Search PubMed⌕ Search

Biomedical subjects

A Gamundí

Publications and source records attributed to A Gamundí.

10 recordsLinked to original sources
PubMed2006

Antioxidant response and oxidative damage in brain cortex after high dose of pilocarpine.

Pilocarpine is a cholinergic agonist capable to induce seizures and an epilepticus-like state in rodents. This status epilepticus (SE) is an useful animal model to study the development and understanding of the neuropathology, behavioural and electroencephalographic alterations of human temporal lobe epilepsy. It has been suggested a relationship between SE and reactive oxygen species (ROS) that can result in seizure-induced neurodegeneration. The aim of this study was to evaluate the existence of oxidative damage and the changes in the antioxidant system in cortex after administration of a high pilocarpine dose. Rats were injected with pilocarpine (350 mg/kg i.p.) or with saline as control and 2h after the animals were sacrificed. Malondialdehyde (MDA) levels, as marker of lipid peroxidation, significantly increased (64%) after pilocarpine treatment evidencing oxidative damage. Antioxidant enzyme activities--catalase (CAT), glutathione peroxidase (GP) and superoxide dismutase (SOD)--significantly increased in response to pilocarpine (28%, 28% and 21%, respectively). GP and Mn-SOD gene expression were induced by pilocarpine treatment. Vitamin E concentration in brain cortex decreased (15%) as result of pilocarpine administration. In conclusion, the high dose of pilocarpine, used in the present study, induces oxidative damage and increases antioxidant enzyme activities and expression in brain cortex. Moreover, increased lipid peroxidation produces the consumption of Vitamin E.

Animals↗
PubMed2006

Antioxidant response analysis in the brain after pilocarpine treatments.

Cholinergic and gabaergic systems play an important role generating electroencephalographic activity and regulating vigilance states. Pilocarpine is a cholinergic agonist commonly used to induce seizures and an epilepticus-like state in rodents. A relationship between status epilepticus and reactive oxygen species has been also suggested which could result in seizure-induced neurodegeneration. The aim of this study was to evaluate the existence of oxidative damage as well as the antioxidant enzyme response in cortex and hippocampus after the administration of an intraperitoneal (350 mg/kg) and an intracerebroventricular (360 microg, 1 microl) pilocarpine injection in rats. The GABA agonist muscimol (1 mg/kg, i.p.), with described neuroprotective properties, was used as a negative control. Only systemic pilocarpine induced oxidative damage. Malondialdehyde levels, as a marker of lipid peroxidation (LP), increased in both regions (55-56%). Catalase (52-80%) and superoxide dismutase (53-60%) activities also rose in both regions but glutathione peroxidase activity only increased in cortex (45%). Glutathione reductase and caspase-3 activity did not change. In conclusion, systemic pilocarpine produced oxidative brain damage, whereas local pilocarpine brain injection had no effects. Moreover, the enzymatic determinations performed in this study are a good tool to study brain injury in pharmacological manipulations such as the ones used in short recording EEG studies.

Animals↗
PubMed2000

Why we sleep: the evolutionary pathway to the mammalian sleep.

The cause of sleep is a complex question, which needs first, a clear distinction amongst the different meanings of a causal relationship in the study of a given behavior, second, the requisites to be met by a suggested cause, and third, a precise definition of sleep to distinguish behavioral from polygraphic sleep. This review aims at clarifying the meaning of the question and at showing the phylogenetic origin of the mammalian and avian sleep. The phylogenetic appearance of sleep can be approached through a study of the evolution of the vertebrate brain. This began as an undifferentiated dorsal nerve, which was followed by the development of an anterior simplified brain and ended with the formation of the multilayered mammalian neocortex or the avian neostriate. The successive stages in the differentiation of the vertebrate brain produced, at least, two different waking types. The oldest one is the diurnal activity, bound to the light phase of the circadian cycle. Poikilotherms control the waking from the whole brainstem, where their main sensorymotor areas lie. Mammals developed the thalamocortical lines, which displaced the waking up to the cortex after acquiring homeothermy and nocturnal lifestyle. In order to avoid competence between duplicate systems, the early waking type, controlled from the brainstem, was suppressed, and by necessity was turned into inactivity, probably slow wave sleep. On the other hand, the nocturnal rest of poikilotherms most probably resulted in rapid eye movement sleep. The complex structure of the mammalian sleep should thus be considered an evolutionary remnant; the true acquisition of mammals is the cortical waking and not the sleep.

Adaptation, Physiological↗
PubMedDate not supplied

Simultaneous determination of vanillylmandelic, homovanillic and 5-hydroxyindoleacetic acids in human urine by thin layer chromatography.

A TLC method for the simultaneous analysis of vanillylmandelic, homovanillic and 5-hydroxyindole-3-acetic acids in urine is described. The sample is cleaned up through a cyano minicolumn and extracted with diethyl ether. The acids are resolved by high-performance TLC, visualized by Folin Ciocalteau reagent and quantificated by densitometry at 600 nm with beta-(4-hydroxy-3-phenyl) acetic acid as the internal standard.

Chromatography, Thin Layer↗
PubMedDate not supplied

A simple thin-layer chromatographic method for the analysis of buprenorphine in urine.

A simple and sensitive (at the ng/mL level) method for buprenorphine assay in urine is described. Buprenorphine is extracted by a C18 cartridge, derivatized with dansyl chloride, resolved by a uni-dimensional, two developing mobile phase high-performance thin layer chromatography system and quantified by fluorescence densitometry at 340 nm.

Analgesics, Opioid↗
PubMedDate not supplied

A simple method for plasma cannabinoid separation and quantification.

A sensitive (up to nanogram level) method for resolving a cannabinoid mixture in plasma is described. Cannabinoids were extracted with a C-18 Sep Pak cartridge and derivatized with dansylchloride. Then the derivatives were resolved on thin layer HPTLC silica plates which were developed and quantified by fluorescence densitometry at 340 nm.

Cannabinoids↗
PubMedDate not supplied

Thin-layer chromatographic determination of brain catecholamines and 5-hydroxytryptamine.

A simple and sensitive (up to nanogram level) method to determine norepinephrine, serotonin and dopamine in rat brain is described. The amines are acetylated and the derivatives are resolved by thin layer chromatography (TLC) on silica high performance thin layer chromatography (HPLC) plates. Quantification is achieved by fluorescence densitometry at 415 nm excitation wavelength.

Animals↗
PubMedDate not supplied

Thin-layer chromatographic determination of catecholamines, 5-hydroxytryptamine, and their metabolites in biological samples: a review.

A review of methodology for separation, detection, and quantitative determination of catecholamines, 5-hydroxytryptamine, and their acidic metabolites in biological tissue and fluids by thin-layer chromatography is presented. Selected procedures, including fluorometric scanning densitometry for catecholamine acetyl derivatives and color scanning densitometry for acids, are described.

Biogenic Amines↗
PubMedDate not supplied

[The work of Santiago Ramón y Cajal in the Revista Trimestral Micrográfica (Trabajos del Laboratorio de Investigaciones Biológicas)].

AIM: This paper is based on a study of Revista Trimestral Micrografica (Trabajos del Laboratorio de Investigaciones Biologicas) between its creation by Santiago Ramon y Cajal in 1896 and his death in 1934. DEVELOPMENT: The journal Revista Trimestral Micrografica was the main way in which Santiago Ramon y Cajal and his school published their work since its creation. Ramon y Cajal created the journal for two main reasons: first, he needed a rapid system to publish his own work; second, the journal could serve to encourage his pupils. The journal published many important reports defending the neuronal theory which expanded the cellular one to include the nervous system.

Bibliometrics↗