Spastic mutant axolotl: identification of a phenocopy pathway with implications for the control of axolotl swimming by the vestibulocerebellum.

Abstract

The spastic mutant axolotl shows abnormal swimming behavior, which includes a preponderance of "embryonic" swimming elements (coils) versus mature swimming elements (sinusoids) and a failure to entrain sinusoids into a prolonged swimming sequence. The mutant also shows anatomical disorganization in the area acousticolateralis and cerebellar auricle, but it is unclear (1) to what extent the behavioral abnormalities are traceable to the vestibulocerebellar defect or (2) how the vestibulocerebellar pathway modulates swimming behavior in the normal axolotl. We have performed quantitative cine analysis of electric shock-induced swimming bouts in normal axolotls, spastic mutants, and a variety of neurosurgically altered wild-type axolotls. We scored the incidence of coil elements (25% in controls, 70-90% in spastics) versus sinusoid elements, as well as length distributions of coilfree intervals (short to long trains of sinusoidal swimming) and of sinusoidfree intervals (of brief of prolonged coiling). We found that bilateral VIIIth nerve lesions or surgical undercutting of the cerebellar auricle in wild-type axolotls almost exactly reproduced the behavioral deficit seen in spastic (75-81% coils, loss of long sinusoid trains, and appearance of prolonged coiling intervals at least some of which coupled several coils into trains of thrashing behavior). By contrast, neither complete transection of the CNS at low midbrain levels nor section of cranial nerves V, VII, or X (lateral line) resulted in an increased incidence of coil elements beyond 26% nor significantly altered the length distributions of S-intervals and C-intervals. Nor did any of the latter lesions disrupt the spasticlike swimming patterns of axolotls already subjected to auricle or VIIIth nerve lesions.(ABSTRACT TRUNCATED AT 250 WORDS)