抄録
We have previously shown that the defense response against stressor was attenuated in prepro-orexin knockout mice (Am J Physiol 285:R581, 2003) and orexin neuron-ablated mice (Am J Physiol 290:R1654, 2006) and proposed that orexin plays as a master switch to elicit multiple efferent pathways of the defense response. It is still open question, however, how information of stressor activates the orexinergic neurons. In this study, we examined possible contribution of the amygdala and bed nucleus of stria terminalis (BNST) as one of the afferent nuclei to activate orexinergic neurons. In urethane-anesthetized mice, a GABA-A receptor antagonist, bicuculline methiodide (0.1-10 mM in 20 nl), was microinjected into the amygdala or BNST, of which electrical stimulation induced simultaneous increases in blood pressure, heart rate, and respiratory frequency. Bicuculline dose-dependently induced cardiorespiratory excitation in both orexin neuron-ablated mice and wild-type controls. However, dose-response curve was rightward shifted in the orexin neuron-ablated mice. In an immunohistochemical study, we confirmed that microinjection of bicuculline to the amygdala or BNST induced c-fos expression in the orexinergic neurons. We conclude that the amygdala and BNST constitute one of the afferent pathways to the orexinergic neurons that involved in the defense response against stressor. [J Physiol Sci. 2007;57 Suppl:S239]
