[Function of glutamate in pattern-gene-rating network is modified by nitric oxide NO].
In previous study on the terrestrial snail Helix pomatia, it has been shown that responsiveness of certain neurons to glutamate is controlled by NO; specifically, the donors of NO produced transformation of inhibitory responses to excitatory ones. Here, we extend this study to buccal neurons related to feeding behavior of the pond snail L. stagnalis. Glutamate is known to operate in the standard three-phase feeding pattern as a phase transmitter which mediates the effects of the second phase interneuron N2v. In isolated CNS, we recorded motor neuron B4 that was inhibited during firing of glutamatergic N2v, but expressed excitatory glutamate receptors as well. In some preparations (n = 17), bath application of 0.1 mM glutamate resulted in profound hyperpolarization of, and cessation of synaptic inputs to, the B4. Following treatment for 10-15 min with the NO donor sodium nitroprusside (n = 9), glutamate effect on B4 became excitatory, and a peculiar, sustained two-phase rhythmic activity of the pattern-generating network appeared. In other non-treated preparations (n = 12), 0.1 mM glutamate produced depolarization and excitation of B4, supplemented, in 8 cases, with emergence of the above mentioned two-phase rhythmic activity. Pretreatment for 10-20 min with the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (n = 7) abolished these effects of glutamate. Our results suggest that 1) glutamate role in buccal rhythm generation depends on NO level, and 2) this mechanism is involved in modification of the feeding behavior in Lymnaea.
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D000818:Animals; D005247:Feeding Behavior / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D008195:Lymnaea / Q000166:cytology / Q000235:genetics / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology
D009569:Nitric Oxide; D018698:Glutamic Acid