Question

You and your fellow deep-sea scientists have discovered a new form of marine invertebrate, and are anxious to determine the similarities and differences to animals already characterized. Chemical analysis reveals the following concentrations of permeable cations:

Ion [in] mM [out] mM
Na⁺ 50 450
K⁺ 420 20
Mg⁺⁺ 10 60
Cl⁻ 50 550
Nernst equation: Eion = 61/z × log [ion]out/[ion]in
Control of the neuromuscular junction in this new invertebrate is found to involve dual innervation, where one motor neuron secretes an excitatory neurotransmitter and another secretes an inhibitory neurotransmitter onto the muscle. How does this compare to the human neuromuscular junction? Propose three different types of inhibitory receptors/channels that would produce inhibition of the invertebrate muscle, specifying ion and direction of ion flow. For each ion, calculate the equilibrium potential. What similarity do you notice in the equilibrium potentials of the ions involved, and how is that significant? How may inhibition be accomplished in human muscle?

Answer 1

In comparison to humans, the newly discovered marine invertebrate shows dual innervation at the neuromuscular junction. Three types of inhibitory channels were proposed that could induce muscle inhibition by hyperpolarization, and their equilibrium potentials were calculated using the Nernst equation, indicating similarity in hyperpolarizing effects aimed at reducing excitability.

Step-by-step explanation:

When you and your fellow deep-sea scientists have discovered a new form of marine invertebrate, understanding the neuromuscular junction's control mechanism is crucial for comparing it with known systems. In humans, the neuromuscular junction typically features a single motor neuron releasing acetylcholine an excitatory neurotransmitter, which results in muscle contraction. In contrast the new invertebrate shows dual innervation with both excitatory and inhibitory neurotransmitter inputs.

In studying invertebrate muscle inhibition, three types of inhibitory receptors/channels can be proposed:

1. Ligand-gated chloride channels allowing Cl− influx, leading to hyperpolarization.
2. GABAA receptors that when activated by the neurotransmitter GABA, typically allow Cl− into the cell.
3. Metabotropic receptors that indirectly open K+ channels, which would lead to K+ efflux and hyperpolarization of the cell.

Using the Nernst equation,
`Eion = 61/z × log([ion]out/[ion]in)` , we can calculate the equilibrium potential for each ion:

• 
  `For Cl−: ECl ≈ −61 × log(50/550) ≈ −65.2 mV`
• 
  `For K+: EK ≈ 61 × log(20/420) ≈ −94.6 mV`

The similarity in equilibrium potentials suggests that both mechanisms aim to hyperpolarize the muscle cell making it less excitable and thus inhibited. In humans, inhibition is typically achieved through the action of inhibitory neurotransmitters like GABA which lead to similar hyperpolarizing effects.