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

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.