Serotoninergic neurotransmission is affected by n-3 polyunsaturated fatty acids in the rat.
Kodas E, Galineau L, Bodard S, Vancassel S, Guilloteau D, Besnard JC, Chalon S. Source
INSERM U316, Laboratoire de Biophysique Medicale et Pharmaceutique, Universite Francois Rabelais, Tours, France. Abstract
We explored the effects of chronic alpha-linolenic acid dietary deficiency on serotoninergic neurotransmission. In vivo synaptic serotonin (5-HT) levels were studied in basal and pharmacologically stimulated conditions using intracerebral microdialysis in the hippocampus of awake 2-month-old rats. We also studied the effects of reversion of the deficient diet on fatty acid composition and serotoninergic neurotransmission. A balanced (control) diet was supplied to deficient rats at different stages of development, i.e. from birth, 7, 14 or 21 days of age. We demonstrated that chronic n-3 polyunsaturated fatty acid dietary deficiency induced changes in the synaptic levels of 5-HT both in basal conditions and after pharmacological stimulation with fenfluramine. Higher levels of basal 5-HT release and lower levels of 5-HT-stimulated release were found in deficient than in control rats. These neurochemical modifications were reversed by supply of the balanced diet provided at birth or during the first 2 weeks of life through the maternal milk, whereas they persisted if the balanced diet was given from weaning (at 3 weeks of age). This suggests that provision of essential fatty acids is durably able to affect brain function and that this is related to the developmental stage during which the deficiency occurs. ------------------------------------------
Then the lesser cite: http://www.nature.com/neuro/journal/v14/n3/full/nn.2736.html
No access for me today but the following is an extract:
How maternal essential fatty acid deficiency impact on its progeny is poorly understood. Dietary insufficiency in omega-3 fatty acid has been implicated in many disorders. Researchers from Inserm and INRA and their collaborators in Spain collaboration, have studied mice fed on a diet low in omega-3 fatty acid. They discovered that reduced levels of omega-3 had deleterious consequences on synaptic functions and emotional behaviours. Details of this work are available in the online version of the journal Nature neuroscience, which can be accessed at: http://dx.doi.org/10.1038/nn.2736
In industrialized nations, diets have been impoverished in essential fatty acids since the beginning of the 20th century. The dietary ratio between omega-6 polyunsaturated fatty acid and omega-3 polyunsaturated fatty acid omega-3 increased continuously over the course of the 20th century. These fatty acids are "essential" lipids because the body cannot synthesize them from new. They must therefore be provided through food and their dietary balance is essential to maintain optimal brain functions.
Olivier Manzoni (Head of Research Inserm Unit 862, "Neurocentre Magendie", in Bordeaux and Unit 901 "Institut de Neurobiologie de la M-diterran-e" in Marseille), and Sophie Lay- (Head of Research at INRA Unit 1286, "Nutrition et Neurobiologie Int-grative" in Bordeaux) and their co-workers hypothesized that chronic malnutrition during intra-uterine development, may later influence synaptic activity involved in emotional behaviour (e.g. depression, anxiety) in adulthood.
To verify their hypotheses, the researchers studied mice fed a life-long diet imbalanced in omega-3 and omega-6 fatty acids. They found that omega-3 deficiency disturbed neuronal communication specifically. The researchers observed that only the cannabinoid receptors, which play a strategic role in neurotransmission, suffer a complete loss of function. This neuronal dysfunction was accompanied by depressive behaviours among the malnourished mice.
Among omega-3 deficient mice, the usual effects produced by cannabinoid receptor activation, on both the synaptic and behavioural levels, no longer appear. Thus, the CB1R receptors lose their synaptic activity and the antioxidant effect of the cannabinoids disappears.
Consequently, the researchers discovered that among mice subjected to an omega-3 deficient dietary regime, synaptic plasticity, which is dependent on the CB1R cannabinoid receptors, is disturbed in at least two structures involved with reward, motivation and emotional regulation: the prefrontal cortex and the nucleus accumbens. These parts of the brain contain a large number of CB1R cannabinoid receptors and have important functional connections with each other.
"Our results can now corroborate clinical and epidemiological studies which have revealed associations between an omega-3/omega-6 imbalance and mood disorders", explain Olivier Manzoni and Sophie Lay-. "To determine if the omega-3 deficiency is responsible for these neuropsychiatric disorders additional studies are, of course, required".
In conclusion, the authors estimate that their results provide the first biological components of an explanation for the observed correlation between omega-3 poor diets, which are very widespread in the industrialized world, and mood disorders such as depression.
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So from my non indeapth understanding
Synaptic activity will be enhanced by fats. To me the mood is the person and electrical activity maybe be reduced/enhanced>
PMCID: PMC1176378 Copyright 2004 by the American Epilepsy Society Dietary Approaches to Epilepsy Treatment: Old and New Options on the Menu Carl E. Stafstrom, M.D., Ph.D.
Full PDF address: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1176378/pdf/epc_46001.pdf
Abstract:
Dietary therapies represent a potentially valuable adjunct to other epilepsy treatments, such as anticonvulsant medications, epilepsy surgery, and vagus nerve stimulation. Although the ketogenic diet (high fat, adequate protein, low carbohydrate) is the most well-established dietary therapy for epilepsy, other possible approaches include the Atkins diet (high fat, high protein, low carbohydrate), a diet enriched in polyunsaturated fatty acids, or overall restriction of calorie intake. This review discusses the current clinical status of each of these dietary approaches and suggests possible mechanisms by which they might suppress neuronal hyperexcitability and seizures.
