Aim: Study was to characterize by immuno-fluorescence, the expression of the serotonin reuptake transporter protein (SERT); 5-HT 1B , 5-HT 2A , and 5-HT 2B serotonin receptors; as well as type 1, and type 2 tryptophan 5-hydroxylase enzymes (TPH1 and TPH2), on the left ventricular free wall and on the interventricular septum of normal hearts of patients who died from non-cardiovascular diseases.Methods: Six different samples taken from the left ventricular free wall and the interventricular septum of six different normal hearts were analyzed by immunehistochemistry by means of specific antibodies.Results: There were found positive immune-reactive cardiomyocytes for SERT and 5-HT 1B , 5-HT 2A , and 5-HT 2B predominantly in the interventricular septum in contrast to the left ventricular free wall. Likewise, immunoreactivity for TPH1 and TPH2 was mainly positive in the interventricular septum in contrast to the left ventricular free wall.Conclusions: On these bases, the presence of SERT, 5-HT 1B , 5-HT 2A , and 5-HT 2B , and both TPH1, and TPH2, suggests the possibility that cardiomyocytes could use, synthesize, release, and reuptake 5-HT, which suggests an intrinsic serotonergic system involved in the autocrine and paracrine modulation of human heart function.

The main objective was to show the decrement of serotoninergic brain activity in depressed women, through the analyses of the slope amplitude of N1/P2 components of the auditory-evoked potentials (AEP), and the measurement of the L-tryptophan free fraction in plasma (FFT). This cross-sectional study was carried out in 60 women, 30 depressed and 30 normal controls. Both groups were measured FFT, glucose, and neutral amino acids (NAA) levels; besides performing AEP to analyses the N1/P2 slope amplitude. It was found a lengthening in the slope amplitude of N1/P2 components of AEP in the group of depressed women, and despite that the level of FFT was low, there were no changes between bound fraction and the total L-Trp. The former suggests a decrease in serotonergic brain activity in the group of depressed women. Otherwise, since the auditory cortex response to sound is regulated by serotonergic innervation, it was expected a change in the behavior of AEP in the group of depressed patients. Thus, the slope amplitude of N1/P2 components of the AEP and the measurement of FFT have proved to be a good clinical indicators of the serotonergic neurotransmission state in the brain of depressed patients, and in another clinical conditions where brain serotonin is involved.

This review aimed to describe and comment on how experimental intrauterine nutritional stress in animals produced some changes in tryptophan-5-hydroxylases (TPH) 1 and 2 in the brain and other key proteins such as plasma albumin, and how the intrauterine nutritional stress could produce long-lasting alterations in serotonin function in the brain of human infants.

Introducción: Los cardiomiocitos poseen la maquinaria bioquímica capaz de sintetizar, utilizar y recapturar serotonina. Objetivo: Determinar si la miocardiopatía hipertrófica (MCH) induce cambios en la expresión de la triptófano-5-hidroxilasa (TPH) 1 y 2, el transportador de serotonina (SERT) y los receptores serotoninérgicos (RS). Métodos: Estudio transversal de cinco bloques de tejido de corazones con MCH y cinco bloques de corazones de control. Se obtuvieron cinco cortes de la pared libre del ventrículo izquierdo (PLVI) y del septum interventricular (SIV) de cada bloque, para determinar la expresión de TPH1 y TPH2, SERT y RS con anticuerpos por inmunofluorescencia. La inmunofluorescencia fue evaluada mediante t de WELCH, con nivel de significación de p < 0.05. Resultados: La PLVI y el SIV de los corazones con MCH mostraron aumento de la expresión de TPH1 y TPH2, así como de los receptores 5-HT 2A y 5-HT 2B en comparación con los controles (p < 0.01). El receptor 5-HT 4 y SERT aumentaron en el SIV de los corazones con MCH (p < 0.01). Conclusiones: Se demostró aumento de las expresiones de TPH, SERT y RS en los cardiomiocitos de los corazones con MCH en comparación con los controles, lo cual podría participar en la fisiopatología de la MCH en los humanos.

Introduction: Diabetes mellitus (DM) inhibits brain serotonin biosynthesis through changes in tryptophan-5-hydroxylase (TPH) activity and expression. Objectives:To determine whether DM-induced changes in brain TPH1 or TPH2 expression and in the number of serotonergic neurons return to normal in diabetic rats treated with insulin. Methods: Rats with streptozotocin-induced diabetes were divided in two groups: one treated with insulin and the other without treatment. On day 14, brain stems were obtained in order to quantify L-tryptophan and 5-hydroxytryptamine levels, as well as to determine TPH activity. The expression of TPH1 and TPH2 by West ern blot, and the number of serotonergic neurons by immunohistochemistry. Results: In diabetic rats, a decrease in the levels of L-tryptophan, 5-hydroxytryptamine, and TPH activity was confirmed, as well as lower TPH1 and TPH2 expression and lower numbers of serotonergic neurons. When diabetic rats were treated with insulin, L-tryptophan returned to normal, but not 5-hy droxytryptamine, TPH expression, or the number of serotonergic neurons. Conclusions: DM chronically inhibits the synthesis of brain 5-hydroxytryptamine through changes in TPH1 and TPH2 expression and a decrease in the number of serotonergic neurons, which persist despite insulin treatment.