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.