There are at least three mechanisms by which the activity of the salivary burster (SB) can be modulated by stretch feedback from the salivary duct: 1) a chemically mediated inhibitory pathway, 2) a proposed single-cell reflex in the SB, 3) polysynaptic routes via other cells that are coupled to the SB. When the inhibitory pathway to the SB is activated by duct stretch, the SB receives a 3- to 5-mV inhibitory postsynaptic potential (IPSP). When the IPSP decays, the SB rebounds with higher frequency activity than was seen prior to stimulation. The strength and duration of salivary duct contractions are a function of the frequency of SB spikes Therefore, the SB rebound from this inhibition causes an increase in the strength and duration of contracture of the salivary duct musculature. It is proposed that a single-cell reflex may also be active in modulating SB activity. When the salivary duct is stretched, an afferent spike or a 2- to 5-mV slow, depolarizing potential is often recorded from the SB soma within 150-500 ms following the stimulus to the duct. This afferent spike or depolarizing potential can excite the spike-initiating zone, which produces efferent bursting activity and results in an efferent phase-advanced SB burst. The details of this proposed mechanism are discussed at length in the text. This scheme implies that the SB has both sensory and motor endings. Alternative explanations are also discussed. Evidence is also presented that other buccal ganglion neurons receive input from salivary duct stretch. Some of the cells receiving synaptic input from duct stretch may synapse on the SB, thereby causing an indirect modulation of SB activity. Some of these inputs to buccal neurons are probably also involved in the activation of the feeding motor program.
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