Before I explain serotonin receptors family I want to go over in deep detail about G-protein coupled receptors, and we will examine closely about specific serotonin subtypes and their functions., This will give us insight of how atypical antipsychotics work and clues of how these agents cause side effects. I have a nice illustration and description to show you below.

Robert T. Dorsam and J. Silvio Gutkind, G-protein-coupled receptors and cancer, Nature Reviews Cancer 7, 79-94 (February 2007)

Various ligands use G-protein-coupled receptors (GPCRs) to stimulate membrane, cytoplasmic and nuclear targets. GPCRs interact with heterotrimeric G proteins composed of , and subunits that are GDP bound in the resting state. Agonist binding triggers a conformational change in the receptor, which catalyses the dissociation of GDP from the subunit followed by GTP-binding to G and the dissociation of G from G subunits.

The subunits of G proteins are divided into four subfamilies: G_s, G_i, G_q and G₁₂, and a single GPCR can couple to either one or more families of G proteins. Each G protein activates several downstream effectors. Typically G_s stimulates adenylyl cyclase and increases levels of cyclic AMP (cAMP), whereas G_i inhibits adenylyl cyclase and lowers cAMP levels, and members of the G_q family bind to and activate phospholipase C (PLC), which cleaves phosphatidylinositol bisphosphate (PIP₂) into diacylglycerol and inositol triphosphate (IP₃).

The G subunits and G subunits function as a dimer to activate many signalling molecules, including phospholipases, ion channels and lipid kinases.

Besides the regulation of these classical second-messenger generating systems, G subunits and G subunits such as G₁₂ and G_q can also control the activity of key intracellular signal-transducing molecules, including small GTP-binding proteins of the Ras and Rho families and members of the mitogen-activated protein kinase (MAPK) family of serine-threonine kinases, including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), p38 and ERK5, through an intricate network of signalling events that has yet to be fully elucidated. Ultimately, the integration of the functional activity of the G-protein-regulated signalling networks control many cellular functions, and the aberrant activity of G proteins and their downstream target molecules can contribute to cancer progression and metastasis.

5-HT, 5-hydroxytryptamine; ECM, extracellular matrix; GABA, gamma-aminobutyric acid; GEF, guanine nucleotide exchange factor; GRK, G protein receptor kinase; LPA, lysophosphatidic acid; PI3K, phophatidylinositol 3-kninase; PKA and PKC, protein kinase A and C; S1P sphingosine-1-phosphate.