PubMed Health⌕ Search

Biomedical subjects

E S Rocha

Publications and source records attributed to E S Rocha.

8 recordsLinked to original sources
PubMed2001

[Common orthopedic problems in adolescents]

OBJECTIVE: Orthopedic problems in children and adolescents are quite frequent. For that reason, our aim was to give a remarkable insight into five selected topics: spinal deformities, osteochondritis, growing pains, back pain, and corrective shoes. METHODS: We analyzed general concepts of spinal deformities, including the general definition of scoliosis and its etiologic classification. We also discussed the definition, etiology, diagnosis, and treatment of osteochondritis, growing pains, back pain, and corrective shoes. The data were obtained from review articles, textbooks, and from the Internet. RESULTS: We describe the epidemiology, diagnosis, and treatment of the selected conditions through review of literature and the authorś own experience. CONCLUSIONS: Comments and relevant aspects concerning general pediatric practice are discussed.

Journal Article↗
PubMed1999

Low concentrations of the organophosphate VX affect spontaneous and evoked transmitter release from hippocampal neurons: toxicological relevance of cholinesterase-independent actions.

In the present study, the patch-clamp technique was applied to cultured hippocampal neurons to evaluate the effects of the nerve agent VX on evoked and spontaneous postsynaptic currents mediated by gamma-aminobutyric acid (GABA) and glutamate. At 0.01 nM, VX reduced the amplitude of evoked GABAergic currents, and only at concentrations >1 nM did it decrease the amplitude of evoked glutamatergic currents. The effect of VX on GABAergic currents, which was partially reversible upon washing of the neurons with VX-free external solution, could be prevented by the muscarinic antagonist atropine. In contrast, the effect of VX on glutamatergic currents, which was not reversible upon washing, appears to be related to the VX-induced reduction of the amplitude and frequency of repetitively firing by action potentials. In the presence of the Na(+)-channel blocker tetrodotoxin (TTX), VX (>/=10 nM) increased the frequency of GABA- and glutamate-mediated miniature postsynaptic currents (MPSCs). This effect of VX was unrelated to cholinesterase inhibition and was Ca(2+) dependent. The lack of effect of VX on MPSC kinetics indicates that VX-induced alterations of evoked and spontaneous currents are exclusively due to alterations of the transmitter release processes. The ability of VX to affect transmitter release in the brain may underlie some of its neurotoxic effects and may provide the basis for the development of therapeutic countermeasures to treat and/or prevent VX-induced neurotoxicity.

Animals↗
PubMed1998

An analysis of low level doses of cholinesterase inhibitors in cultured neurons and hippocampal slices of rats.

Recent data indicate that the neurotoxic effects of organophosphate compounds, including those of the nerve agents VX and sarin, are not solely due to irreversible cholinesterase inhibition. In this study we applied the patch clamp technique to hippocampal neurons in culture and slices to investigate the effects of VX, sarin and huperzine A on transmitter release and the mechanisms related with such effects. The nerve agents VX and sarin at very low concentrations significantly reduced the evoked release of GABA and glutamate. This effect was dependent of the activation of muscarinic receptors. In the presence or absence of the Na(+)-channel blocker tetrodotoxin (TTX), VX increased the frequency of spontaneous glutamate and GABA-induced postsynaptic currents. The effect of VX on TTX-insensitive spontaneous currents appears to be unrelated to cholinesterase inhibition, because it could be detected even after cholinesterase was blocked by high concentrations of the nerve agent soman. The ability of the nerve gases to decrease evoked release of GABA and increase spontaneous transmitter release may underlie some of the neurotoxic effects of the compounds. Huperzine A did not affect spontaneous or evoked release of GABA and glutamate, suggesting that this compound may be a pure cholinesterase inhibitor and had no effect on postsynaptic GABAA or AMPA receptors.

Alkaloids↗
PubMed1997

Methamidophos: an anticholinesterase without significant effects on postsynaptic receptors or transmitter release.

Methamidophos (O,S-dimethyl phosphoroamidothiolate, Tamaron), an organophosphate (OP) anticholinesterase of limited toxicity, is widely used as an insecticide and acaricide. To provide additional insight into the molecular basis of its action, we have used electrophysiological and biochemical techniques to study the effects of methamidophos on the neuromuscular junction of rat and frog and on the central nervous system of rat. Methamidophos has a relatively weak inhibitory action on cholinesterases in rat diaphragm muscle, brain and hippocampal homogenates, with IC50 values on the order of 20-20 microM. An even weaker anticholinesterase activity was found in frog muscle homogenates, with the IC50 being above 300 microM. As further evidence of anticholinesterase activity, methamidophos (1-100 microM) was able to reverse the blockade by d-tubocurarine (0.5-0.7 microM) of neuromuscular transmission in rat phrenic nerve-hemidiaphragm preparations. Inhibition of cholinesterase activity by methamidophos was long lasting, which is consistent with the formation by the agent of a covalent bond with the enzyme's active serine residue. The action was also slowly reversible, which suggests spontaneous reactivation of the enzyme. electrophysiological studies at the rat neuromuscular junction showed that, due to its anticholinesterase activity, methamidophos increased the amplitude and prolonged the decay phase of nerve-evoked and spontaneous miniature end-plate potentials. In contrast to other OP compounds, e.g., paraoxon (Rocha et al., 1996a), methamidophos did not affect neurotransmitter release, nor did it interact directly with the muscle nicotinic acetylcholine receptor. Moreover, it contrast to paraoxon, methamidophos did not affect the whole-cell currents induced by application of acetylcholine, glutamate or gamma-aminobutyric acid recorded to cultured hippocampal neurons. Based on these data, methamidophos appears to have a selective effect on cholinesterase.

Animals↗
PubMed1996

Paraoxon: cholinesterase-independent stimulation of transmitter release and selective block of ligand-gated ion channels in cultured hippocampal neurons.

Paraoxon (O,O-diethyl O-p-nitrophenyl phosphate) is the neurotoxic metabolite of the insecticide parathion (O,O-diethyl O-p-nitrophenyl phosphorothioate). The effects of organophosphorus compounds on peripheral synapses have been attributed to inhibition of cholinesterase and to direct actions on muscarinic and nicotinic receptors, but less is known about the actions of organophosphorus compounds, including paraoxon, in the central nervous system. We investigated initially the effects of paraoxon on spontaneous transmitter release by recording miniature postsynaptic currents (MPSCs) from cultured rat hippocampal neurons using the whole-cell mode of the patch-clamp technique. Paraoxon (0.3 microM) in the presence of tetrodotoxin (0.3 microM) and atropine (1 microM) caused a significant increase in the frequency of gamma-aminobutyric acid- and glutamate-mediated MPSCs, but did not change the peak amplitudes or decay-time constants of these MPSCs. In contrast, application of nicotinic agonists or antagonists did not change the MPSC frequency. The presynaptic effect of paraoxon shown here was not mediated by actions on muscarinic or nicotinic receptors, or by elevated acetylcholine levels secondary to inhibition of cholinesterase. In addition, agonists were applied to assess the postsynaptic effects of paraoxon on excitatory and inhibitory amino acid receptors. Paraoxon (30 microM-1 mM) blocked the ion channels of glycine, gamma-aminobutyric acidA, N-methyl-D-aspartic acid and nicotinic acetylcholine receptors, but not the ion channels of kalnate- and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors. The combined effects of paraoxon on spontaneous transmitter release and on the functions of several ligand-gated receptors may constitute mechanisms relevant to the neurotoxicity of paraoxon.

Animals↗
PubMed1996

Diversity of nicotinic acetylcholine receptors in rat brain. V. alpha-Bungarotoxin-sensitive nicotinic receptors in olfactory bulb neurons and presynaptic modulation of glutamate release.

The presence of functional nicotinic acetylcholine receptors (nAChRs) on cultured neurons of the rat olfactory bulb was evaluated using the whole-cell patch-clamp technique. Application of acetylcholine (ACh) to 78% of the tested olfactory bulb neurons evoked whole-cell currents (referred to as direct response), which are very similar in characteristics to type IA currents. Their peak amplitude increased, while their rise-time and decay-time constants decreased with increasing agonist concentration. In 12% of the neurons, ACh evoked single or multiple miniature postsynaptic currents (referred to as indirect response) for which amplitude, rise time, and decay-time constants were not dependent upon the ACh concentration. Methyllycaconitine (1 nM), a selective competitive antagonist at the alpha-bungarotoxin-sensitive neuronal nAChR, reversibly blocked both responses, whereas 6-cyano-7-nitroquinoxaline-2,3-di-one (10 microM) reversibly blocked only the indirect responses. Whereas tetrodotoxin (0.2-2 microM) failed to affect the indirect response, Ca(+2)-free, Mg(+2)-containing external solution decreased reversibly and significantly the frequency of ACh-evoked miniature postsynaptic currents. The pharmacology and kinetics of the two types of responses are consistent with the existence in the olfactory bulb neurons of alpha-bungarotoxin-sensitive nAChRs at both postsynaptic and presynaptic sites, the presynaptic receptors being located on glutamatergic synapses where they modulate the release of the transmitter. The dimensions of the soma and dendrites of the neurons suggest that the direct response is obtained from periglomerular and/or granular neurons, and the indirect response from short-axon and/or external tufted cells. The present results suggest that 1) nicotinic synaptic transmission could play an important role in modulating the bulbar output at the glomerular level, and 2) a presynaptic modulatory effect is one of the functions for the alpha-bungarotoxin-sensitive nAChRs in the mammalian central nervous system.

Acetylcholine↗
PubMed1989

Aortic input impedance during hypovolemic shock and after hyperosmotic solution infusion.

Aortic input impedance (Zin) was determined in 7 chloralose-urethane-anesthetized dogs. Flow and pressure were recorded in the ascending aorta during random cardiac pacing. These signals were processed on a spectrum analyzer utilizing the Fast Fourier Transform. Measurements were made 1) under control conditions; 2) every 5 min throughout 1 hr of hypovolemic shock; 3) every 5 min for 30 min after ending infusion of hyperosmotic solution (7.5% NaCl, 4.5 ml/kg body weight). We conclude that the determination of characteristic impedance (Zc) (average value of Zin from 4 to 10 Hz) can be useful for determining the initial phase of vascular decompensation in hypovolemic shock. After hyperosmotic solution infusion we observed a reduction in peripheral resistance, Zin, Zc, frequency of minimal Zin and frequency of phase crossover. These data strongly suggest a decrease in arterial vascular tonus.

Animals↗