http://hdl.handle.net/10366/4613 2026-06-26T20:48:43Z http://hdl.handle.net/10366/171852 [ES]Introducción La imaginería motora (IM) es una herramienta ampliamente utilizada en campos como el deporte o la neurorrehabilitación ya que se ha demostrado que provoca una activación cerebral similar a la que se produce durante el movimiento. Sin embargo, la evidencia sobre su capacidad para inducir activación muscular periférica en el miembro inferior es limitada. El objetivo de este estudio fue analizar la actividad electromiográfica (EMG) durante diferentes condiciones de ejecución real e IM del miembro inferior. Materiales y métodos Participaron 17 adultos sanos, en los que se registró la actividad EMG superficial del recto y el bíceps femoral durante cuatro condiciones: ejecución real e IM guiada de un patrón motor simple (extensión de rodilla) y de un programa motor orientado a objetivo (golpeo de balón). Todos los participantes realizaron una única sesión experimental. La señal EMG se procesó de forma estandarizada y se normalizó respecto al máximo observado durante la ejecución real. Resultados La IM del patrón simple se asoció a incrementos subumbrales, pero significativos de la actividad EMG respecto al reposo, mientras que la IM del programa motor mostró mayor variabilidad interindividual y ausencia de diferencias consistentes frente al nivel basal. No se observaron correlaciones significativas entre la actividad EMG y la capacidad global de IM. Conclusión Estos resultados sugieren que la IM puede inducir activación muscular periférica de baja amplitud, especialmente en tareas motoras simples, mientras que el aumento de la complejidad funcional podría reducir la consistencia de dicha activación. 2026-01-01T00:00:00Z http://hdl.handle.net/10366/171838 [ES] Introducción: La esclerosis múltiple (EM) es una patología neurodegenerativa de carácter crónico, cuya fisiopatología se caracteriza por la presencia de procesos inflamatorios recurrentes y desmielinización a nivel del sistema nervioso central. En el abordaje terapéutico de esta enfermedad, las intervenciones de neurorehabilitación, como los métodos Vojta y Bobath, son comúnmente empleadas en la práctica clínica. No obstante, la evidencia científica disponible sobre su impacto en biomarcadores relacionados con la mielinización, así como en parámetros clínicos específicos, sigue siendo limitada, lo que pone de manifiesto la necesidad de investigaciones adicionales que permitan esclarecer su efectividad en este contexto. Objetivo: Comparar los efectos de la Terapia de Locomoción Refleja de Vojta frente al Método Bobath en sujetos con Esclerosis Múltiple, sobre la presión inspiratoria máxima (PIMax), el equilibrio, la espasticidad, el tiempo de reacción y el perfil lipidómico de ácidos grados relacionados con procesos neuroinflamatorios. Métodos: Se llevó a cabo un ensayo clínico aleatorizado con el objetivo de evaluar la eficacia comparativa de dos enfoques terapéuticos de neurorehabilitación en pacientes diagnosticados con EM. El estudio fue desarrollado en la Clínica de Fisioterapia Aymara Abreu, mientras que el análisis lipidómico se realizó en el Instituto de Neurociencias de Castilla y León (INCYL). La muestra estuvo compuesta por dos grupos: Un grupo de intervención, correspondiente al enfoque de locomoción refleja, el cual recibió sesiones individuales de fisioterapia (n = 16); y el segundo grupo “tratamiento habitual”, basado en el concepto Bobath (n = 12), que recibió un número equivalente de sesiones. Ambos grupos participaron en un programa de intervención de dos sesiones semanales durante un período de 12 meses. Las variables de resultado incluyeron: la Escala de Equilibrio de Berg, la Escala Tardieu, los tiempos de reacción (visual, auditivo y táctil) evaluados mediante el programa Cognifit, la presión inspiratoria máxima (PImax) y los biomarcadores lipídicos presentes en la lágrima. Resultados: La intervención basada en la Terapia de Locomoción Refleja de Vojta, en comparación con el enfoque terapéutico del concepto Bobath, evidenció mejoras significativas en diversos parámetros clínicos y fisiológicos. En particular, se observó un incremento en la presión inspiratoria máxima (PImax), una optimización de la estabilidad postural evaluada mediante la Escala de Equilibrio de Berg, y una disminución de la espasticidad, según los registros obtenidos a través de la Escala de Tardieu. Adicionalmente, se constató una reducción en la latencia de los tiempos de reacción visual, auditivo y táctil, medidos mediante el programa Cognifit. En el ámbito bioquímico, el análisis lipidómico de la lágrima reveló una disminución en los niveles de ácido araquidónico, lo cual podría indicar un menor proceso neuroinflamatorio. Conclusiones: La Terapia Vojta mostró una evolución funcional más consistente que el Método Bobath, observándose ligeras modificaciones en los ácidos grasos estudiados. Asimismo, se evidenciaron mejoras en parámetros fisiológicos funcionales como equilibrio, espasticidad, tiempo de reacción y PIMax. Su aplicación podría representar una estrategia terapéutica prometedora en la neurorrehabilitación. 2026-01-01T00:00:00Z http://hdl.handle.net/10366/171751 [EN]This study aims to design, build, and optimize the performance of a small-scale thermoacoustic engine (TAE) prototype hybrid (piezoelectric/thermoelectric) power generation. Independent variables are predicted using the quadratic model, which are selected based on ANOVA analysis for best fit of experimental data. A Box-Behnken Design (BBD) is applied with 20 treatments. The independent variables considered for evaluation included run time (5–15 min), hot-side heat exchanger (HX) temperature (400–600 °C), resonator length (0.402–0.604 m), cold-side HX temperature (0–27 °C) and working gas (air, N2, CO₂). The results show that the hot-side HX temperature had a significant impact on the total output power (P total), whereas the cold-side HX temperature and resonator length had a relatively mild effect on P total. The working gas type and run time also do not have a significant impact on P total. The optimal conditions for a maximum P total of 65 mW were achieved using nitrogen (N2) as the working gas, under a hot-side HX temperature of 585 °C, resonator length of 0.518 m, and cold-side HX temperature of 2.025 °C. The good fit between experimental and predicted values under optimal conditions confirms the accuracy of the model. Results demonstrate this TAE potential for industrial waste heat recovery application, despite long-term material stability at high temperatures need to be further investigated. 2026-05-01T00:00:00Z http://hdl.handle.net/10366/171673 Auditory mismatch responses—mismatch negativity (MMN) and mismatch fields (MMF)—are well established electrophys-iological markers of automatic auditory discrimination supported by short-term sensory memory. These responses, typicallyelicited using passive oddball paradigms, are increasingly used to investigate sensory and language processing in autism. Thissystematic review synthesizes findings from 55 studies comparing MMN and MMF responses in autistic and typically developing(TD) individuals across childhood, adolescence, and adulthood. Using the Synthesis Without Meta-analysis (SWiM) framework,we identified consistent evidence for smaller MMN amplitudes and reduced MMF power in autistic children and adolescentsrelative to TD peers, particularly in response to frequency, duration, and speech-based deviants. Studies also frequently reportedlonger mismatch latencies in autistic participants and associated these delays with language difficulties and heightened auditorysensitivity. Although some studies reported age-related convergence in MMN and MMF measures between autistic and TDgroups in later childhood or adolescence, greater right-hemisphere lateralization in autistic individuals emerged as a consistentfinding across both speech and non-speech paradigms, suggesting differences in hemispheric weighting for auditory process-ing of linguistic and non-linguistic cues. To explain interindividual and developmental variability in mismatch responses, wepropose a precision-weighted predictive coding account, in which divergent assignment of confidence to sensory predictionerrors may contribute to autism-related differences. While study quality was generally fair, methodological heterogeneity, un-derrepresentation of females, and limited cross-cultural sampling constrain generalizability. Future research should prioritizelongitudinal, sex-stratified, and culturally diverse designs, using standardized protocols and collaborative data practices. MMNand MMF responses hold promise as non-invasive translational biomarkers of early-stage sensory prediction and neurodevelop-mental variation in autism 2026-05-17T00:00:00Z http://hdl.handle.net/10366/171672 [EN] In autism, sensory differences have been linked to altered contextual processing and to how temporal structure supports the formation of regularities and predictions. Here, we examined how temporal and contextual auditory processing are shaped by sex, development, and prenatal valproic acid (VPA) exposure in the non-lemniscal inferior colliculus at low sound levels. Single-unit recordings from control and VPA-exposed rats were obtained using oddball and cascade paradigms, allowing dissociation of mismatch (iMM), repetition suppression (iRS), and prediction-error (iPE) components in both response magnitude and latency.In control animals, maturation selectively reorganized contextual and predictive processing in females, shifting responses toward reduced repetition suppression and increased prediction-error signaling. This shift was accompanied by longer response latencies, indicating a broader temporal integration window. Compared to male rats, adult females displayed prediction-driven, with reduced adaptation bias, of mismatch responses.In contrast, prenatal VPA exposure disrupted this sex- and age-dependent pattern, particularly in females, producing reduced response magnitude together with earlier response peaks. These findings reveal a female-specific reorganization of subcortical contextual processing and demonstrate that sex, age, and prenatal VPA exposure-related effects can dissociate response strength from temporal deployment. Collectively, our results highlight the role of temporal dynamics in contextual computation within the auditory midbrain and support the contribution of early subcortical circuits to autism-related sensory processing 2026-05-10T00:00:00Z http://hdl.handle.net/10366/171671 Brain-derived neurotrophic factor (BDNF) is a master regulator of neuronal differentiation and inhibitory circuit maturation in the mammalian brain. Yet, its downstream mediators in distinct neuronal populations remain incompletely defined. Here, we identify mitogen- and stress-activated kinase 1 (MSK1) as a critical mediator of BDNF signalling during postnatal striatal development. MSK1 expression predominates in GABAergic neurons across the cortex and striatum, with region-specific dynamics: MSK1 expression in cortical GABAergic interneurons declines from postnatal day 5 (P5) to day 30 (P30), while expression in striatal GABAergic medium spiny neurons (MSNs) persists into adulthood. Using a novel Msk1IV KO mouse model, generated by deleting exon IV of Msk1, we find that striatal volume and MSN dendritic complexity decrease by P60, without cortical neuron alterations, underscoring MSK1´s striatal-specific role. Mechanistically, MSK1 drives BDNF-induced MeCP2 phosphorylation at serine 421 in MSNs via MAPK/ERK, independently of CaMKII, forming a nuclear complex with MeCP2, thus amplifying MSK1´s role in transcriptional regulation. This MSK1-MeCP2 signalling is also involved in BDNF-dependent and independent morphological developmental processes of cultured striatal neurons. Accordingly, Msk1IV KO striatum shows dysregulated GABAergic (Gad1, Gabrg3) and dopaminergic (Drd1, Drd2, Drd3) gene expression, mirroring profiles in MeCP2 deficient models. Behaviourally, Msk1IV KO mice display hypersociability, impaired nest-building, and increased depressive-like behaviour in the forced swimming test, contributing to striatal circuit dysfunction. These findings link MSK1-mediated molecular disruptions to inhibitory circuit imbalances and behaviours reminiscent of psychiatric disorders, positioning MSK1 as a potential therapeutic target for neurodevelopmental and psychiatric disorders, including those associated with MeCP2 dysfunction. 2026-05-18T00:00:00Z http://hdl.handle.net/10366/171519 [EN]Nociception, the neural process underlying pain detection, is modulated by the NGF/TrkA signaling axis. Although anti-NGF antibodies can alleviate chronic pain, their clinical application is limited by adverse effects, underscoring the need to identify downstream regulators of this pathway. One such mechanism involves TrkA ubiquitination mediated by Nedd4 E3 ubiquitin ligases, whose activity is modulated by Nedd4 family interacting protein 2 (Ndfip2). Notably, Ndfip2 expression is regulated by TrkA signaling under pain conditions. Here, we characterize the physiological and molecular roles of Ndfip2 in sensory neurons. We demonstrate that Ndfip2 localizes to the endoplasmic reticulum and Golgi apparatus and interacts with TrkA in sensory neurons. Conditional deletion of Ndfip2 in TrkA-expressing cells selectively alters mechanical nociception. Mechanistically, loss of Ndfip2 decreases total TrkA protein levels, downstream activation, and cell-surface exposition, particularly in male-derived dorsal root ganglia neurons. Conversely, Ndfip2 expression reduces mature glycosylated TrkA and promotes the accumulation of non-glycosylated forms, consistent with impaired receptor maturation. Together, these findings identify Ndfip2 as a post-translational regulator of TrkA in TrkA-lineage sensory neurons and establish its in vivo role in mechanical nociception. 2026-03-31T00:00:00Z http://hdl.handle.net/10366/171518 [EN]Cell therapy is a promising strategy for tackling neurodegenerative diseases. The most outstanding results with this approach usually involve neuroprotection of damaged neurons at risk of death, but only with limited success. Current therapies are often based on the idea of “one gene, one disease, one drug” for single targets, a concept that limits their actual effectiveness. In contrast, combining different strategies can establish an advanced cell therapy that can slow down neuronal degeneration. In this study, we took advantage of the combination of cell and gene therapy, by transplanting bone marrow stem cells genetically modified to overexpress insulin-like growth factor 1 (IGF1) into a model of selective neurodegeneration, the PCD mouse. This animal is characterized by progressive neuronal loss in the olfactory bulb and alterations in IGF1 levels, among other symptoms. Using different techniques (cell cultures, viral transduction, cell transplants, flow cytometry, qPCR, ELISA, immunohistochemistry, advanced image analysis), our findings showed that neuronal death was virtually blocked, even 130 days after cell transplantation, a result clearly more successful than previous studies. The effects of this transplant are based in part on the regulation of neuroinflammation, increasing the proportion of reactive microglia and reducing that of proinflammatory microglia. In addition, IGF1 overexpression dramatically reduced DNA damage in mutant animals via IGF binding protein 3 pathway: this enhances neuroprotection by complementing the basal effect of cell therapy itself. In summary, our work supports the idea that combining therapeutic approaches and their synergies is a more effective tactic for combating neuronal loss. 2026-05-16T00:00:00Z http://hdl.handle.net/10366/171410 [EN] Experimental evidence indicates that a high seizure burden can induce cerebral overexpression of P-glycoprotein (P-gp) at the blood–brain barrier, a phenomenon associated with drug-resistant epilepsy under the “transporter hypothesis”, but also at the neuronal level, linked to a reduced seizure threshold, increased seizure severity (SS), status epilepticus (SE), and a high spontaneous death (SD) rate. In contrast, we recently described a progressive reduction in SS and the absence of SE and SD in GASH/Sal hamsters subjected to 45 audiogenic seizures. Here, we examined SS, SE, and the SD, and the expression of P-gp, erythropoietin receptor (EPO-R), hypoxia-inducible factor 1 alpha subunit (HIF-1α) and cyclooxygenase 2 (COX-2), in the brains of GASH/Sal hamsters following 20 audiogenic kindling stimulations (AUK-20). SS was evaluated using the midbrain and limbic severity scales; gene expression was assessed by RT-qPCR and P-gp protein levels were measured by immunohistochemistry and Western blot (IHC/WB) analysis. A modest decrease in midbrain SS was observed, without an increase in the already low limbic SS scores, and no SE or SD events occurred. P-gp levels remained low in both IHC and WB analyses. At the mRNA level, we detected increased EPO-R expression, decreased HIF-1α, and increased COX-2 without an accompanying increased in Abcb1b. Unlike findings from other experimental epilepsy models, AUK-20 in GASH/Sal hamsters does not enhance limbic SS, trigger SE or SD, or induce P-gp overexpression in the brain. Independently of the implications for drug resistance, the lack of cerebral P-gp overexpression without increased SS in the AUK-20-GASH/Sal model supports a potential role of P-gp in modulating seizure severity and epilepsy-associated mortality risk. 2026-04-09T00:00:00Z http://hdl.handle.net/10366/171359 [EN]The cytoskeleton relies heavily on the dynamic nature of microtubules, regulated by posttranslational modifications such as polyglutamylation and deglutamylation. Disruption of its internal balance, particularly through the absence of cytosolic carboxypeptidase 1 (CCP1), leads to cytoskeletal collapse and cell death. An example of this occurrence exists in the Purkinje Cell Degeneration (PCD) mouse, a direct animal model for childhood-onset neurodegeneration with cerebellar atrophy (CONDCA) human disease. Both CONDCA patients and PCD mice suffer a dramatic degeneration of Purkinje cells. Intriguingly, lobe X appears less vulnerable to this insult. This study revealed in wild-type mice that lobe X expresses less Ccp1 compared to other lobes, correlating with its delayed degeneration in PCD mice. Further expression analysis of other deglutamylating enzymes (CCP4 and CCP6) and glutamylating enzymes (TTLL1) revealed distinctive patterns: Ccp4 showed minimal relevance in cerebellum, while Ccp6 displayed a compensatory increase during critical stages. Meanwhile, Ttll1 expression remained consistent across lobes, suggesting that the resistance of lobe X may be related to a more dynamic, hyperglutamylated cytoskeleton. Unraveling the neuroresistance mechanisms of Purkinje cells may help mitigate neuronal loss in CONDCA patients and may offer a glimmer of hope for alleviating the symptoms of other neurodegenerative diseases. 2025-01-01T00:00:00Z http://hdl.handle.net/10366/171255 [ES]La tesis titulada “Sex, age, and etiology effects on auditory processing in two rat models of autism: evidence from auditory brainstem responses and contextual neural and behavioral measures” investiga cómo el procesamiento auditivo varía en función del sexo biológico, la etapa del desarrollo y la etiología en modelos animales de autismo. Partiendo del marco teórico de la codificación predictiva, el trabajo analiza cómo el sistema auditivo extrae regularidades del entorno y detecta desviaciones, integrando niveles de análisis que abarcan desde el tronco encefálico hasta el comportamiento. Para ello, se emplean dos modelos de autismo en rata: uno ambiental, basado en la exposición prenatal al ácido valproico (VPA), y otro genético, mediante deleción heterocigota del gen Grin2b. Además, se incluye un modelo farmacológico basado en la administración del antagonista NMDA MK-801 para estudiar el uso conductual de regularidades auditivas. Metodológicamente, la tesis combina tres aproximaciones complementarias: (1) registros de respuestas auditivas del tronco encefálico (ABRs) para evaluar la sincronía y el tiempo de conducción subcortical; (2) registros de actividad neuronal de unidad única en el colículo inferior para caracterizar el procesamiento contextual auditivo mediante índices de mismatch (iMM), supresión por repetición (iRS) y error de predicción (iPE); y (3) tareas conductuales tipo oddball para evaluar el uso de regularidades auditivas en la toma de decisiones. Los resultados muestran que el procesamiento auditivo no se altera de manera uniforme, sino que depende de la interacción entre sexo, edad y etiología. Se observan diferencias específicas en la latencia y amplitud de las ABRs, así como en los mecanismos neuronales de procesamiento contextual en el colículo inferior, especialmente en regiones no lemniscales. Asimismo, las manipulaciones farmacológicas revelan alteraciones en la capacidad de utilizar regularidades auditivas para guiar la conducta. En conjunto, la tesis demuestra que la variabilidad auditiva en el autismo refleja interacciones estructuradas entre factores biológicos y del desarrollo, y no una alteración única. Estos hallazgos aportan un marco integrador que conecta mecanismos neurofisiológicos con procesos conductuales, contribuyendo a una comprensión multiescala del procesamiento auditivo en el autismo. 2026-01-01T00:00:00Z http://hdl.handle.net/10366/171017 [EN] This study assesses the performance of no-fee GNSS augmentation systems for tractor guidance. Five no-fee augmentation systems: EGNOS, GLIDE, RTK, VRS-NRTK, and on-site RTK were evaluated in both static and guidance tests over short- and long‑term periods using three GNSS receiver types: low-cost Navilock NL8022MP, mid-range Novatel Smart2, and high-end Harxon TS108PRO. Static tests recorded 24 h of position data from 14 receiver-augmentation configurations on a fixed surface. Guidance tests recorded trajectory data from the 14 configurations during straight-line guidance using a tractor equipped with two GNSS receivers, one under test and one high-precision reference. Results found that: (i) unaugmented GNSS resulted in guidance errors of 2–3 m, reduced below 1 m in pass-to-pass intervals shorter than 15 min; (ii) EGNOS reduced these guidance errors by ∼41%; (iii) GLIDE reduced guidance errors to below 20 cm for pass-to-pass intervals shorter than 15 min, with no long-term improvement; (iv) RTK guidance error decreased as baseline length shortened: >100 km yielded > 17 cm, 20–100 km yielded 3–20 cm, and < 20 km yielded 2–3 cm; (v) VRS-NRTK slightly outperformed RTK with similar baseline lengths; and (vi) on-site RTK enabled 1 cm guidance error. In summary: low-cost receivers without augmentation or with EGNOS result in metre-level errors; mid-range receivers with GLIDE deliver decimetre-level guidance errors in the short term; and high-end receivers using on-site RTK or VRS-NRTK on baselines up to 100 km achieve centimetre-level errors, enabling farmers to replicate tractor trajectories consistently year to year. 2026-03-24T00:00:00Z http://hdl.handle.net/10366/170947 [EN]Age-related hearing loss (ARHL) disrupts ascending auditory inputs, impairing auditory signal transmission, triggering cortical hyperexcitability, and increasing the risk of age-related cognitive decline. In early aging, multisession epidural direct current stimulation (DCS) of the auditory cortex (AC) preserves auditory thresholds and prevents cortical hyperexcitability in Wistar rats. Here, we hypothesized that multisession DCS could halt transcriptional dysregulation in the AC at the earliest stages of aging. We have characterized age-related transcriptional changes in the AC to assess DCS-mediated effects by RNA-seq. At 18.13 months, non-stimulated, aged rats (NES) showed 194 differentially expressed genes (DEGs) in relation to young controls (YG), with enrichment in pathways associated with GABAergic, glutamatergic, and dopaminergic synapses, long-term potentiation/depression, inflammaging, autophagy, apoptosis and neurodegeneration. The upregulated genes included Gabrb1, Grin2b, Rac3c, Tnr, and Ndst1, suggesting compensatory hyperactivity, excitatory/inhibitory imbalance, and stiffening of perineuronal nets (PNN) around parvalbumin (PV) interneurons. Electrically stimulated (ES) rats showed 86 DEGs in relation to YG, with no significant enrichment in aging-related pathways. By contrast, NES vs ES showed 1393 DEGs, with strong enrichment in aging-related pathways. Also, many of the 121 common DEGs across comparisons, which are upregulated in NES and downregulated in ES, are related to neurotransmission (Gabrb1, Grin2b), synaptic scaffolding (Dlg2, Prkca), trophic signaling (Ntrk2, Igf1r) and PNN (Tnr, Ndst1). Based on these findings, multisession DCS curbs maladaptive genomic reprogramming in the aged AC most likely by preserving excitatory/inhibitory balance and maintaining PNN integrity, thereby protecting the AC from ARHL and cognitive vulnerability. 2026-02-19T00:00:00Z http://hdl.handle.net/10366/170888 [EN] Atypical sensory processing is a common feature of autism, yet the neural computations that give rise to these differences, particularly in relation to biological sex and etiological origin, remain unclear. Here we examine predictive auditory processing at the single-neuron level in the inferior colliculus of two adult rat models of autism: a genetic model with a heterozygous Grin2b deletion (Grin2b + /-) and an environmental model based on prenatal valproic acid exposure. We recorded neuronal responses to an auditory oddball paradigm and a cascade control sequence across lemniscal and non-lemniscal IC divisions under high-intensity stimulation, allowing us to derive indices of repetition suppression, prediction error and neuronal mismatch. Using generalized linear mixed-effects models that accounted for animal identity, inferior colliculus division, sex, and rat model, followed by hierarchical group-level comparisons, we identified robust alterations in predictive processing in both autism-like models. These effects varied across inferior colliculus divisions and differed between sexes, revealing distinct phenotype-specific signatures. The results indicate that sex and etiology jointly modulate early auditory computations in autism. More broadly, our findings highlight the translational value of predictive coding frameworks and support the use of complementary animal models to capture neurobiological heterogeneity across the autism spectrum 2026-01-30T00:00:00Z http://hdl.handle.net/10366/170643 [EN]This paper delves into the prosodic features of speech affected in AD and MD, the type of pathology they are associated with (aphasia, apraxia or aprosodia), as well as the contribution of these alterations to the neurolinguistic field (hemispheric specialization).We used a corpus of spontaneous speech from patients with AD (n=10) and MD (n=10), and a control group with HS (n=10). The results showed a discriminatory significance of VnPVI (in MD), and (Δ)f0 and %V; furthermore, %V is a strong variable to distinguish between speakers with and without pathology, as well as to discriminate between AD and MD along with other variables. There is, however, no correlation with verbal fluency (semantic and phonological) or with MMSE, which would imply a motor type deficit: apraxic type in AD and aprosodic type in MD. These results show certain phonological and typological conditioning, among other issues. 2025-01-01T00:00:00Z http://hdl.handle.net/10366/170624 [EN] Under the predictive coding framework, perception is understood as an inferential process in which the brain continuously generates predictions about incoming sensory input and updates its internal models when reality deviates from expectation. Auditory deviance detection provides a tractable paradigm to investigate how the brain encodes prediction errors. While these computations are well characterized within the auditory hierarchy, their extension to memory-related and cross-modal structures remains unclear. This thesis examines auditory predictive processing beyond the auditory pathway, focusing on the hippocampus and the primary visual cortex (V1) as potential nodes in a distributed predictive network. Using extracellular recordings in urethane-anesthetized rats, I measured single- and multi-unit activity and local field potentials (LFPs) from hippocampal subfields (dentate gyrus [DG], cornu ammonis 1 [CA1]) and infragranular layers (IV–VI) of V1. Classical oddball paradigms and no-repetition control sequences were employed to dissociate repetition suppression from genuine prediction error components. Approximately one-fifth of hippocampal neurons responded to auditory stimulation, with a subset (~20%) showing enhanced activity to deviant tones. DG neurons displayed shorter latencies and larger mismatch and prediction error indices than CA1, suggesting a distinct contribution to novelty-related processing. Spiking responses reflected prediction error, while LFPs showed distinct contributions from repetition suppression and prediction error that varied across subfields. Early LFP components were enhanced for randomly presented deviants, whereas later components were more pronounced for predictable deviants. In V1, more than half of infragranular neurons responded to tones despite the absence of visual input, 50% showing larger responses to deviant than standard stimuli. These responses predominantly reflected prediction error rather than adaptation and were amplified under temporally uncertain (random) conditions. Layer V neurons exhibited rapid, phasic responses, whereas layer VI responses were broader and more sustained, consistent with laminar specialization in hierarchical predictive coding. Together, these results demonstrate that auditory prediction errors are encoded in both hippocampal and visual circuits, extending predictive processing beyond classical sensory boundaries, positioning both regions as integral components of a distributed predictive coding architecture that underlies hierarchical inference across the brain. 2026-01-01T00:00:00Z