Preface

Serotonin is a monoamine neurotransmitter in the central nervous system (CNS), whose well-known biological functions include modulating cognition, sleep, emotion, learning, memory, and numerous physiological processes.

At any given time, over 4% of the global population suffers from a major depressive disorder. Among approved depression treatments are selective serotonin reuptake inhibitors (SSRIs). These are based on the serotonin hypothesis, which holds that low levels of extracellular serotonin causes depression; consequently, increasing extracellular serotonin can treat depression. Since the introduction of SSRIs, many books about serotonin have been published.

I started my neuroscience career by measuring serotonin in the brain of different animals during my PhD study. Later on, I became involved in depression mechanisms research and drug discovery. This scientific journey brought me from Lanzhou in China, Leuven in Belgium, Bethesda in the USA, all the way to San Diego.

Sometimes I pick up an assortment of scattered seashells while walking along the beautiful Torrey Pines Beach in San Diego. Likewise, this book contains an assortment of discussions of different aspects of serotonin to enrich our knowledge and understanding of this neurochemical.

> **Ying Qu, PhD** Leulan Bioscience, San Diego, CA

**1**

**Figure 1.**

*AA release. This figure adapted from [23].*

**Chapter 1**

*Ying Qu*

**1. Introduction**

Introductory Chapter:

Transduction

From Measuring Serotonin

Neurotransmission to Evaluating

Serotonin or 5-hydroxytryptamine (5-HT) is a well-established monoamine neurotransmitter in the central nervous system (CNS). The discovery of 5-HT dates as far back as 1868 and can be traced to its presence in the blood and in the gastrointestinal tract [1]. Its well-known biological functions include modulating cognition, sleep, emotion, learning, memory, and numerous physiological processes. 5-HT is primarily found in the enteric nervous system located in the gastrointestinal tract [2], where it

*Model explaining PLA2 activation in response to serotonergic drugs. Under normal conditions, the 5-HT that is released from presynaptic vesicles into the synaptic cleft binds to postsynaptic 5-HT receptors coupled via a G-protein to PLA2, thus hydrolyzing arachidonic acid (AA) from membrane phospholipids (PL). Administration serotonergic drugs activate PLA and increase incorporation of AA by different routes. (1) 5-HT2A/2C agonist, DOI directly binds to 5-HT2 receptors to activate this signal; (2) fluoxetine (SSRI) inhibits 5-HT uptake, thus increasing 5-HT in the synaptic cleft so as to increase PLA activation and* 

Serotonin Post-Receptor Signaling

### **Chapter 1**
