Elevated brain GABA correlates with systemic dysfunctions in paroxysmal chick

Altered brain GABA, phosphocreatine and adenosine triphosphate have been documented in paroxysmal (px) chicks in earlier studies, suggesting perturbations in energy metabolism as a causative factor in this syndrome that is characterized by spontaneous neural degeneration of several central sensory systems, grand mal seizures, and progressive anorexia. In this study, brain sections from 5-, 7-, and 10-day-old px and normal White Leghorn-cross chicks were stained by immunocytochemistry to localize and quantify GABA. Serum glucose was measured to assess adequacy of circulating energy substrate. Differences between px and normal brains were found in GABA staining intensity in nuclei and tracts associated with auditory, vestibular and oculomotor function, and in several septal areas. Staining appeared to be confined primarily to terminals, 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 circulating glucose, suggesting that alterations in brain energy substrates are not a function of inadequate supply.