Our laboratory has reported that pentobarbital-induced anesthesia reduced t
he incorporation of intravenously injected radiolabeled palmitic acid into
brain phospholipids. To determine if this decrease reflected a pentobarbita
l-induced decrease in palmitate turnover in phospholipids, we applied our m
ethod and model to study net flux and turnover of palmitate in brain phosph
olipids (1). Awake, light and deep pentobarbital (25-70 mg/kg, iv) anesthet
ized rats were infused with [9,10-H-3]palmitate over a 5 min period. Brain
electrical activity was monitored by electroencephalography. An isoelectric
electroencephalogram characterized deep pentobarbital anesthesia. Net inco
rporation rates (J(FA,i)) and turnover rates (F-i) of palmitate were calcul
ated. J(FA,i) for palmitate incorporated into phospholipids was dramaticall
y reduced by pentobarbital treatment in a dose-dependent manner, by 70% and
90% respectively for lightly and deeply anesthetized animals, compared wit
h awake controls. Turnover rates for palmitate in total phospholipid and in
dividual phospholipid classes were decreased by nearly 70% and 90% for ligh
tly and deeply anesthetized animals, respectively. Thus, pentobarbital decr
eases, in a dose-dependent manner, the turnover of palmitate in brain phosp
holipids. This suggests that palmitate turnover is closely coupled to brain
functional activity.