Altered brain GABA, phosphocreatine and adenosine triphosphate have be
en documented in paroxysmal (px) chicks in earlier studies, suggesting
perturbations in energy metabolism as a causative factor in this synd
rome that is characterized by spontaneous neural degeneration of sever
al central sensory systems, grand mal seizures, and progressive anorex
ia. In this study, brain sections from 5-, 7-, and 10-day-old px and n
ormal White Leghorn-cross chicks were stained by immunocytochemistry t
o localize and quantify GABA. Serum glucose was measured to assess ade
quacy of circulating energy substrate. Differences between px and norm
al brains were found in GABA staining intensity in nuclei and tracts a
ssociated with auditory, vestibular and oculomotor function, and in se
veral septal areas. Staining appeared to be confined primarily to term
inals, and increasingly larger numbers of stained terminals were found
in older px brains. This progressive increase appears to parallel the
degenerative changes that occur over time in px brain and progressive
manifestation of clinical signs. Px chicks appear to have adequate ci
rculating glucose, suggesting that alterations in brain energy substra
tes are not a function of inadequate supply.