We investigated the brain-stem pathway(s) by which electrical stimulation of the central cut end of the lingual nerve (LN) evokes parasympathetic reflex vasodilatation in the palate contralateral to the stimulated side. This occurs in artificially ventilated, cervically vagosympathectomized cats deeply anesthetized with α-chloralose and urethane. For this purpose, we made microinjections within the brain stem to produce nonselective, reversible local anesthesia (lidocaine) or soma-selective, irreversible neurotoxic damage (kainic acid). Local anesthesia of the trigeminal spinal nucleus (Vsp) ipsilateral to the stimulated side produced by microinjection of lidocaine (2%; 1 μl/site) reversibly and significantly reduced the LN stimulus-evoked palatal blood flow (PBF) increases. PBF increases ipsilateral and contralateral to the stimulated nerve were equally affected. In contrast, microinjection of lidocaine into the Vsp contralateral to the stimulated side did not affect these responses. Microinjection of kainic acid (10 mM/site; 1 μl) into the Vsp ipsilateral to the stimulated side led to a bilateral irreversible reduction in reflex vasodilatation in the palate. Microinjection of lidocaine into either superior salivatory nucleus (SSN) attenuated the PBF increase only on the side ipsilateral to the microinjection site. Hexamethonium (1.0 mg/kg iv) significantly reduced the vasodilator responses to electrical stimulation of Vsp by blocking ganglionic transmission on both sides. The simplest interpretation of these results is that the LN-evoked parasympathetic reflex vasodilatation in the contralateral palate depends on activation of a pathway originating from the Vsp ipsilateral to the stimulated nerve and crossing to the contralateral SSN.
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