Evidence that L-type calcium channels do not contribute to static vestibular function in the guinea pig vestibular nucleus.

Abstract:

:Labyrinthine-intact guinea pigs received unilateral, brainstem cannula injections of (1) 2.5 micrograms of the selective dihydropyridine L-type Ca2+ channel agonist, Bay K 8644 (n = 4 animals); (2) 10 micrograms Bay K 8644 (n = 4); 12.5 micrograms of the selective dihydropyridine L-type Ca2+ channel antagonist, nifedipine (n = 4); or 40 micrograms nifedipine (n = 4). In 11/16 cases, the lesion associated with the cannula tip was located within or near the border of the right vestibular nucleus (VN) complex. All cannula injections were delivered in a 1 microliter volume of artificial cerebrospinal fluid (ACSF) and dimethylsulphoxide (DMSO) (70% DMSO, 30% ACSF for Bay K 8644; 80% DMSO, 20% ACSF for nifedipine), adjusted to a pH of approx. 7.0. The effects of these injections were compared with control injections of ACSF/DMSO in our previous studies. Animals were observed for signs of a labyrinthine syndrome (i.e. spontaneous ocular nystagmus, yaw and roll head tilt) directed to the contralateral or ipsilateral side. In no case did Bay K 8644 or nifedipine cause ocular motor or postural symptoms similar to those produced by a unilateral labyrinthectomy. These results suggest that L-type Ca2+ channels do not contribute significantly to the resting activity of VN neurons and therefore do not contribute to static vestibular function at the level of the VN.

journal_name

Brain Res

journal_title

Brain research

authors

Sansom AJ,Smith PF,Darlington CL

doi

10.1016/0006-8993(93)90677-f

subject

Has Abstract

pub_date

1993-12-10 00:00:00

pages

349-52

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(93)90677-F

journal_volume

630

pub_type

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