labelled cross‑section of a cholinergic synapse showing the presynaptic terminal, synaptic vesicles, voltage‑gated Ca²⁺ channels, synaptic cleft, acetylcholinesterase, nicotinic receptors on the motor end‑plate, and the flow of ions during an action potential.
Key Equation – Nernst Potential for Ca²⁺
The equilibrium potential for calcium ions can be estimated using the Nernst equation:
where R is the gas constant, T temperature in kelvin, z the charge (+2 for Ca²⁺), and F Faraday’s constant.
Conclusion
The cholinergic synapse exemplifies how precise structural organisation and ionic movements translate an electrical signal in a neuron into a mechanical response in muscle. Calcium ions are indispensable, acting as the immediate trigger that couples membrane depolarisation to the release of acetylcholine, thereby initiating the cascade that leads to muscle contraction.