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Romer et al. (2009) concluded from a study of primary culture of mouse hepatocytes that a serotonin 2A receptor-mediated mechanism is involved in hepatocyte proliferation after partial hepatectomy, and that the effects of various serotonergic drugs (serotonin agonists, antagonists, and receptor subtype‐specific antagonists) may reflect a primary effect on serotonin receptor populations within the hepatocyte. These findings indicate that post‐hepatectomy liver regeneration occurs via a central mechanism, and that it is unclear whether serotonin plays a role as the transmitter in the central component of this process.
Serotonin (5-HT; 5-HT1A and 5-HT2C receptors) stimulation of the 5-HT2C receptor inhibits hepatic glucose production in a time‐ and dose‐dependent manner, and reports show that the pharmacological blockade of the 5-HT2 receptor subtype can activate NST and cause major hepatic glycogen depletion (Park et al., 2000). Besides 5-HT2C receptors, which are widely distributed on serotonergic neurons, 5-HT1A autoreceptors have been localized on serotonergic raphe neurons and in pituitary, hypothalamus, and CNS (Van Belle et al., 1992; Biber et al., 1995), which implies that 5-HT1A autoreceptors have an important role in serotonergic neurotransmission. The 5-HT1A receptor mRNA was found in the rat liver. Thus, previous findings obtained by directly applying 5-HT2C or 5-HT1A receptor agonists and antagonists in the liver may be at least partially mediated by the autoreceptors located in the raphe‐parahypothalamic region. The 5-HT1A receptor antagonist NAN-190 has been found to reversibly inhibit hepatic glucose output in temporal correlation with the amount of receptor binding (Petersen et al., 1994). Peters et al. (2000) reported that the 5-HT2C receptor agonist Ro60-0175 does not activate 5-HT1A autoreceptors in the rat liver. Thus, a liver glycogenolytic effect may be 5-HT2C receptor mediated. Pharmacological studies conducted in particular ligands and range of concentrations should determine whether a dose or inhibitor can inhibit the action of 5-HT on target molecules. d2c66b5586
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