Vestibulo-oculomotor behaviour in rats following a transient unilateral vestibular loss induced by lidocaine.
The effects of a transient vestibular nerve blockade, achieved by intra-tympanic instillation of lidocaine, were studied in rats by recording horizontal eye movements in darkness. Evaluation of the dose-response relationship showed that a maximal effect was attained with a concentration of 4% lidocaine. Within 15 min of lidocaine instillation, a vigorous spontaneous nystagmus was observed which reached maximal frequency and velocity of the slow phase after about 20 min. Subsequently, the nystagmus failed for approximately half an hour before it reappeared. This could be avoided by providing visual feedback in between the recordings in darkness or by a contralateral instillation of 2.5% lidocaine. It is suggested that the failure reflects an overload of the vestibulo-oculomotor circuits. After recovery from the nerve blockade, when the gaze was stable, dynamic vestibular tests were performed. They revealed that a decrease of the slow phase velocity gain and the dominant time constant during, respectively, sinusoidal- and step stimulation toward the unanaesthetised side, had developed with the nerve blockade. These modulations were impaired by a nodulo-uvulectomy but not by bilateral flocculectomy, which is consistent with the concept of vestibular habituation. A GABA(B) receptor antagonist, CGP 56433A, given systemically during the nerve blockade, aggravated the vestibular asymmetry. The same effect has previously been demonstrated in both short- (days) and long-term (months) compensated rats, by antagonising the GABA(B) receptor. In summary, this study provides the first observations of vestibulo-oculomotor disturbances during the first hour after a rapid and transient unilateral vestibular loss in the rat. By using this method, it is possible to study immediate behavioural consequences and possible neural changes that might outlast the nerve blockade.
Magnusson
A K
AK
Department of Biomedicine and Surgery, Faculty of Health Sciences, SE-581 85, Linköping, Sweden. amgnusson@nefo.med.uni-muenchen.de
Tham
R
R
D000222:Adaptation, Physiological; D000779:Anesthetics, Local / Q000494:pharmacology*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D001565:Benzoates / Q000494:pharmacology; D003714:Denervation; D004305:Dose-Response Relationship, Drug; D005133:Eye Movements / Q000187:drug effects / Q000502:physiology; D007839:Functional Laterality; D018756:GABA Antagonists / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology*; D008297:Male; D009760:Nystagmus, Physiologic; D010721:Phosphinic Acids / Q000494:pharmacology; D011187:Posture; D051381:Rats; D011919:Rats, Inbred Strains; D012027:Reflex, Vestibulo-Ocular / Q000187:drug effects* / Q000502:physiology; D012438:Saccades / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D014722:Vestibule, Labyrinth / Q000187:drug effects* / Q000502:physiology / Q000601:surgery
D000779:Anesthetics, Local; D001565:Benzoates; D018756:GABA Antagonists; D010721:Phosphinic Acids; C105509:(3-(1-((3-(cyclohexylmethyl)hydroxyphosphinyl)-2-hydroxypropyl)amino)ethyl)benzoic acid; D008012:Lidocaine