Fos induction in the rat deep cerebellar and vestibular nuclei following central administration of colchicine: a qualitative and quantitative time-course study.
The present study was conducted to demonstrate Fos expression at four levels (anterior, prefastigial, postfastigial, posterior) of the cerebellar-vestibular nuclear complex in rats exposed to 1, 6, 24, and 48h of colchicine treatment using a light microscopic avidin biotin peroxidase (ABC) immunohistochemistry. Intracerebroventricular administration of colchicine (60microg per 10microl saline) elicited a continuous increase in the number of Fos-positive cells in the main cerebellar (fastigial, interpositus, dentatus) and vestibular (superior, medial, lateral, spinal, Y) nuclei. One and six hours after colchicine treatment, intensive Fos labeling was observed only in the pyriform cortex and the hypothalamic paraventricular nucleus, respectively, and there was no Fos immunolabeling in any of the cerebellar or vestibular structures investigated. On the other hand, moderate number of Fos-positive cells was visible in each of the cerebellar and vestibular nuclei 24h after colchicine treatment. Exposure of the animals to 48h of colchicine treatment induced an additional, more than 50%, rise in the accumulation of Fos-positive profiles in almost all the cerebellar and vestibular nuclei. In addition, at this time-point, a characteristic pattern of Fos distribution appeared almost in all of the cerebellar and vestibular nuclei, however, the numerical incidence of Fos-positive profiles in paired structures along the neuroaxis was bilaterally symmetric. The present data demonstrate for the first time that the central administration of colchicine causes a persistent and, in comparison with other brain areas, time-delayed activation of certain population of neurons in both cerebellar and vestibular nuclei. We assume that the delayed Fos activation in these structures indicate that the cerebellar and vestibular nuclei are not the primary targets of the central effect of colchicine and their activation seems to be rather a result of a postponed functional consequences of the central action of colchicine probably related to the coordination of motor performance.
Pirnik
Zdeno
Z
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06, Bratislava, Slovak Republic.
Mikkelsen
Jens D
JD
Kiss
Alexander
A
D000818:Animals; D002452:Cell Count; D002529:Cerebellar Nuclei / Q000187:drug effects* / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects; D006074:Gout Suppressants / Q000494:pharmacology; D007150:Immunohistochemistry; D007276:Injections, Intraventricular / Q000379:methods; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014726:Vestibular Nuclei / Q000187:drug effects* / Q000378:metabolism
D006074:Gout Suppressants; D016760:Proto-Oncogene Proteins c-fos; D003078:Colchicine