Publications by authors named "Alfonso Boyzo Montes de Oca"

Article Synopsis
  • Parkinson's disease affects dendritic spines in specific brain regions, impacting their shape and function, which is essential for understanding treatment options.
  • This study examined the effects of 6-OHDA lesions in male rats on behavior and dendritic spine changes, testing the combined treatment of pramipexole and rasagiline.
  • Despite the lesions leading to balance issues and decreased dendritic spine density in some neurons, the combined treatment did not improve symptoms but did modify the types of dendritic spines in certain brain areas, highlighting their potential as targets for new therapies.
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Background: Early appearance of serotonin in the fetal brain and its effects on brain morphogenesis support its neurotrophic role.

Objective: To determine the presence of serotonergic cells and the expression of tryptophan-5-hydroxylase (TPH), 5-hydroxytryptamine (5-HT), serotonin transporter (SERT), 5-HT receptor and Pet-1 during the development of the cerebral cortex, both in situ and in tissue cultures.

Material And Methods: A descriptive, observational study was carried out in pregnant Wistar rats.

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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.

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Background: The diabetic cardiomyopathy occurs in both type 1 and type 2 diabetes mellitus. Hyperglycemia and associated metabolic changes participate in the pathogenesis of this disease.

Objective: To characterizes various pathological changes occurring during the development of diabetic cardiomyopathy in rats.

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Objective: To determine concentrations of serotonin and dopamine in the hypothalamus of undernourished rats and controls during pregnancy and lactation and body composition of their offspring.

Methods: Malnourished rats along with control rats were used during pregnancy and lactation. At birth of their offspring, control mothers nursed their young and malnourished rats and the undernourished mothers nursed their offspring and control pups.

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The aim of this study was to determine whether intrauterine malnutrition (IUM) produces a change in the expression of tryptophan-5-hydroxylase (TPH) 1 and/or 2 as the primary mechanism to explain the observed chronic cerebral acceleration of the synthesis of 5-hydroxytryptamine (5-HT). We used an IUM model and controls with ages of 1, 15 and 21 days. The brainstem was obtained to determine L-tryptophan, 5-HT and TPH activity.

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The aim of this study was to determine the differences between two groups of adolescents with metabolic syndrome (MetS) and normal controls in relation to brain serotonergic activity through intensity-dependent auditory-evoked potentials (IDAEPs) and plasma free fraction of L-tryptophan. Eighteen adolescents with MetS and thirteen controls were studied. Free fraction, bound and total plasma L-tryptophan, glucose, cholesterol, triglycerides, HDL-cholesterol, albumin and IDAEPs were determined.

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The aim of this study was to determine whether intrauterine growth restriction produces an increase of dihydropteridine reductase activity as a compensatory mechanism that maintains the necessary concentration of cofactor, tetrahydrobiopterin, during accelerated brain serotonin biosynthesis. Intrauterine growth-restricted offspring and controls were used. On days 1, 10, 15 and 21 of life, the brainstem was dissected and l-tryptophan, serotonin, tryptophan-5-hydroxylase and dihydropteridine reductase activities were determined.

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Background: We undertook this study to present biochemical and morphological characterization of serotonergic cells during fetal heart development.

Methods: Wistar rats (10, 12, 16 and 20 days of gestation) were used. After obtaining the fetuses by Cesarean section, the hearts were removed and fixed for immunohistochemical assay of tryptophan-5-hydroxylase (Tph), in addition to Western blot for enzyme.

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