We studied the effects of MNR stimulation on phrenic (Phr) electroneurogram and external intercoastal muscles (EI)electromiogram in spontaneously breathing rabbits.Additionally, experiments were performed before and after lignocaine blockade of nucleus tractus solitarii (NTS) to determine whether the information from MNR is transmitted via NTS neurones.The completness of the blockade of NTS region was checked by studying the Hering-Breuer reflex.Stimulation at the rostral part of this region produced inhibition of phasic inspiratory activity, whereas stimulation in the caudal part elicited tonic activity throughout the respiratory cycle.These effects were more pronounced on EI than on Phr.Responses to MNR stimulation were attenuated after lignocaine blockade, suggesting that the neurones located in NTS take part inthe transmission of the modulatory information from the MNR to respiratory motoneurones.
Stimulation of the superior laryngeal nerve (SLN) causes a potentiation of hypoglossal nerve activity persisting after cessation of stimulation. The mechanism of this phenomenon is uncertain. We investigated a potential role of the nitric oxide (NO) pathway in modulation of the after-effects of SLN stimulation on phrenic and hypoglossal activity in rabbits. L-Arginine, a substrate for NO synthesis and NG-Nitro-L-Arginine (L-NNA) an inhibitor of NO synthase (NOS), were administered systemically. L-Arginine and L-NNA alone caused small changes in respiratory activity. During pre-treatment with NO precursor the amplitude and duration of hypoglossal potentiation evoked by SLN stimulation were reduced. Systemic NO synthase inhibition partially reversed these effects of L-Arginine. The results showed that interference with NO production by NO substrate and NOS inhibitor modulates the effects of SLN stimulation on hypoglossal activity. Nitric oxide might be a negative modulator of the transmission of short-term potentiation (STP) in hypoglossal activity.
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