Biomedical subjects

C Pedroarena

Publications and source records attributed to C Pedroarena.

8 recordsLinked to original sources

PubMed2000

Neurotrophin-induced rapid enhancement of membrane potential oscillations in mesencephalic trigeminal neurons.

We have proposed that neurotrophins, in addition to their trophic actions, act as neuromodulators in the adult central nervous system. As a first step to test this hypothesis, we examined in the adult rat slice preparation whether nerve growth factor and neurotrophin-3 are capable of altering the excitability of neurons of the mesencencephalic trigeminal nucleus. In contrast to vehicle pressure microapplication, which did not evoke changes in the electrophysiological properties of these neurons, neurotrophin application produced a significant increase in amplitude of the membrane potential oscillatory activity that is observed in these cells and a significant decrease in their threshold current. The latency of these effects ranged from 2 to 80 s and the duration ranged from 2 to 11 min. Neurotrophin-3 induced a decrease in input resistance and resting membrane potential in 58% of the cells; nerve growth factor induced a decrease in input resistance and resting membrane potential in 35% of the neurons. The spike configuration and action potential afterhyperpolarization potential remained unchanged following neurotrophin application. Tetrodotoxin blocked the membrane potential oscillatory activity of trigeminal mesencephalic neurons. Neurotrophin-induced effects were not blocked by the tyrosine kinase inhibitor K-252a, whereas IgG-192, an antibody directed to the neurotrophin low-affinity receptor, enhanced excitability, as did neurotrophins. These results demonstrate that neurotrophins are capable of producing a rapid increase in the excitability of trigeminal mesencephalic neurons and suggest that their effects may be mediated by low-affinity neurotrophin receptors.

Action Potentials↗

PubMed1998

The neuronal basis for consciousness.

Attempting to understand how the brain, as a whole, might be organized seems, for the first time, to be a serious topic of inquiry. One aspect of its neuronal organization that seems particularly central to global function is the rich thalamocortical interconnectivity, and most particularly the reciprocal nature of the thalamocortical neuronal loop function. Moreover, the interaction between the specific and non-specific thalamic loops suggests that rather than a gate into the brain, the thalamus represents a hub from which any site in the cortex can communicate with any other such site or sites. The goal of this paper is to explore the basic assumption that large-scale, temporal coincidence of specific and non-specific thalamic activity generates the functional states that characterize human cognition.

Animals↗

PubMed1997

Dendritic calcium conductances generate high-frequency oscillation in thalamocortical neurons.

Cortical-projecting thalamic neurons, in guinea pig brain slices, display high-frequency membrane potential oscillations (20-80 Hz), when their somata are depolarized beyond -45 mV. These oscillations, preferentially located at dendritic sites, are supported by the activation of P/Q type calcium channels, as opposed to the expected persistent sodium conductance responsible for such rhythmic behavior in other central neurons. Short hyperpolarizing pulses reset the phase and transiently increase the amplitude of these oscillations. This intrinsic thalamic electroresponsiveness may serve as a cellular-based temporal binding mechanism that sharpens the temporal coincidence of cortical-feedback synaptic inputs, known to distribute at remote dendritic sites on thalamic neurons.

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PubMed1995

Experimental analysis of the method of 'peeling' exponentials for measuring passive electrical properties of mammalian motoneurons.

Trigeminal motoneurons of the guinea pig brain stem slice preparation were studied using intracellular recording techniques. The voltage response to a 100-ms constant-current pulse was studied and a population of cells was found which did not exhibit sag or overshoot of their voltage response to a pulse of hyperpolarizing current of < 1 nA but did exhibit both phenomena when a current pulse of > 1 nA was used. The sag and overshoot observed with large-current pulses were reduced or blocked when 4 mM CsCl was added to the bathing solution. This observation supports the hypothesis that these phenomena were due to the voltage- and time-dependent activation of the Q-current. The method of peeling exponentials was then used to correct raw voltage data from cells in which the Q-current was present. The mean membrane time constant was within 1% and the mean input resistance was within 2% of the means for these parameters when measured in these same cells under conditions in which the Q-current was absent. We conclude from these experiments that the method of peeling exponentials is valid for obtaining estimates of the membrane time constant and input resistance from cells that exhibit sag and overshoot due to voltage- and time-dependent changes in the magnitude of the Q-current.

Action Potentials↗

PubMed1994

The control of jaw-opener motoneurons during active sleep.

Brainstem and spinal cord motoneurons that innervate somatic musculature serving antigravity functions are postsynaptically inhibited during active sleep. However, it has been reported that hypoglossal motoneurons (which do not innervate antigravity muscles) are not postsynaptically inhibited during active sleep, but are disfacilitated. In the present report we describe changes, during active sleep, in the excitability and membrane potential of digastric and synergistic motoneurons of the trigeminal motor pool; these neurons do not perform antigravity functions. The experiments described in the present report were performed in chronic cats that were prepared for intracellular recording. The motoneurons hyperpolarized an average of 11 mV (S.D. +/- 1.29, n = 8, P < 0.005) during active sleep compared to quiet sleep. Hyperpolarization was accompanied by a reduction in the excitability of the somadendritic regions of the neurons, as indicated by an increase in the delay of propagation of antidromic spikes from the initial segment to the somadendritic portion of the cell. High gain membrane potential recordings from these motoneurons revealed the occurrence of a remarkably large number of hyperpolarizing potentials during active sleep. When K-chloride-filled microelectrodes were utilized and chloride ions were injected intracellularly, the polarity of these potentials was reversed. During phasic episodes of active sleep, there was a clear increase in hyperpolarizing potential activity, a blockade of somadendritic spikes and phasic reductions in the amplitude of the initial segment spikes. Hyperpolarizing potentials occurred in conjunction with ponto-geniculo-occipital waves.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1991

Strychnine blockade of the non-reciprocal inhibition of trigeminal motoneurons induced by stimulation of the parvocellular reticular formation.

Stimulation of a region within the parvocellular medullary reticular formation (PcRF) that contains somas of premotor interneurons produces short latency inhibitory synaptic potentials (IPSPs) in cat trigeminal motoneurons. The present study was undertaken to determine whether glycinergic synapses are responsible for these IPSPs. The intravenous administration of strychnine, an established glycine antagonist, abolished these PcRF-IPSPs. This effect appears to be specific for glycinergic inhibitory synapses because the short lasting component of the IPSP produced by inferior alveolar nerve (IAN) stimulation was also abolished, whereas, in contrast, the long lasting non-glycinergic component of this IPSP was not suppressed. These results indicate that a glycinergic system in the reticular formation is responsible for the non-reciprocal postsynaptic inhibition of trigeminal motoneurons.

Animals↗

PubMed1991

A medullary inhibitory region for trigeminal motoneurons in the cat.

The present report describes the effects on trigeminal motoneurons of stimulation of a circumscribed site within the parvocellular region of the medullary reticular formation. This medullary site was selected because anatomical studies have shown that premotor interneurons project from this site to the trigeminal motorpool. Electrical stimulation of this site induced IPSPs (PcRF-IPSPs) in jaw-closer motoneurons. A population of these IPSPs, recorded contralateral to the site of stimulation, exhibited latencies shorter than 1.5 ms (mean 1.16 +/- 0.08 SD). Their mean amplitude was 1.72 mV +/- 1.13 SD and their mean duration was 3.52 ms +/- 2.15 SD. We believe that these PcRF-IPSPs arose as the result of activation of a monosynaptic pathway. A comparable inhibitory input from this site to ipsilateral jaw-closer motoneurons and to both contra and ipsilateral digastric motoneurons was also observed. We therefore conclude that this medullary PcRF site contains premotor interneurons that are capable of postsynaptically inhibiting motoneurons that innervate antagonistic jaw muscles.

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PubMed1990

Non-reciprocal postsynaptic inhibition of digastric motoneurons.

This study was undertaken to explore the effects, on digastric motoneurons, of electrical stimulation of a site within the parvocellular medullary reticular formation (PcRF). This site is located lateral to the hypoglossal nucleus and ventral to the dorsal motor nucleus of the vagus nerve. Within this site are somas of premotor interneurons that project to trigeminal motor nuclei. Stimulation of this site resulted in the generation of IPSPs in digastric motoneurons. We postulate that these IPSPs were due to the activation of a monosynaptic path from the PcRF to digastric motoneurons. The present results, in conjunction with those previously reported which indicate that the PcRF also induces monosynaptic IPSPs in masseter motoneurons, demonstrate that this is a site of origin for the postsynaptic inhibitory control of motoneurons that innervate both jaw opening and closing muscles.

Animals↗