POSTNATAL DEVELOPMENT OF ｙ-AMINOBUTYRIC ACID (GABA) NEURONS IN THE CEREBELLUM OF JAUNDICED GUNN RATS: A STUDY WITH ANTI-GABA ANTISERUM

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In the cerebellum of jaundiced homozygous (ji) Wistar Gunn rats, specific activity of glutamate decarboxylase (GAD) on a wetweight basison andafterpostnatal day 10was significantly lower than in non-jaundiced heterozygous (j+) rats (2). In the present study, wehaveexaminedthepostnatal developmentofGAD activityin another strain of Gunn rats (Sprague-Dawley Gunn rat). Thejj rats ofthis strain also showeda considerably low rate ofincrease in GAD activity from days 10 to 15 compared withj+ rats. To clarify a histological basis of the impaired development of GAD activity inji rats, the postnatal development of cerebellar y-aminobutyric acid (GABA)ergic neurons was studied immunocytochemically using anti-GABA antiserum raised in rabbits. Golgi andPurkinje cellswere stainedwiththeanti-GABA antiserum atthe dayofbirth in both jj andj+ rats. Many Purkinje cells, which showed some degenerative changesalready at day 1 injj rats, suffered from severe damages at day 10, and disappeared before day 15. Golgi cells also showed some degenerative changes at day 15, though they still maintained their immunoreactivity to the antiserum. Basket cells, which appearedat day 10,weresmallin number injjratsatday15, suggestingthattheyhadbeenseverelydamaged during this period. The results suggest that bilirubin sensitivity ofGABAergic neurons isheterogeneous, anddestruction bybilirubin ofPurkinje andbasketcells before day 15 is mainly responsible for a low rate ofincrease in GAD activity from postnatal days 10 to 15.