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After unilateral vestibular neurectomy (UVN) many molecular and neurochemical mechanisms underlie the neurophysiological reorganizations occurring in the vestibular nuclei (VN) complex, as well as the behavioral recovery process. As a key regulator, the histaminergic system appears to be a likely candidate because drugs interfering with histamine (HA) neurotransmission facilitate behavioral recovery after vestibular lesion. This study aimed at analyzing the post-lesion changes of the histaminergic system by quantifying binding to histamine H 3  receptors (H 3 R; mediating namely histamine autoinhibition) using a histamine H 3  receptor agonist ([ 3 H]N-α-methylhistamine). Experiments were done in brain sections of control cats ( N  = 6) and cats submitted to UVN and killed 1 ( N  = 6) or 3 ( N  = 6) weeks after the lesion. UVN induced a bilateral decrease in binding density of the agonist [ 3 H]N-α-methylhistamine to H 3 R in the tuberomammillary nuclei (TMN) at 1 week post-lesion, with a predominant down-regulation in the ipsilateral TMN. The bilateral decrease remained at the 3 weeks survival time and became symmetric. Concerning brainstem structures, binding density in the VN, the prepositus hypoglossi, the subdivisions of the inferior olive decreased unilaterally on the ipsilateral side at 1 week and bilaterally 3 weeks after UVN. Similar changes were observed in the subdivisions of the solitary nucleus only 1 week after the lesion. These findings indicate vestibular lesion induces plasticity of the histamine H 3 R, which could contribute to vestibular function recovery.

Plasticity of the histamine H3 receptors after acute vestibular lesion in the adult cat