NEURONAL REGULATION OF COCHLEAR BLOOD-FLOW IN THE GUINEA-PIG

Citation
Ea. Laurikainen et al., NEURONAL REGULATION OF COCHLEAR BLOOD-FLOW IN THE GUINEA-PIG, Journal of physiology, 480, 1994, pp. 563-573
Citations number
41
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
480
Year of publication
1994
Part
3
Pages
563 - 573
Database
ISI
SICI code
0022-3751(1994)480:<563:NROCBI>2.0.ZU;2-W
Abstract
1. Previous studies have shown that electrical stimulation (ES) of the guinea-pig cochlea causes a neurally mediated increase in cochlear bl ood flow (CBF). It is known that the centrifugal neuronal input to the cochlea comes through the perivascular sympathetic plexus from the ce rvical sympathetic chain and along the vestibular nerve (VN) from the periolivary area of the brainstem. Both of these neuronal systems are distributed topographically in the cochlea. 2. In order to study the n eural origins of ES-evoked CBF increase, laser Doppler flowmetry was u sed to test the following hypotheses. (a) The response is regional, th at is, limited to the area of the cochlea stimulated. To test this we performed differential ES of the cochlear turns. CBF was measured from either the third or the first turn. (b) The response is mediated via autonomic receptors within the cochlea. To study this, we applied atro pine, succinylcholine and idazoxan locally to the cochlea. (c) The res ponse is influenced by neuronal input via the sympathetic cervical cha in (SC) and components of the VN. We stimulated and sectioned the SC, and sectioned the VN, to test this hypothesis.3. We observed that the CBF response was topographically restricted to the stimulated region. Locally applied muscarinic or nicotinic antagonists (atropine and succ inylcholine respectively) did not affect the response. However, local idazoxan (an alpha(2)-blocker) eliminated the response. Locally applie d adrenaline and SC stimulation modified the dynamic range of the resp onse. SC sectioning enhanced the responsiveness of the cochlear vascul ature to ES. The VN section caused a temporary decrease in CBF and eli mination of the ES-evoked CBF response. 4. We conclude that the releas e of dilating agents is topographical with respect to ES current flow, the ES-evoked CBF increase is peripherally mediated via alpha(2)-rece ptors, and the response is influenced by input via the SC. The elimina tion of the response by VN sectioning proximal to the brainstem indica ted that fibres of the VN mediate the CBF increase during direct cochl ear ES. The data suggest that these fibres may be the efferent limb of a neural loop involved with the regulation of CBF. Such a system coul d provide a mechanism for the rapid increase in CBF with organ stress.