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Cholinergic action on the heart of the leech, Hirudo medicinalis
Insights
Acetylcholine (ACh) activates nicotinic receptors on leech heart muscle, increasing membrane conductance. The HE motor neuron uses ACh for transmission, while the HA neuron does not.
Area of Science:
- Neuroscience
- Pharmacology
- Physiology
Background:
- Neuromuscular transmission in the Hirudo medicinalis heart is not fully understood.
- Acetylcholine (ACh) is a key neurotransmitter in many systems, but its role in leech cardiac function requires clarification.
Purpose of the Study:
- To investigate the role of acetylcholine (ACh) in neuromuscular transmission within the Hirudo medicinalis heart.
- To identify the type of acetylcholine receptors present on leech heart muscle cells and determine if specific neurons utilize ACh.
Main Methods:
- Experiments involved superfusion and iontophoretic application of ACh and related compounds to isolated leech heart preparations.
- Electrophysiological recordings measured membrane depolarization and conductance changes.
- Histochemical localization of acetylcholinesterase was performed.
- Pharmacological agents, including agonists and antagonists, were used to probe receptor function.
Main Results:
- Acetylcholine (ACh) caused dose-dependent depolarization and increased membrane conductance in leech heart muscle cells, with a reversal potential of -9 mV.
- Nicotinic agonists mimicked ACh effects, while nicotinic antagonists (e.g., curare) blocked ACh responses.
- The HE motor neuron's fast excitatory transmission was blocked by curare, suggesting it is cholinergic.
- The HA modulatory neuron's effects were unaffected by curare, indicating it is likely not cholinergic.
Conclusions:
- Leech heart muscle cells possess nicotinic acetylcholine receptors.
- The HE motor neuron utilizes acetylcholine as a neurotransmitter for neuromuscular transmission.
- The HA modulatory neuron does not appear to use acetylcholine in its cardiac modulation.
Abstract:
Experiments were performed to determine the role of acetylcholine (ACh) in neuromuscular transmission in the heart of the leech Hirudo medicinalis. Superfused or iontophoretically applied ACh rapidly depolarized both isolated heart muscle cells and muscle cells in isolated hearts in a dose-dependent manner. the depolarization was associated with a conductance increase of the muscle membrane that had a reversal potential of -9 mV. Eserine potentiated the response to superfused ACh, reducing the threshold from 10(-6) to 10(-8) mol l-1. Acetylcholinesterase was localized histochemically to be in the immediate area of neuromuscular terminals. Superfused nicotinic agonists mimicked the effects of ACh, while superfused nicotinic antagonists reversibly blocked the iontophoretic response of heart muscle fibres to ACh. 5 X 10(-7) mol l-1 curare, 5 X 10(-5) mol l-1 nicotine and 1 X 10(-4) mol l-1 atropine reduced the iontophoretic response to half its original amplitude. Alpha-bungarotoxin did not block the response of heart muscle cells to iontophoretically applied ACh. Curare was used to determine whether the neurones that innervate the heart-HE motor neurones and HA modulatory neurone--use ACh as a neuromuscular transmitter. The fast depolarizing component of the HE cell's neuromuscular transmission was reversibly blocked by 10(-4) mol l-1 curare, while the HA cell's modulatory effects on the heart were apparently unaffected by 10(-4) mol l-1 curare. Our results indicate that heart muscle cells have nicotinic acetylcholine receptors that open in the presence of ACh, thereby increasing membrane conductance. The HE motor neurone is probably cholinergic and engages these receptors in its neuromuscular transmission, while the HA modulatory neurone is probably not cholinergic.