Effect of unilateral vestibular stimulation on histamine release from the hypothalamus of rats in vivo

Abstract

1. We investigated the effect of unilateral vestibular stimulation on histamine release from the anterior hypothalamic area of urethan-anesthetized rats in vivo, using a brain microdialysis method coupled with high-performance liquid chromatography fluorometry. 2. The histamine release was increased to approximately 180% of the basal release by the electrical stimulation of the inner ear with 1 Hz, 500 microA, and 200 ms for 20 min. This effect was dependent on the current intensity. 3. Activation of the unilateral horizontal semicircular canal by middle ear irrigation for 15 min with 45 degrees C water increased the histamine release to approximately 200% of the basal release. 4. Irrigation of the middle ear with ice water for 15 min increased the histamine release to approximately 190% of the basal release. 5. The histamine release was not changed by the irrigation of the middle ear with 37 degrees C water and the irrigation of the auricle with ice water, which suggests that neither somatosensory stimulation to the middle ear nor nonspecific cold stress affects the histamine release. 6. All these findings suggest that the sensory mismatch signals induced by caloric stimulation and unilateral electrical vestibular stimulation activate the histaminergic neuron system in the brain.

Brain Activation by H1 Antihistamines Challenges Conventional View of Their Mechanism of Action in Motion Sickness: A Behavioral, c-Fos and Physiological Study in Suncus murinus (House Musk Shrew)

“…Unfortunately, there have been no studies where intracerebral administration of histamine receptor antagonists have been made into any of these nuclei during motion-induced emesis experimentation. However, it is thought that during provocative motion, a neural mismatch signal activates histaminergic neurons in the hypothalamus, and the histaminergic descending pathway to potentially stimulate H 1 receptors in the brainstem's “emetic center” (Takeda et al, 1986; Horii et al, 1993; Uno et al, 1997; Schmäl, 2013). Whilst the precise role of neuron and mast cell sources of histamine are not known, it is known that H 1 receptors are densely located in the NTS and DMNV, and also the vestibular nucleus; all areas are behind the blood brain barrier.…”

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

“…The mechanism of action of histamine on to the VN helps to explain the functional role of this neural loop activated when asymmetrical inputs reach the central vestibular structures (Horii et al, 1993). This loop could convey signals that promote the regulation of HDC gene expression leading to the release of histamine in the VN.…”

“…Histamine is highly implicated with the arousal level (Brown et al, 2001; Haas et al, 2008) and it has been shown that the horizontal vestibulo-ocular-reflex gain was very sensitive to the state of alertness (Flandrin et al, 1979; Matta and Enticott, 2004). Stimulation of the vestibular nerve enhances HA release in the hypothalamus and brainstem (Takeda et al, 1986; Horii et al, 1993, 1996; Uno et al, 1997). In vitro intracellular recordings from neurons in the medial and the lateral vestibular nuclei (VN; MVN and LVN) revealed HA induced depolarization via postsynaptic histamine H 1 (H 1 R; Inverarity et al, 1993) or H 2 receptors (H 2 R; Phelan et al, 1990; Serafin et al, 1993; Wang and Dutia, 1995; Zhang et al, 2008, 2013; Zhuang et al, 2013).…”

Betahistine, Vestibular Function and Compensation: In Vitro Studies of Vestibular Function and Plasticity

“…Histamine is known to be released in the medulla and hypothalamus during the stress that accompanies vestibular dysfunction, such as in animal models of motion sickness (9) and after unilateral vestibular stimulation (10). Similarly, the histamine immunoreactivity in the vestibular nuclei is decreased following UL (5), thus indicating increased histamine release and depletion of central histamine stores.…”