Discharge induction in molluscan peptidergic cells requires a specific set of autoexcitatory neuropeptides

The peptidergic caudodorsal cells of the pond snail Lymnaea stagnalis generate long lasting discharges of synchronous spiking activity to release their products. During caudodorsal cell discharges a peptide factor is released which induces similar discharges in silent caudodorsal cells [Ter Maat A....

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Veröffentlicht in:Neuroscience 1990, Vol.39 (2), p.479-491
Hauptverfasser: Brussaard, A.B., Schluter, N.C.M., Ebberink, R.H.M., Kits, K.S., Maat, A. Ter
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Sprache:eng
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Zusammenfassung:The peptidergic caudodorsal cells of the pond snail Lymnaea stagnalis generate long lasting discharges of synchronous spiking activity to release their products. During caudodorsal cell discharges a peptide factor is released which induces similar discharges in silent caudodorsal cells [Ter Maat A. et al. (1988) Brain Res. 438, 77–82]. To identify this factor, the electrophysiological effects of putative caudodorsal cell gene products, calfluxin, caudodorsal cell hormone, four a caudodorsal cell peptides and three βcaudodorsal cell peptides, were tested individually and in various combinations. Calfluxin, a caudodorsal cell peptide 3–9 and β 1caudodorsal cell peptide each had no effect on membrane potential or excitability of the caudodorsal cells. All other caudodorsal cell peptides caused excitatory responses, but did not induce discharges. Instead, only a specific combination of four caudodorsal cell peptides, caudodorsal cell hormone and a caudodorsal cell peptide (1–11, 3–11 and 3–10), evoked caudodorsal cell discharges with similar characteristics to electrically evoked discharges. Incomplete versions of this combination failed to cause a discharge. In addition, antibodies to caudodorsal cell hormone or αcaudodorsal cell peptide reduced caudodorsal cell excitability and prevented the generation of discharges by electrical stimulation. These results suggest that excitatory autotransmission caused by four caudodorsal cell peptides provides a means to amplify excitatory inputs, thus leading to the generation of the all-or-nothing caudodorsal cell discharge.
ISSN:0306-4522
1873-7544
DOI:10.1016/0306-4522(90)90284-B