Amerikanische Gesellschaft für Hirudotherapie

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.

Research article published in The Journal of physiology (1987)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: In vitro / laboratoryGenomik & ProteomikSpeichel-PharmakologieDeitmer et al. · The Journal of physiology, 1987

Abstract

1. Double-barrelled, neutral-carrier pH-sensitive micro-electrodes were used to measure the intracellular pH (pHi) and the pHi regulation of neuropile glial (n.g.) cells and of identified neurones of the leech Hirudo medicinalis. 2. The distribution of H+ in the n.g. cells and in the neurones was found not to be in electrical equilibrium. The mean pHi of the n.g. cells was 6.87 +/- 0.13 (mean +/- S.D. of mean here and for all following data n = 27) in HEPES-buffered leech saline (pHo = 7.4) and 7.18 +/- 0.19 (n = 13) in 2% CO2-11 mM-HCO3(-)-saline. The mean pHi was 7.28 +/- 0.1 (n = 20) in Retzius neurones and 7.32 +/- 0.15 (n = 12) in noxious neurones in HEPES-buffered leech saline, and 7.20 +/- 0.15 (n = 10) and 7.27 +/- 0.16 (n = 6) in 2% CO2-11 mM-HCO3(-)-buffered saline in these two types of neurones, respectively. 3. The cytoplasmic buffering power, as calculated by the change in pHi following the change from 2% CO2-11 mM-HCO3- to 5% CO2-22 mM-HCO3- in the leech saline, was 20-30 mM/pH unit in the n.g. cells and between 12 and 33 mM/pH unit in the neurones. 4. The recovery of pHi in n.g. cells from an experimentally induced acidification (addition and removal of 20 mM-NH4Cl) was dependent on the presence of external Na+. Independent of the buffer system used, pHi recovery was inhibited when external Na+ was exchanged by N-methyl-D-glucamine. Amiloride (2-3 mM) reduced the rate of pHi recovery by about 50% in these n.g. cells. 5. In CO2-HCO3(-)-free saline, or in the presence of the anion exchange blocker 4-acetamido-4'-isothiocyanostilbene-2, 2'-disulphonic acid (SITS, 0.5 mM), pHi recovery from an acid load was often slowed by up to 50% in n.g. cells. This suggests that there is a significant contribution of a HCO3(-)-dependent membrane transport to pHi regulation in n.g. cells. 6. When a HEPES-buffered saline was exchanged by a 2% CO2-11 mM-HCO3(-)-buffered saline, the pHi of n.g. cells increased by 0.31 pH units. This alkaline shift was reversible upon removal of the CO2-HCO3- and was absent in the Na+-free saline. It was not inhibited by 1 mM-furosemide or by 0.5 mM-SITS.(ABSTRACT TRUNCATED AT 400 WORDS)

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

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH terms4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAmilorideAnimalsBicarbonatesCarbon DioxideCentral Nervous SystemHomeostasisHydrogen-Ion ConcentrationIn Vitro TechniquesLeechesNeurogliaNeurons

Zusammenfassung

1. Double-barrelled, neutral-carrier pH-sensitive micro-electrodes were used to measure the intracellular pH (pHi) and the pHi regulation of neuropile glial (n.g.) cells and of identified neurones of the leech Hirudo medicinalis.

Warum dies für die Hirudotherapie relevant ist

This study examined the regulation of intracellular pH in identified glial cells and neurons within the central nervous system of the medicinal leech, Hirudo medicinalis. By characterizing the fundamental neurophysiology and homeostatic mechanisms of the leech, the study provides basic biological insights into the very organism utilized in clinical hirudotherapy. However, its relevance to the American Society of Hirudotherapy is strictly foundational, as it does not investigate the leech secretome, therapeutic applications, or any clinical outcomes related to leech therapy. The scope is limited to in vitro cellular physiology.

Zitation

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.

Deitmer et al. · The Journal of physiology, 1987

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