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Juriquilla, Mexico

Merchant H.,Institute Neurobiologia | Yarrow K.,City University London
Current Opinion in Behavioral Sciences | Year: 2016

Several lines of evidence suggest that motoric brain structures may form the core amodal component of a neural network supporting a wide range of timed behaviours. Here, we review recent findings which elucidate the neural computations that occur within motor regions, and in particular the supplementary motor area, in order to support precisely timed actions. Although motor activity may help us represent time, it is also clear that action both enriches and complicates the interpretation of sensory inputs. Hence, in the second half of this review, we consider the latest findings regarding the perceptual distortions that our actions can impose upon our subjective perception of time. © 2016 Elsevier Ltd. Source


Cruz-Martinez R.,Institute Neurobiologia | Gratacos E.,Institute dinvestigacions Biomediques August Pi i Sunyer IDIBAPS
Ginecologia y Obstetricia de Mexico | Year: 2014

At present, the fetus is already considered a "patient" and as such, can develop diseases with fatal outcome in which the only therapeutic option can be fetal surgery. Currently, fetal surgery is limited almost exclusively to endoscopic surgery. Different techniques have gained clinical acceptance for improving the prognosis of various lethal fetal pathologies. Laser therapy for twin to twin transfusion syndrome and cord occlusion in monochorionic twins with selective intrauterine growth restriction are the procedures of choice for the management of monochorionic twins complications, and are associated with survival rates of up to 80-90% for at least one fetus. In fetuses with isolated congenital diaphragmatic hernia and severe pulmonary hypoplasia, fetal endoscopic tracheal occlusion has shown to improve the survival probabilities from 5% to 55% and from 1% to 33% in left and right congenital diaphragmatic hernia, respectively, and a decrease in the rate of pulmonary hypertension and neonatal morbidity. In selected cases with low urinary tract obstruction (megacystis) and without renal failure; fetal cystoscopy is a diagnostic method that excludes the possibility of urethral stenosis or atresia and may be used to ablate posterior urethral valves by laser, restoring urethral patency and potentially preserving respiratory and bladder function. In fetuses with pulmonary masses, either primary or due to airway obstruction, there is high risk of fetal death due to cardiac compression and contralateral pulmonary hypoplasia. In such cases fetal bronchoscopy can provide a successful therapeutic option to release airway obstruction. Source


Ortiz-Miranda S.I.,University of Massachusetts Medical School | Dayanithi G.,French Institute of Health and Medical Research | Dayanithi G.,Academy of Sciences of the Czech Republic | Velazquez-Marrero C.,University of Massachusetts Medical School | And 4 more authors.
Journal of Cellular Physiology | Year: 2010

Opioids modulate the electrical activity of magnocellular neurons (MCN) and inhibit neuropeptide release at their terminals in the neurohypophysis. We have previously shown that μ-opioid receptor (MOR) activation induces a stronger inhibition of oxytocin (OT) than vasopressin (AVP) release from isolated MCN terminals. This higher sensitivity of OT release is due, at least in part, to the selective targeting of R-type calcium channels. We now describe the underlying basis for AVP's weaker inhibition by MOR activation and provide a more complete explanation of the complicated effects on neuropeptide release. We found that N-type calcium channels in AVP terminals are differentially modulated by MOR; enhanced at lower concentrations but increasingly inhibited at higher concentrations of agonists. On the other hand, N-type calcium channels in OT terminals were always inhibited. The response pattern in co-labeled terminals was analogous to that observed in AVP-containing terminals. Changes in intracellular calcium concentration and neuropeptide release corroborated these results as they showed a similar pattern of enhancement and inhibition in AVP terminals contrasting with solely inhibitory responses in OT terminals to MOR agonists. We established that fast translocation of Ca2+ channels to the plasma membrane was not mediating current increments and thus, changes in channel kinetic properties are most likely involved. Finally, we reveal a distinct Ca-channel β-subunit expression between each type of nerve endings that could explain some of the differences in responses to MOR activation. These results help advance our understanding of the complex modulatory mechanisms utilized by MORs in regulating presynaptic neuropeptide release. © 2010 Wiley-Liss, Inc. Source


Honing H.,University of Amsterdam | Merchant H.,Institute Neurobiologia
Behavioral and Brain Sciences | Year: 2014

The gradual audiomotor evolution hypothesis is proposed as an alternative interpretation to the auditory timing mechanisms discussed in Ackermann et al.'s article. This hypothesis accommodates the fact that the performance of nonhuman primates is comparable to humans in single-interval tasks (such as interval reproduction, categorization, and interception), but shows differences in multiple-interval tasks (such as entrainment, synchronization, and continuation). Copyright © Cambridge University Press 2014. Source


Velazquez-Marrero C.M.,University of Massachusetts Medical School | Velazquez-Marrero C.M.,Institute Neurobiologia | Marrero H.G.,University of Massachusetts Medical School | Marrero H.G.,Institute Neurobiologia | Lemos J.R.,University of Massachusetts Medical School
Journal of Cellular Physiology | Year: 2010

Release of neurotransmitter is activated by the influx of calcium. Inhibition of Ca 2+ channels results in less calcium influx into the terminals and presumably a reduction in transmitter release. In the neurohypophysis (NH), Ca 2+ channel kinetics, and the associated Ca 2+ influx, is primarily controlled by membrane voltage and can be modulated, in a voltage-dependent manner, by G-protein subunits interacting with voltage-gated calcium channels (VGCCs). In this series of experiments we test whether the κ- and μ-opioid inhibition of Ca 2+ currents in NH terminals is voltage-dependent. Voltage-dependent relief of G-protein inhibition of VGCC can be achieved with either a depolarizing square pre-pulse or by action potential waveforms. Both protocols were tested in the presence and absence of opioid agonists targeting the κ- and μ-receptors in neurohypophysial terminals. The κ-opioid VGCC inhibition is relieved by such pre-pulses, suggesting that this receptor is involved in a voltage-dependent membrane delimited pathway. In contrast, μ-opioid inhibition of VGCC is not relieved by such pre-pulses, indicating a voltage-independent diffusible second-messenger signaling pathway. Furthermore, relief of κ-opioid inhibition during a physiologic action potential (AP) burst stimulation indicates the possibility of activity-dependent modulation in vivo. Differences in the facilitation of Ca 2+ channels due to specific G-protein modulation during a burst of APs may contribute to the fine-tuning of Ca 2+-dependent neuropeptide release in other CNS terminals, as well. © 2010 Wiley-Liss, Inc. Source

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