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Published September 1, 1987 | Published
Journal Article Open

On the termination of ingestive behaviour by the medicinal leech

Abstract

Hungry leeches, Hirudo medicinalis, ingest blood meals averaging 890% of their mass in 29 min. Ingestion is terminated as a result of distension of the body: experimentally distending leeches as they feed causes an immediate cessation of ingestion and inhibits any subsequent biting behaviour; if distension is circumvented by various experimental procedures, leech ingestive periods are prolonged significantly. Ingestion is not terminated as a result of fatigue, chemical cues or mass change. Distension also underlies satiation, for removing blood from the crops of recently fed leeches qualitatively alters their satiated behaviour to biting. Biting is not a defensive reaction to injury. In rostral ganglia, impulses of the serotonergic Retzius (RZ) and LL neurones evoke the physiological components of ingestion. Localized warming of the prostomial lip induces impulses in these large effector neurones. Distending the body wall tonically hyperpolarizes the RZ and LL cells. This inhibitory response to distension is conducted from the mid-body to the anterior neurones via the ventral nerve cord. Distensive inhibition antagonizes the synaptic excitation evoked in RZ and LL neurones by thermal stimulation. Thus, a stimulus which evokes feeding synaptically excites 5-HT neurones and a stimulus which terminates ingestion inhibits them. The integration of these inputs controls the expression of leech feeding behaviour and these connections match precisely a model proposed to regulate the ingestive behaviour of blowflies.

Additional Information

© 1987 by Company of Biologists. Accepted 7 May 1987. We thank Karsten Fliegner and Edward Freedman for technical assistance with experiments. We also thank Susan Durham and Dr Robert Parmenter for guidance with statistical analyses. Some of this research was conducted when the authors were associated with the Division of Biology and Medicine of Brown University, Providence, RI 02912, USA. Supported by PHS grant NS-14482 and NS-24077 to CML.

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