Javier Yajeya

ORCID: 0000-0003-1617-4227
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Alzheimer's disease research and treatments
  • Neurogenesis and neuroplasticity mechanisms
  • Migraine and Headache Studies
  • Sleep and Wakefulness Research
  • Nicotinic Acetylcholine Receptors Study
  • Tryptophan and brain disorders
  • Receptor Mechanisms and Signaling
  • Nerve injury and regeneration
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuropeptides and Animal Physiology
  • Neuroscience and Neural Engineering
  • Neural and Behavioral Psychology Studies
  • Ion channel regulation and function
  • Pain Mechanisms and Treatments
  • Visual perception and processing mechanisms
  • Neuroscience of respiration and sleep
  • Medicinal Plants and Neuroprotection
  • 14-3-3 protein interactions
  • Neural dynamics and brain function
  • Drug Transport and Resistance Mechanisms
  • Sympathectomy and Hyperhidrosis Treatments
  • Spatial Neglect and Hemispheric Dysfunction
  • Neuroendocrine regulation and behavior

Universidad de Salamanca
2009-2020

Instituto de Estudios de Ciencias de la Salud de Castilla y León
2000-2020

Instituto de Neurociencias de Castilla y León
1999-2020

University of Central Florida
2010

University of California, Los Angeles
1988-1989

Significance Disruption of neuronal dendrites causes cognitive impairment in Alzheimer’s disease (AD). Rock2, a kinase the Rho family proteins, is dendrite destabilizer that accumulates AD brain. However, why Rock2 aberrantly aggregates, causing integrity loss, unknown. Here, we show protein stability controlled by ubiquitin ligase APC/C Cdh1 . Accordingly, loss function adult neurons increases and activity, disruption cortex hippocampus, along with memory neurodegeneration, mice. These...

10.1073/pnas.1616024114 article EN Proceedings of the National Academy of Sciences 2017-04-10

During early stages of Alzheimer's disease (AD), synaptic dysfunction induced by toxic amyloid-β (Aβ) is present before the accumulation histopathological hallmarks disease. This scenario produces impaired functioning neuronal networks, altered patterns synchronous activity and severe functional deficits mainly due to hyperexcitability hippocampal networks. The molecular mechanisms underlying these alterations remain unclear but evidence, shown our laboratory others, points involvement...

10.1371/journal.pone.0134385 article EN cc-by PLoS ONE 2015-07-28

Patellar tendinopathy has a high prevalence rate among athletes. Different therapeutic options can be found in the current literature, but none of them been clearly established as gold standard. The purpose this study is to compare, randomized controlled trial, clinical efficacy eccentric exercise combined with either an ultrasound-guided galvanic electrolysis technique (USGET) or conventional electrophysiotherapy treat patellar tendinopathy.Sixty patients diagnosed were into two groups....

10.1186/s40634-016-0070-4 article EN cc-by Journal of Experimental Orthopaedics 2016-11-16

Hippocampal synaptic plasticity disruption by amyloid-β (Aβ) peptides + thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures neuronal excitability maintenance seems an underlying mechanism. G-protein-gated inwardly rectifying potassium (GirK) channels control neural hyperpolarization response many G-protein-coupled receptors activation. Here, vitro vivo amyloidosis mouse models, we study whether GirK take part of the hippocampal...

10.1111/jnc.14946 article EN cc-by Journal of Neurochemistry 2019-12-26

The hippocampus plays a critical role in learning and memory. Its correct performance relies on excitatory/inhibitory synaptic transmission balance. In early stages of Alzheimer's disease (AD), neuronal hyperexcitability leads to network dysfunction observed cortical regions such as the hippocampus. G-protein-gated potassium (GirK) channels induce neurons hyperpolarize, contribute resting membrane potential could compensate any excesses excitation. Here, we have studied relationship between...

10.1038/s41598-017-15306-8 article EN cc-by Scientific Reports 2017-11-01

Last evidences suggest that, in Alzheimer's disease (AD) early stage, Amyloid-β (Aβ) peptide induces an imbalance between excitatory and inhibitory neurotransmission systems resulting the functional impairment of neural networks. Such alterations are particularly important septohippocampal system where learning memory processes take place depending on accurate oscillatory activity tuned at fimbria-CA3 synapse. Here, acute effects Aβ CA3 pyramidal neurons their synaptic activation from septal...

10.3389/fncel.2013.00117 article EN cc-by Frontiers in Cellular Neuroscience 2013-01-01

An exciting topic regarding integrative properties of the nervous system is how transient motor commands or brief sensory stimuli are able to evoke persistent neuronal changes, mainly as a sustained, tonic action potential firing. A persisting firing seems be necessary for postural maintenance after previous movement. We have studied in vitro and vivo generation activity responsible eye fixation spontaneous movements. Rat sagittal brainstem slices were used intracellular recording prepositus...

10.1523/jneurosci.0235-04.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-06-02

The central terminals of the primary sensory trigeminal ganglion (TG) neurons projecting into caudal nucleus (CTN) rat exhibit neurokinin A (NKA)-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)-immunoreactivities (IRs). We stimulated TG in to induce some alterations which might occur during migraine (neurogenic inflammation). Under a stereotaxic apparatus by means bipolar electrode, one-side animals were electrically (7.5 Hz, 5 ms, 0.8-1. 4 mA) with square pulses for min....

10.1016/s0304-3959(99)00240-7 article EN Pain 2000-02-01

Intracellular recordings in slice preparations of the basolateral amygdala were used to test which excitatory amino acid receptors mediate postsynaptic potentials due stimulation external capsule. These also examine action muscarinic agonists on evoked potentials. from amygdaloid pyramidal neurons revealed that carbachol (2-20 microM) suppressed, a dose-dependent manner, responses by capsule (EC). This effect was blocked atropine. The estimated effective concentration produce half-maximal...

10.1002/1098-2396(200011)38:2<151::aid-syn6>3.0.co;2-k article EN Synapse 2000-01-01

We previously demonstrated that the administration of GH immediately after severe motor cortex injury, in rats, followed by rehabilitation, improved functionality affected limb and reexpressed nestin contralateral cortex. Here, we analyze whether these effects depend on a time window injury reexpression actin. Injured animals were treated with (0.15 mg/kg/day) or vehicle, at days 7, 14, 35 cortical ablation. Rehabilitation was applied short long term (LTR) lesion then sacrificed. Nestin...

10.1155/2018/6125901 article EN cc-by Neural Plasticity 2018-01-01

To maintain horizontal eye position on a visual target after saccade, extraocular motoneurons need persistent (tonic) neural activity, called “eye-position signal,” generated by prepositus hypoglossi (PH) neurons. We have shown previously in vitro and vivo that this activity depends, among others mechanisms, the interplay of glutamatergic transmission cholinergic synaptically triggered depolarization. Here, we used rat sagittal brainstem slices, including PH nucleus paramedian pontine...

10.1523/jneurosci.2061-05.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-10-26

Abstract The medial septum/diagonal band region, which participates in learning and memory processes via its cholinergic GABAergic projection to the hippocampus, is one of structures affected by beta amyloid (βA) deposition Alzheimer's disease (AD). acute effects βA (25–35 1–40) on action potential generation glutamatergic synaptic transmission slices septal area rat brain were studied using current patch‐clamp techniques. mechanism through M1 muscarinic receptors voltage‐dependent calcium...

10.1002/jnr.21150 article EN Journal of Neuroscience Research 2006-12-14
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