Heterosynaptic modulation by the octopaminergic OC interneurons increases the synaptic outputs of protraction phase interneurons (SO, N1L) in the feeding system of Lymnaea stagnalis.
We examined the cholinergic synapses between protraction phase interneurons (SO or N1L) and their targets (N1M interneuron, B1 motoneuron) in the buccal ganglia of the pond snail Lymnaea stagnalis. We have tested the hypothesis that the OC (octopamine-containing) interneuron, an intrinsic modulator of the feeding network, can increase the synaptic efficacy from the SO or N1L to their targets. Prestimulation of the OC interneuron, 4 s before the activation of the SO or N1L increases the strength of their output synapses by 75% (SO)-110% (N1L). The individual excitatory postsynaptic potentials evoked by SO or N1L stimulation increase in size. OC prestimulation also produces an increase in the firing rate of these presynaptic interneurons: SO 40%; N1L 33%. The facilitation lasts up to 6 s after the end of the OC burst. The enhancement of PSPs is seen at all the output synapses (both excitatory and inhibitory) of the SO and N1L interneurons. The output synapses of the non-cholinergic swallowing phase N3p interneuron are not affected, even when the same postsynaptic target is selected. The SO-->N1M, SO-->B1 and N1L-->N1M synapses are also strengthened by bath application of 1-5 microM octopamine (average increase 60%). The major effect is an increased excitability of the SO; the B1 motoneuron response to the main transmitter of the SO, acetylcholine, is unaffected. Increased synaptic outputs of the protraction phase SO and N1L interneurons is functionally significant for generation of feeding pattern in the Lymnaea CNS. Strengthening the connections of SO and N1L to the central pattern generator (N1M) interneurons enhances their ability to drive fictive feeding. Thus heterosynaptic facilitation by the octopaminergic OC interneurons in the central pattern generator network may contribute to the behavioral plasticity of feeding in the intact animal.
Vehovszky
A
A
Department of Biology, University of York, P.O. Box 373, UK. agnes@tres.blki.hu
Elliott
C J H
CJ
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D004357:Drug Synergism; D005247:Feeding Behavior / Q000502:physiology*; D007395:Interneurons / Q000187:drug effects / Q000502:physiology*; D008195:Lymnaea; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D009655:Octopamine / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology
D000316:Adrenergic alpha-Agonists; D018377:Neurotransmitter Agents; D009655:Octopamine; D000109:Acetylcholine