Background
Prior clinical studies suggest a shared mechanism between vestibular symptoms and migraine headache. However, the specific neuroanatomical substrate connecting vestibular symptoms with migraine remains to be largely unknown. Thus, the
Conclusions
Together, we reveal a modulatory role of glutamatergic TNC-VN projection neurons in vestibular dysfunction of migraine.
Methods
A chronic-NTG rat model was established by recurrent intermittent administration of nitroglycerin (NTG). Pain- and vestibular-related behaviors were assessed. To selectively inhibit the glutamatergic neurons and trigeminal nucleus caudalis (TNC) to VN projection neurons, the AAVs encoding engineered Gi-coupled hM4D receptor were administered in the TNC or VN area.
Results
We identify a glutamatergic projection from TNC to VN that mediates vestibular dysfunction in a chronic-NTG rat model. Inhibition of the GlutamateTNC neurons alleviates vestibular dysfunction in the chronic-NTG rat. Calcitonin gene-related peptide (CGRP)-expressing neurons in the VN received glutamatergic projections from TNC neurons. Silencing the glutamatergic TNC-VN projection neurons attenuates vestibular dysfunction in the chronic-NTG rat. Conclusions: Together, we reveal a modulatory role of glutamatergic TNC-VN projection neurons in vestibular dysfunction of migraine.