α-Linolenic Acid Deficiency Modifies Distractibility but Not Anxiety and Locomotion in Rats during Aging

Abstract

In rodents, chronic dietary alpha-linolenic acid deficiency decreases learning and memory and alters dopaminergic and serotoninergic neurotransmission. However, these two neurotransmitter systems are related mainly to attention, emotion and locomotion. Therefore, we decided to investigate the effects of dietary alpha-linolenic acid deficiency in rats tested with animal models of distractibility (the distractometer procedure), anxiety (the elevated plus maze) and ambulatory activity (a circular corridor). Moreover, because these neurochemical modifications persist during aging, we decided to study the effects of aging on these behaviors by using rats aged 2, 6, 12 and 24 mo. An age-related decline in distractibility was observed that was accelerated by linolenic acid deficiency. Indeed, an age-related reduction in distractibility was found in so far as distraction time was reduced at the age of 12 mo in controls and at the age of 24 mo in deficient groups compared with 2-mo-old rats. Moreover, distraction time was significantly lower in 6- and 24-mo-old rats fed a deficient diet compared with age-matched controls. Anxiety was not modified by diet or age. Finally, a parallel decrease in locomotion was exhibited by rats fed both diets between 6 and 12 mo of age. Locomotion was not modified by diet. These results show that dietary alpha-linolenic deficiency alters behavior in a very specific way; distractibility is modified by diet, whereas anxiety and locomotion are not, suggesting that particular brain areas may be altered.

Exposure to a maternal n-3 fatty acid-deficient diet during brain development provokes excessive hypothalamic–pituitary–adrenal axis responses to stress and behavioral indices of depression and anxiety in male rat offspring later in life

“…These studies suggest that DHA deficiency during brain development may lead to irreversible damage to certain brain functions. In contrast, DHAdeficient mice or rats fed an n-3 fatty acid-deficient diet from the embryo throughout their entire life, as opposed to only in early life, as in this study, showed either no difference in or lower anxiety-like behavior in the plus-maze test and depressive-like behavior in the forced swimming task compared to animals fed an n-3 fatty acidadequate diet [44][45][46][47][48]. This may be partly due to the different experimental design regarding the period of DHA deficiency.…”

Long-term omega-3 supplementation modulates behavior, hippocampal fatty acid concentration, neuronal progenitor proliferation and central TNF-α expression in 7 month old unchallenged mice

“…Similarly, various studies have shown different effects on anxiety behavior in animals after altering Ω-3:Ω-6 PUFA levels in their diet (Fedorova and Salem, 2006). Ω-3 deficient mice have previously been shown to have everything from decreased anxiety (Nakashima et al, 1993; Francès et al, 1995), increased anxiety (Carrié et al, 2000a; Fedorova and Salem, 2006), or no change in anxiety measured by time spent in the open arm of an elevated plus maze (Belzung et al, 1998; Moriguchi et al, 2000). …”

EFA supplementation in children with inattention, hyperactivity, and other disruptive behaviors

“…This result suggests that the amount of these FA in cell membranes could influence neurological processes that affect behavior. Previous studies in rats found that altered composition of n-3 FA in neurological membranes due to dietary insufficiency of ALA can influence both serotoninergic and dopaminergic neurotransmission (90,91). n-3 FA insufficiency has been associated with deficits in learning and memory (92), but effects on attention have not been as clear (93,94).…”