In this chapter, we have attempted to provide an overview of some fundamental aspects of neurotransmitters, signal transduction pathways, and second messengers. For most psychiatrists, molecular and cellular biology have not traditionally played a major role in day-to-day clinical practice. However, new insights into the molecular and cellular basis of disease and drug action are being generated at an ever-increasing rate and will ultimately result in a transformation of our understanding and management of diseases. Indeed, the last decade of the twentieth century was truly a remarkable one for biomedical research. The "molecular medicine revolution" has utilized the power of sophisticated cellular and molecular biological methodologies to tackle many of society's most devastating illnesses. The rate of progress has been exciting indeed, and hundreds of G protein-coupled receptors and dozens of G proteins and effectors have now been identified and characterized at the molecular and cellular levels. These efforts have allowed the study of a variety of human diseases that are caused by abnormalities in cell-to-cell communication; studies of such diseases are offering unique insights into the physiological and pathophysiological functioning of many cellular transmembrane signaling pathways.

Psychiatry, like much of the rest of medicine, has entered a new and exciting age demarcated by the rapid advances and the promise of molecular and cellular biology and neuroimaging. There is a growing appreciation that severe psychiatric disorders arise from abnormalities in cellular plasticity cascades, leading to aberrant information processing in synapses and circuits mediating affective, cognitive, motoric, and neurovegetative functions. Thus, these illnesses can be best conceptualized as genetically influenced disorders of synapses and circuits rather than simply as deficits or excesses in individual neurotransmitters (Carlson et al. 2006). Furthermore, many of these pathways play critical roles not only in synaptic (and therefore behavioral) plasticity but also in long-term atrophic processes. Targeting these cascades in treatment may stabilize the underlying disease process by reducing the frequency and severity of the profound mood cycling that contributes to morbidity and mortality. The role of cellular signaling cascades offers much explanatory power for understanding the complex neurobiology of bipolar illness (Goodwin and Jamison 2007). Signaling cascades regulate the multiple neurotransmitter and neuropeptide systems implicated in psychiatric disorders and are targets for the most effective treatments. The highly integrated monoamine and prominent neuropeptide pathways are known to originate in and project heavily to limbic-related regions, such as the hippocampus, hypothalamus, and brain stem, which are likely associated with neurovegetative symptoms. Abnormalities in cellular signaling cascades that regulate diverse physiological functions likely explain the tremendous medical comorbidity associated with psychiatric disorders.

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