The uptake, metabolism, and cellular distribution of 3H-docosahexaenoic acid (3H-22:6) in the frog retina during in vitro incubation were studied. An initial diffuse labeling throughout the retina was detected by autoradiography and was followed by an active steady increase in labeled photoreceptor cells. After 6 hr of incubation, 92% of the label was concentrated in photoreceptor cells. Among these cells, 435 rods (green rods) labeled heavily and showed two to three times higher uptake than the 502~rods (red rods). Cone uptake labeling was the lowest, showing negligible labeling throughout the cytoplasm. However, oil droplets of the 575 cones actively concentrated 22:6. The high uptake of 3H-22:6 by photoreceptor cells was followed by its rapid esterification into phospholipids. After 6 hr of labeling, only 5% of the radioactivity in the retina was free 22:6, whereas 66% was esterified into phospholipids. The remaining 22:6 was distributed equally in triacylglycerols (TAGS) and diacylglycerols. When 3H-22:6 (0.11 PM) of high specific activity was used, early incubation times showed phosphatidylinositol (PI) labeling to be of the same order of magnitude or greater than that of phosphatidylcholine (PC) or phosphatidylethanolamine (PE). Although the amount of endogenous 22:6 esterified into PI accounted for less than 2% of the 22:6 in retinal phospholipids, 27% of 3H-22:6 labeling was recovered in this phospholipid. When 'C-22:6 at a final concentration of 70 PM was used, a different profile of lipid labeling was observed. Forty percent of the labeling remained in the free fatty acid pool, followed by TAG (24%), PC (14%), and PE (12%). PI showed the smallest increase in picomoles of 14C-22:6 incorporated, when compared with 3H-22:6. In conclusion, a selective and differential uptake of 3H-22:6 by photoreceptor cells is coupled to its active utilization for phospholipid biosynthesis, mainly that of PC, PE, and PI. The differential uptake of 3H-22:6 among photoreceptor cells may reflect involvement of this fatty acid in cell-specific functions.

Abstract— The size of the free fatty acid pool in rat brain was significantly increased following convulsions induced by pentylenetetrazol as well as by electroconvulsive shock. Other convulsants such as d‐methionine‐dl‐sulphoximine and the dibutyryl analog of adenosine 3′,5′‐monophosphate did not alter the levels of free fatty acids. Diethyl ether anaesthesia suppressed the stimulatory effect of electroshock on the generation of free fatty acids in brain, but the effect was not seen with the anaesthetic pentobarbitone sodium. The lack of an inhibitory effect of either anaesthetic on the free fatty acid production which was induced in brain by ischaemia supported the view that the action of electroshock was not merely the result of anoxia. The prominent increase in size of the free fatty acid pool in brain thus appeared to be specific for electroshock‐ and pentylenetetrazol‐convulsed rats. We have proposed that the changes in the free fatty acids might be involved in the regulation of membrane functioning.

Bicuculline-induced status epilepticus was found to be associated with increased amounts of free fatty acids and diacylglycerols in the rat cerebrum. The predominant fatty acid in both lipid pools was arachidonic acid. The accumulation of arachidonoyl-diglycerols decreased at the time of and during behavioral seizures induced by bicuculline, while the amount of free arachidonic acid appeared to increase. We propose a metabolic relationship between these lipids to explain the described changes. The similarities between the composition of the lipid pools and the fatty acid composition of phosphatidylinositol support the hypothesis that these changes may be a result of a convulsion-activated degradation of this phospholipid from excitable membranes.