Abstract
The superior vestibular nucleus (SVN), which holds a key position in vestibulo-ocular reflexes and nystagmus, receives direct hypothalamic histaminergic innervations. By using rat brainstem slice preparations and extracellular unitary recordings, we investigated the effect of histamine on SVN neurons and the underlying receptor mechanisms. Bath application of histamine evoked an excitatory response of the SVN neurons, which was not blocked by the low-Ca<sup>2+</sup>/high-Mg<sup>2+</sup> medium, indicating a direct postsynaptic effect of the amine. Selective histamine H<sub>1</sub> receptor agonist 2-pyridylethylamine and H<sub>2</sub> receptor agonist dimaprit, rather than VUF8430, a selective H<sub>4</sub> receptor agonist, mimicked the excitation of histamine on SVN neurons. In addition, selective H<sub>1</sub> receptor antagonist mepyramine and H<sub>2</sub> receptor antagonist ranitidine, but not JNJ7777120, a selective H<sub>4</sub> receptor antagonist, partially blocked the excitatory response of SVN neurons to histamine. Moreover, mepyramine together with ranitidine nearly totally blocked the histamine-induced excitation. Immunostainings further showed that histamine H<sub>1</sub> and H<sub>2</sub> instead of H<sub>4</sub> receptors existed in the SVN. These results demonstrate that histamine excites the SVN neurons via postsynaptic histamine H<sub>1</sub> and H<sub>2</sub> receptors, and suggest that the central histaminergic innervation from the hypothalamus may actively bias the SVN neuronal activity and subsequently modulate the SVN-mediated vestibular functions and gaze control.
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