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1. Previous studies have shown that electrical stimulation (ES) of the guinea-pig cochlea causes a neurally mediated increase in cochlear blood flow (CBF). It is known that the centrifugal neuronal input to the cochlea comes through the perivascular sympathetic plexus from the cervical 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 neural origins of ES-evoked CBF increase, laser Doppler flowmetry was used to test the following hypotheses. (a) The response is regional, that 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 atropine, succinylcholine and idazoxan locally to the cochlea. (c) The response is influenced by neuronal input via the sympathetic cervical chain (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 succinylcholine respectively) did not affect the response. However, local idazoxan (an alpha 2-blocker) eliminated the response. Locally applied adrenaline and SC stimulation modified the dynamic range of the response. SC sectioning enhanced the responsiveness of the cochlear vasculature to ES. The VN section caused a temporary decrease in CBF and elimination of the ES-evoked CBF response. 4. We conclude that the release of dilating agents is topographical with respect to ES current flow, the ES-evoked CBF increase is peripherally mediated via alpha 2-receptors, and the response is influenced by input via the SC. The elimination of the response by VN sectioning proximal to the brainstem indicated that fibres of the VN mediate the CBF increase during direct cochlear 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 could provide a mechanism for the rapid increase in CBF with organ stress.
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 1989,
Acta oto-laryngologica,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
September 1995,
Hearing research,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
October 1994,
Arzneimittel-Forschung,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
March 1994,
Acta oto-laryngologica,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 1991,
Acta oto-laryngologica,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
September 1995,
Hearing research,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 2002,
Advances in oto-rhino-laryngology,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 1991,
ORL; journal for oto-rhino-laryngology and its related specialties,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 1987,
Hearing research,
E A Laurikainen, and
O Costa, and
J M Miller, and
A L Nuttall, and
T Y Ren, and
R Masta, and
W S Quirk, and
P J Robinson
January 1990,
Hearing research,
