## 2 Arachidic Acid Sources  
Recently, lines of evidence suggest that the membrane lipid component to Gs\(\alpha\)-protein, tubulin, and state of consciousness are related in a complex way. Depending on the lipid concentration phase of the membrane, tubulin can serve as a regulator of the hydrolysis of membrane phospholipids as well as G-proteins [9]. In this context, the state of continuous renewal and exchange of fatty acids can be thought of in terms of a mechanical force on the cytoskeleton both in physiological and pathological conditions [10; 15; 16; 17]. Arachidic acid (AA) is an abundant PUFA of the membrane phospholipids. It is an integral component of cell membranes, conferring to the mammalian cell membranes their fluidity at physiological temperatures. A complex molecular sequence affects the entire molecular mechanism and may affect the production of regulatory molecules, including enzyme activities and metabolic reactions, which can influence the viscosity of the membrane. The principal effect of AA is its conversion via cyclooxygenase (COX) and lipoxygenase (LOX) enzymes and, consequently, the stimulus to produce a variety of oxygenated PUFA bioactive derivatives known as eicosanoids (prostaglandins, PGE, thromboxanes, lipoxins, leukotrienes, hydroxyeicosattarenaoic, and epoxyeicosatetraenoic acids), and docosatrienes (neuroprotectins and resolvins) which are locally acting hormone-like compounds and are known modulate inflammation status (Figure 1). These molecules play roughly some role in depression. In particular, AA processing follows the release of some cytosolic and secretory enzymes belonging to the rate-limiting phospholipase A2 (PLA\({}_{2}\)) enzymes. In the brain, AA is specifically hydrolyzed by cytosolic PLA\({}_{2}\) (c PLA\({}_{2}\)) in a Ca\({}^{2+}\)-dependent manner in response to a wide range of stimuli [18]. PLA\({}_{2}\) hydrolyzes the _sn_-2 fatty acyl bond of membrane glycerophospholipids, including phosphatidycholine (PC) and phosphatidylethanolamine (PE). Arachidic acid metabolites play crucial roles in maintaining health conditions by regulating physiological processes, development, and growth of skeletal muscle, resolution of the inflammation process, and production of angiogenic factors. AA and its metabolites are also implicated in various processes, including hypoxia, ischemia, and hypoglycemia [19]. The release of AA has been well characterized in both neural and non-neural cells. The lipo-soluble metabolites of AA spread rapidly across membranes. Therefore, in addition to acting within the cell that produced them, these molecules can act on neighboring cells acting as transcellular messengers [20]. Patients suffering from major depression displayed a higher level of PLA\({}_{2}\) activity [21]. An increased AA/omega-3 fatty acid ratio, especially docosahexaenoic acid (DHA), is associated with depression [11]. LOX generates anti-inflammatory docosahexaenoic acid(DHA)-derived metabolites and lipoxins derived from AA via the 5-LOX pathway. Studies on 5-LOX-deficient transgenic mice models suggested that 5-LOX activity may contribute to depression-like behaviors [22]. In addition, 5-LOX inhibitors, by increasing phosphorylation of glutamatergic receptor type 1, might normalize synaptic plasticity in depression state and produce antidepressant effects [23]. Drugs commonly used to treat BD, such as lithium, carbamazepine, and valpro acid, significantly reduce AA turnover in the brain. This evidence suggests the possibility of a role for the benefit observed from using omega-3 PUFA in mood disorders because omega-3 PUFA competitively inhibits the metabolism of AA to eicosanoids [24]. Lithium also influences downstream in the AA pathway by inhibiting the COX-2 and reducing the inflammation condition [24]. Eicosanoids families are modulated by neuroglia such as microglia and astrocyte. In particular, eicosanoids are produced by microglia [25]. COX-1 is constitutively expressed in the body and acts as a \"house-keeping\" enzyme.