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Leech giant glial cell: functional role in a simple nervous system
Author(s) -
Deitmer Joachim W.,
Rose Christine R.,
Munsch Thomas,
Schmidt Joachim,
Nett Wolfgang,
Schneider HansPeter,
Lohr Christian
Publication year - 1999
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199912)28:3<175::aid-glia1>3.0.co;2-7
Subject(s) - neuroscience , biology , leech , hirudo medicinalis , nervous system , neuropil , neuroglia , neuron , ionotropic effect , glutamate receptor , central nervous system , receptor , biochemistry , world wide web , computer science
The giant glial cell in the central nervous system of the leech Hirudo medicinalis has been the subject of a series of studies trying to link its physiological properties with its role in neuron–glia interactions. Isolated ventral cord ganglia of this annelid offer several advantages for these studies. First, single giant glial cells can easily be identified and are quite accessible to electrophysiological and microfluorometric studies. Second, only two giant macroglial cells are located in the neuropil of each ganglion, rendering them well suited for studying neuron–glia interactions. Third, many neurons can be identified and are well known with respect to their physiology and their roles in controlling simple behaviors in the leech. This review briefly outlines the major recent findings gained by studying this preparation and its contributions to our knowledge of the functional role of glia in nervous systems. Emphasis is directed to glial responses during neuronal activity and to the analysis of intracellular Ca 2+ and H + transients mediated by neurotransmitter receptors and ion‐driven carriers. Among its numerous properties, the leech giant glial cell prominently expresses a large K + conductance, voltage‐dependent Ca 2+ channels, ionotropic non‐NMDA glutamate receptors, and an electrogenic, reversible Na + ‐HCO 3 − cotransporter. GLIA 28:175–182, 1999. © 1999 Wiley‐Liss, Inc.