American Society of Hirudotherapy

Postactivation inhibition of spontaneously active neurosecretory neurons in the medicinal leech

Research article published in Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology (2007)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: In vitro / laboratoryGenomics & ProteomicsGocht et al. · Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology, 2007

Abstract

Spontaneously active neurosecretory neurons in vertebrate and invertebrate nervous systems share similarities in firing frequencies, spike shapes, inhibition by the transmitters they themselves release and postactivation inhibition, an intensity-dependent period of suppressed spontaneous generation of action potentials following phases of high-frequency activity. High-frequency activation of spontaneously active serotonin-containing Retzius cells in isolated ganglia of the leech Hirudo medicinalis induced prolonged membrane hyperpolarisations causing periods of postactivation inhibition of up to 33 s. The duration of the inhibitory periods was directly related to both the number and rate of spikes during activation and was inversely proportional to a cell's spontaneous firing frequency. The periods of postactivation inhibition remained unaffected by both serotonin depletion through repeated injections of 5,7-dihydroxytryptamine and suppressing the afterhyperpolarisation following each action potential with tetraethylammonium (TEA), iberiotoxin or charybdotoxin, suggesting that neither autoinhibition by synaptic release of serotonin nor calcium-activated potassium channels contribute to the underlying mechanism. In contrast, the postactivation inhibitory period was significantly affected both by differential electrical stimulation of the same Retzius cells via microelectrodes filled with molar concentrations of either Na(+)-acetate or K(+)-acetate, and by partial inhibition of Na(+)/K(+)-ATPase with ouabain. Thus, postactivation inhibition in Retzius cells results from prolonged hyperpolarising activity of Na(+)/K(+)-ATPase stimulated by the accumulation of cytosolic Na(+ )during phases of high-frequency spike activity.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsAction PotentialsAnimalsElectric StimulationEnzyme InhibitorsGanglia, InvertebrateHirudo medicinalisIn Vitro TechniquesNeural InhibitionNeuronsNeurosecretory SystemsOuabainPotassiumSerotoninSodiumSodium-Potassium-Exchanging ATPaseTime Factors

Summary

In isolated Hirudo medicinalis ganglia, high-frequency activation of serotonin-containing Retzius cells produced postactivation inhibition up to 33 s; experiments excluding serotonin autoinhibition and calcium-activated potassium channels implicated Na+/K+-ATPase driven by cytosolic sodium accumulation.

Why This Matters for Hirudotherapy

This study examined postactivation inhibition in spontaneously active neurosecretory neurons, specifically the serotonin-containing Retzius cells in isolated ganglia of the medicinal leech, Hirudo medicinalis. The researchers investigated the mechanisms causing prolonged membrane hyperpolarization following high-frequency activation, finding it is driven by Na+/K+-ATPase activity rather than calcium-activated potassium channels or serotonin autoinhibition. It explores the fundamental neurophysiology of the primary leech species used in hirudotherapy. However, the scope is strictly limited to basic invertebrate neuroscience using in vitro techniques, providing no insight into the leech secretome, anticoagulant properties, or clinical hirudotherapy applications.

Citation

Reference (Vancouver style)

Gocht D, Heinrich R. Postactivation inhibition of spontaneously active neurosecretory neurons in the medicinal leech. J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2007;193(3):347-361. doi:10.1007/s00359-006-0190-x. PMID: 17123088

Bibliographic details (authors, volume, pages, DOI) are taken from the PubMed record.

Added to ASH library: May 28, 2026 · Site last updated: June 18, 2026

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