a major depressive episode. Classification Different members of the NOS family are encoded by separate genes. There are three known isoforms in mammals, two are constitutive (cNOS) and the third is inducible (iNOS). Cloning of NOS enzymes indicates that cNOS include both brain constitutive (NOS1) and endothelial constitutive (NOS3); the third is the inducible (NOS2) gene. Recently, NOS activity has been demonstrated in several bacterial species, including notorious pathogens Bacillus anthracis and Staphylococcus aureus. The different forms of NO synthase have been classified as follows: nNOS Neuronal NOS (nNOS) produces NO in nervous tissue in both the central and peripheral nervous systems. Its functions include: Synaptic plasticity in the central nervous system (CNS) Smooth muscle relaxation Central regulation of blood pressure Vasodilatation via peripheral nitrergic nerves Neuronal NOS also performs a role in cell communication and is associated with plasma membranes. nNOS action can be inhibited by NPA (N-propyl-L-arginine). This form of the enzyme is specifically inhibited by 7-nitroindazole. The subcellular localisation of nNOS in skeletal muscle is mediated by anchoring of nNOS to dystrophin. nNOS contains an additional N-terminal domain, the PDZ domain. The gene coding for nNOS is located on Chromosome 12. iNOS As opposed to the critical calcium-dependent regulation of constitutive NOS enzymes (nNOS and eNOS), iNOS has been described as calcium-insensitive, likely due to its tight non-covalent interaction with calmodulin (CaM) and Ca2+. The gene coding for iNOS is located on Chromosome 17. While evidence for ‘baseline’ iNOS expression has been elusive, IRF1 and NF-κB-dependent activation of the inducible NOS promoter supports an inflammation mediated stimulation of this transcript. iNOS produces large quantities of NO upon stimulation, such as by proinflammatory cytokines (e.g. Interleukin-1, Tumor necrosis factor alpha and Interferon gamma). Induction of the high-output iNOS usually occurs in an oxidative environment, and thus high levels of NO have the opportunity to react with superoxide leading to peroxynitrite formation and cell toxicity. These properties may define the roles of iNOS in host immunity, enabling its participation in anti-microbial and anti-tumor activities as part of the oxidative burst of macrophages. It has been suggested that pathologic generation of nitric oxide through increased iNOS production may decrease tubal ciliary beats and smooth muscle contractions and thus affect embryo transport, which may consequently result in ectopic pregnancy. eNOS Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3), generates NO in blood vessels and is involved with regulating