Acute toxicity of organic and inorganic compounds on the freshwater cyclopoid copepod Eucyclops neumani neumani (Pesta, 1927).
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Animals↗
Biomedical subjects
E Soto
Publications and source records attributed to E Soto.
Relationship between beta-amyloid degradation and the 26S proteasome in neural cells.
Beta-amyloid peptide (Abeta) plays a central role in mediating neurotoxicity and in the formation of senile plaques in Alzheimer's disease (AD). The investigation of the roles of ubiquitin (Ub) in the process underlying the association of abnormal protein with the inclusion bodies that characterize AD is of great importance for the further understanding of this disorder. We have used primary cultures of cortical neurons and astrocytes to investigate the participation of the Ub-proteasome pathway in the degradation of Abeta and the effect of Abeta(1-42) and of the fragment Abeta(25-35) upon neural cells. We have found that Abeta(25-35) and Abeta(1-42) produce a significant increase in Ub-protein conjugates and in the expression of the Ub-activating enzyme E1. On the other hand, beta peptides inhibited the proteolytic activities of the 26S proteasome. When the proteolytic activity of the 26S proteasome was inhibited with lactacystin, there was a marked decrease in Abeta(1-42) degradation, suggesting that the peptide, in both astrocytes and neurons, could be a possible substrate of this enzymatic complex. Treatment of the cultures with lactacystin prior to the exposure to Abeta produced a significant decrease in cell viability, possibly as a consequence of the inhibition of Abeta degradation leading to a persistent exposure of the cells to the amyloidogenic peptide which results in cell death. Alterations in the Ub-proteasome pathway in AD could affect the normal proteolytic removal of Abeta, leading to an abnormal accumulation of Abeta(1-42).
Acetylcysteine↗
Opioid receptors mediate a postsynaptic facilitation and a presynaptic inhibition at the afferent synapse of axolotl vestibular hair cells.
This study was designed to determine the effects of opiate drugs on the electrical activity of afferent neurons and on the ionic currents of hair cells from semicircular canals. Experiments were done on larval axolotls (Ambystoma tigrinum). The multiunit spike activity of afferent neurons was recorded in the isolated inner ear under both resting conditions and mechanical stimulation. Ionic currents were recorded using voltage clamp of hair cells isolated from the semicircular canal. In the isolated inner-ear preparation, microperfusion of either non-specific opioid receptor antagonist naloxone (10 nM to 1 mM), mu receptor agonist [D-Ala(2), N-Me-Phe(4),Gly(5)-ol]-enkephalin (1 pM to 10 microM), or kappa receptor antagonist nor-binaltorphimine (10 nM to 100 microM) elicited a dose-dependent long-lasting (>5 min) increase of the electrical discharge of afferent neurons. The mu receptor agonist funaltrexamine (1 nM to 100 microM) and the kappa receptor agonist U-50488 (1 nM to 10 microM) diminished the basal spike discharge of vestibular afferents. The delta receptor agonist D-Pen(2)-D-Pen(5)-enkephalin (1 nM to 10 mM) and the antagonist naltrindole (1 nM to 10 mM) were without a significant effect. The only drug that displayed a significant action on hair-cell ionic currents was trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl) benzeneacetamide methanesulfonate (U-50488) that reduced the Ca(2+) current in a dose-dependent fashion. On its own, mu receptor agonist [D-Ala(2), N-Me-Phe(4),Gly(5)-ol]-enkephalin (0.01 and 10 microM) significantly potentiated the response of afferent neurons to the excitatory amino acid agonist (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (0.1 microM), while synaptic transmission was blocked by the use of high-Mg(2+), low-Ca(2+) solutions. Our data indicate that the activity of vestibular afferent neurons may be regulated in a complex fashion by opioid receptors: mu opioid receptors mediating an excitatory, postsynaptic modulatory input to afferent neurons, and kappa receptors mediating an inhibitory, presynaptic input to hair cells.
Afferent Pathways↗
Induction of apoptosis in cerebellar granule cells by 2,4-dichlorophenoxyacetic acid.
2,4-Dichlorophenoxyacetic acid (2,4-D) and derivatives are herbicides widely used in Argentina and other parts of the world. Exposure to 2,4-D, its ester and salt formulations, have been associated with a range of adverse health effects in humans and different animal species, from embryotoxicity and teratogenicity to neurotoxicity. In this work, we demonstrate that after 24 hs of treatment with 1 and 2 mM 2,4-D there is an induction of apoptosis in cerebellar granule cells (CGC) in culture. However, with 2 mM 2,4-D one population of CGC developed features of apoptosis while another appeared to die by necrosis. This process is associated with an increase in caspase-3 activity after 12 hs of treatment with the herbicide, which is preceded by cytochrome c release from the mitochondria. Treatment of CGC with 2,4-D appears to induce apoptosis by a direct effect on mitochondria producing cytochrome c release and consequently activation of caspase-3, being mitochondrial damage sufficient for triggering the events that may cause apoptosis.
2,4-Dichlorophenoxyacetic Acid↗
Immunohistochemical localization and electrophysiological action of nociceptin/orphanin-FQ in the snail (Helix aspersa) neurons.
We report the existence and anatomical distribution to nociceptin/orphanin-FQ (N/O FQ)-like immunoreactivity in neurons and fibers in the perioesophageal ganglia of the snail (Helix aspersa). Intracellular recordings from perioesophageal ganglion neurons showed that the application of 10 microM N/O FQ produced an excitatory action in 22% of the neurons studied and an inhibitory action in 33% of the neurons regardless of their origin (cerebral or parietal ganglion). Our result provides evidence that N/O FQ-like peptide is located in whole perioesophageal ganglia (mainly in the cerebral one), and that it may serve as a neuromodulator of the neuronal spike discharge. These data support the idea that the N/O FQ opioid system has an early phylogenetic origin and a functional continuity during the course of evolution.
Action Potentials↗
Nitric oxide in the afferent synaptic transmission of the axolotl vestibular system.
This study was performed using intracellular and multiunit extracellular recording techniques in order to characterize the role of nitric oxide in the afferent synaptic transmission of the vestibular system of the axolotl (Ambystoma tigrinum). Bath application of nitric oxide synthase inhibitors N(G)-nitro-L-arginine (0.01microM to 10microM) and N-nitro-L-arginine methyl ester hydrochloride (0.1microM to 1000microM) elicited a dose-dependent decrease in the basal discharge of the semicircular canal afferent fibers. N(G)-Nitro-L-arginine also diminished the response to mechanical stimuli. Moreover, N(G)-nitro-L-arginine (1microM) produced a hyperpolarization associated with a decrease in the spike discharge and diminished the frequency of the excitatory postsynaptic potentials on afferent fibers recorded intracellularly. Nitric oxide donors were also tested: (i) S-nitroso-N-acetyl-DL-penicillamine (0.1microM to 100microM) increased the basal discharge and the response to mechanical stimuli. At the maximum effective concentration (100microM) this drug affected neither the amplitude nor the frequency of the excitatory postsynaptic potentials. However, it slightly depolarized the afferent neurons and decreased their input resistance. (ii) 3-Morpholino-sydnonimine hydrochloride did not significantly affect the basal discharge or the mechanically evoked peak response of afferent neurons at any of the concentrations used (1microM to 1000microM). However, after 10min of perfusion in the bath, 1microM and 10microM 3-morpholino-sydnonimine hydrochloride significantly modified the baseline of the mechanically evoked response, producing an increase in the mean spike discharge of the afferent fibers. These results indicate that nitric oxide may have a facilitatory role on the basal discharge and on the response to mechanical stimuli of the vestibular afferent fibers. Thus, nitric oxide probably participates in the sensory coding and adaptative changes of vestibular input in normal and pathological conditions.
Action Potentials↗
Betahistine produces post-synaptic inhibition of the excitability of the primary afferent neurons in the vestibular endorgans.
Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work was to study the action of betahistine in the vestibular endorgans. Experiments were done in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 microM to 10 mM; n = 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 microM. To define the site of action of betahistine, its interactions with the nitric oxide synthase inhibitor NG-nitro-L-arginine (3 microM) and with the cholinergic antagonists atropine (10 microM; n = 3) and d-tubocurarine (10 microM; n = 3) were studied. The action of betahistine when co-administered with these drugs was the same as that in control experiments, indicating that its effects did not include nitric oxide production or the activation of cholinergic receptors. In contrast, 0.01-1 mM betahistine reduced the excitatory action of kainic acid (10 microM; n = 6) and quiscualic acid (1 microM; n = 13). These results indicate that the action of betahistine on the spike discharge of afferent neurons seems to be due to a post-synaptic inhibitory action on the primary afferent neuron response to the hair cell neurotransmitter.
Ambystoma↗
Effects of betahistine and of its metabolites on vestibular sensory organs.
Betahistine is widely used in the treatment of peripheral and central vestibular disorders. Till now the anti-vertigo effect of the drug was though to be mainly due to an action of betahistine on inner ear or cerebral microcirculation or on some structures of the CNS, chiefly the vestibular nuclei. Vertigo, however is, in most cases, of peripheral origin but it remains unknown whether betahistine, or some of its metabolities, may directly affect the vestibular system at peripheral level. Pharmacokinetic studies have in fact demonstrated that betahistine is transformed, mainly at the hepatic level, in aminoethylpyridine (M1), hydroxyethylpyridine (M2) and, finally, in pyridylacetic acid (M3) which is excreted with the urine. All these substances are therefore present in the body fluids of subjects treated with betahistine, and thus might have pharmacological effects. The goal of the present study was to investigate whether betahistine or some of its metabolites could exert any effect on vestibular receptors. To this end, the effects of the drugs (10(-7)-10(-2) M) have been examined on frog semicircular canals, an animal model well suited for this purpose. The effects of betahistine and of its metabolites have been evaluated by recording ampullar receptor activity both at rest and during mechanical stimulation of the sensory organ. The results demonstrated that both betahistine and one of its metabolites, the aminoethylpyridine (M1), exert effects quite similar on ampullar receptors; both these substances in fact could reduce greatly ampullar receptor resting discharge but had scanty effects on mechanically-evoked responses. This observation might justify betahistine and possibly M1 anti-vertigo effects. In fact vertigo is normally due to uncontrolled changes in vestibular receptor resting discharge. It is therefore probable that any factor able to reduce vestibular receptor resting firing rate and, in consequence, its variations, may have, as final effect, an anti-vertigo action. The observation that betahistine and M1 have similar effects might be of some clinical interest. In fact, on the basis of our data, the hypothesis may be put forward that the anti-vertigo action of betahistine is at first achieved by betahistine itself and then sustained and prolonged in time by M1.
Animals↗
Action mechanism of betahistine in the vestibular end organs.
Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work was to study the betahistine action mechanism at the vestibular end organs. Experiments were carried out in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 microM to 10 mM, n = 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 microM. To define the site of action of betahistine, its interactions with antagonists of nitric oxide sintethizing enzyme, cholinergic drugs, and excitatory amino acids were studied. Betahistine 1 mM (n = 5) was coadministered with NG-nitro-L-arginine 3 microM. The action of betahistine remained as in control experiments. Betahistine 1 mM reduced the excitatory action of carbachol (200 microM, n = 5) in a 30 +/- 3.4%. Cholinergic antagonists atropine (10 microM, n = 3) and d-tubocurarine (10 microM, n = 3) did not modify betahistine actions. Betahistine 1 mM also reduced kainic acid (10 microM, n = 4) excitatory action in 45.5 +/- 9.8%. These results corroborate that betahistine has a peripheral inhibitory action in the spike discharge of the afferent neurons in the vestibule. This action seems to involve neither NO production nor modifications in the release of acetylcholine from the efferent fibers. The inhibitory action of betahistine seems to be due to a postsynaptic binding site on the afferent neurons.
Ambystoma↗
BgK anemone toxin inhibits outward K(+) currents in snail neurons.
We studied the effects of BgK toxin on outward K(+) currents in isolated neurons of the snail Helix aspersa, using the whole cell patch clamp technique. BgK partially and reversibly blocked K(+) currents in the 1 pM to 100 nM concentration range (n=53). The dose-response curve for BgK current inhibition had a maximum blocking effect at 100 nM. Our results indicate that BgK is a potent, apparently non-selective, K(+) channel blocker in molluscan neurons.
Animals↗
Calcium channels functional roles in the frog semicircular canal.
Different types of voltage-operated calcium channels have been described in hair cells; however, no clear functional role has been assigned to them. As a first functional characterization of vestibular calcium channels, we studied the effect of several calcium channel agonists and antagonists on whole nerve firing rate in an isolated frog semicircular canal preparation. Resting activity was affected by all dihydropyridines tested and by omegaconotoxin GVIA, whereas only nimodipine was able to reduce the mechanically evoked activity. These results indicate that nimodipine-sensitive channels play a major role in afferent transmitter release, and omega-conotoxin GVIA sensitive channels regulate the afferent firing (possibly on the postsynaptic side) but with a less important role.
Animals↗
Sensitivity of Ampelisca araucana juveniles (Crustacea: amphipoda) to organic and inorganic toxicants in tests of acute toxicity.
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Animals↗
Microcomputer program for automated action potential waveform analysis.
A program for action potential waveform analysis based on a PC compatible computer is described. Single or averaged action potentials are analyzed by obtaining its first derivative and using criteria which allow automatic measurement of several action potential components, including: depolarization rate, repolarization rate, amplitude, duration, resting membrane potential and afterhyperpolarization amplitude and slope. Data can be imported from pClamp (Axon Instruments) and exported to other software such as Excel, Sigmaplot and MatLab for example.
Action Potentials↗
[Experience with laparoscopic surgery for adnexal masses at the Regional Hospital of Temuco, Chile].
BACKGROUND: Laparoscopic surgery has clear advantages over open surgical procedures. In gynecology, laparoscopic surgery for adnexal masses in pre or post menopausal women has been used for several years. AIM: To report the experience with gynecologic laparoscopic surgery at the Temuco Regional Hospital. PATIENTS AND METHODS: Between 1996 and 1998, laparoscopic surgery was done in 96 patients aged 16 to 56 years and open surgery in 56 patients aged 15 to 74 years, with a clinical or ultrasound diagnosis of adnexal masses or ovarian dermoid cysts. RESULTS: The most frequent tumors excised were epithelial and germinal cell. Laparoscopic surgery required a mean operative time of 69.9 min and it had a 3.1% of complications. Women subjected to this type of surgery had a mean hospital stay of 3.1 days and the mean postoperative stay was 2 days. Open surgery required an operative time of 69 min and it had no postoperative complications. The mean hospital stay for women subjected to this type of procedure was 9.5 days. CONCLUSIONS: Women subjected to laparoscopic surgical procedures for adnexal masses had a shorter hospital stay than women subjected to open surgical procedures.
Adnexal Diseases↗
Assessment of sediment toxicity in San Vicente Bay, central Chile, using the amphipod Ampelisca araucana.
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Animals↗
Sensitivity of the meiofaunal copepod Tisbe longicornis to K2Cr2O7 under varying temperature regimes.
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Animals↗
Microcomputer decision support system for intensive care.
This article describes a computer system to support decisions in Intensive Medicine developed for a multipurpose Intensive Care Unit (13 beds and about 700 yearly patients). The system is used in a microcomputer (486DX4). Works done in this area are mentioned; and the different programs which integrate the system, the advantages of its use and the results accomplished are described. Some of the most important results are the quality increment of the medical care given, physicians' possibilities of dedicating more time to their patients, cost reductions, and improvements in the development of teaching and in the conditions to carry out research work in the Intensive Care Unit (ICU). An analysis is made of the system requirements that guarantee its integration to the Unit work, and the easy and safe use of it by the physicians and nurses.
Critical Care↗
A microcomputer program for automated neuronal spike detection and analysis.
A system for on-line spike detection and analysis based on an IBM PC/AT compatible computer, written in TURBO PASCAL 6.0 and using commercially available analog-to-digital hardware is described here. Spikes are detected by an adaptive threshold which varies as a function of signal mean and its variability. Since the threshold value is determined automatically by the signal-to-noise ratio analysis, the user is not actively involved in controlling its level. This program has been reliably used for the detection and analysis of the spike discharge of vestibular system afferent neurons. It generates the interval-joint distribution graph, the interval histogram, the autocorrelation function, the autocorrelation histogram, and phase-space graphs, thus, providing a complete set of graphical and statistical data for the characterization of the dynamics of neuronal spike activity. Data can be exported to other software such as Excel, Sigmaplot and MatLab, for example.
Ambystoma↗