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Aging is a major risk factor to develop neurodegenerative diseases and is associated with decreased buffering capacity of the proteostasis network. We investigated the significance of the unfolded protein response (UPR), a major signaling pathway activated to cope with endoplasmic reticulum (ER) stress, in the functional deterioration of the mammalian brain during aging. We report that genetic disruption of the ER stress sensor IRE1 accelerated age-related cognitive decline. In mouse models, overexpressing an active form of the UPR transcription factor XBP1 restored synaptic and cognitive function, in addition to reducing cell senescence. Proteomic profiling of hippocampal tissue showed that XBP1 expression significantly restore changes associated with aging, including factors involved in synaptic function and pathways linked to neurodegenerative diseases. The genes modified by XBP1 in the aged hippocampus where also altered. Collectively, our results demonstrate that strategies to manipulate the UPR in mammals may help sustain healthy brain aging.
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Envelhecimento , Encéfalo , Proteínas Serina-Treonina Quinases , Resposta a Proteínas não Dobradas , Proteína 1 de Ligação a X-Box , Animais , Camundongos , Envelhecimento/genética , Encéfalo/metabolismo , Estresse do Retículo Endoplasmático/genética , Proteínas Serina-Treonina Quinases/genética , Proteômica , Transdução de Sinais/fisiologia , Proteína 1 de Ligação a X-Box/genética , Proteína 1 de Ligação a X-Box/metabolismoRESUMO
Alzheimer's disease (AD) is one of the most significant health challenges of our time, affecting a growing number of the elderly population. In recent years, the retina has received increased attention as a candidate for AD biomarkers since it appears to manifest the pathological signatures of the disease. Therefore, its electrical activity may hint at AD-related physiological changes. However, it is unclear how AD affects retinal electrophysiology and what tools are more appropriate to detect these possible changes. In this study, we used entropy tools to estimate the complexity of the dynamics of healthy and diseased retinas at different ages. We recorded microelectroretinogram responses to visual stimuli of different nature from retinas of young and adult, wild-type and 5xFAD-an animal model of AD-mice. To estimate the complexity of signals, we used the multiscale entropy approach, which calculates the entropy at several time scales using a coarse graining procedure. We found that young retinas had more complex responses to different visual stimuli. Further, the responses of young, wild-type retinas to natural-like stimuli exhibited significantly higher complexity than young, 5xFAD retinas. Our findings support a theory of complexity-loss with aging and disease and can have significant implications for early AD diagnosis.
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Doença de Alzheimer , Idoso , Envelhecimento , Doença de Alzheimer/patologia , Animais , Modelos Animais de Doenças , Entropia , Humanos , Camundongos , Retina/patologiaRESUMO
We propose a novel, scalable, and accurate method for detecting neuronal ensembles from a population of spiking neurons. Our approach offers a simple yet powerful tool to study ensemble activity. It relies on clustering synchronous population activity (population vectors), allows the participation of neurons in different ensembles, has few parameters to tune and is computationally efficient. To validate the performance and generality of our method, we generated synthetic data, where we found that our method accurately detects neuronal ensembles for a wide range of simulation parameters. We found that our method outperforms current alternative methodologies. We used spike trains of retinal ganglion cells obtained from multi-electrode array recordings under a simple ON-OFF light stimulus to test our method. We found a consistent stimuli-evoked ensemble activity intermingled with spontaneously active ensembles and irregular activity. Our results suggest that the early visual system activity could be organized in distinguishable functional ensembles. We provide a Graphic User Interface, which facilitates the use of our method by the scientific community.
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Rede Nervosa/fisiologia , Células Ganglionares da Retina/fisiologia , Animais , Simulação por Computador , Eletrodos , Modelos Neurológicos , Análise de Componente Principal , Células Ganglionares da Retina/citologiaRESUMO
Gender bias in Science, Technology, Engineering, and Mathematics (STEM) has been identified since a long time ago. However, gender imbalance in neuroscience has not yet been adequately explored worldwide. Here we report the first study on the development of the careers of men and women neuroscientists in Latin America in relation to family life and their perceptions of obstacles to success. Apart from revealing gender inequality in the neuroscience field, distinctive Latin American traits have become evident, thus providing novel insights into the global comprehension of gender imbalance in the region, which is required for guiding future actions, including the design of public policies in the region.
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BACKGROUND: Alzheimer's disease (AD) is the most prevalent form of dementia worldwide. This neurodegenerative syndrome affects cognition, memory, behavior, and the visual system, particularly the retina. OBJECTIVE: This work aims to determine whether the 5xFAD mouse, a transgenic model of AD, displays changes in the function of retinal ganglion cells (RGCs) and if those alterations are correlated with changes in the expression of glutamate and gamma-aminobutyric acid (GABA) neurotransmitters. METHODS: In young (2-3-month-old) and adult (6-7-month-old) 5xFAD and WT mice, we have studied the physiological response, firing rate, and burst of RGCs to various types of visual stimuli using a multielectrode array system. RESULTS: The firing rate and burst response in 5xFAD RGCs showed hyperactivity at the early stage of AD in young mice, whereas hypoactivity was seen at the later stage of AD in adults. The physiological alterations observed in 5xFAD correlate well with an increase in the expression of glutamate in the ganglion cell layer in young and adults. GABA staining increased in the inner nuclear and plexiform layer, which was more pronounced in the adult than the young 5xFAD retina, altering the excitation/inhibition balance, which could explain the observed early hyperactivity and later hypoactivity in RGC physiology. CONCLUSION: These findings indicate functional changes may be caused by neurochemical alterations of the retina starting at an early stage of the AD disease.
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Doença de Alzheimer/genética , Doença de Alzheimer/metabolismo , Modelos Animais de Doenças , Neurotransmissores/genética , Neurotransmissores/metabolismo , Células Ganglionares da Retina/metabolismo , Fatores Etários , Doença de Alzheimer/fisiopatologia , Animais , Feminino , Ácido Glutâmico/metabolismo , Masculino , Camundongos , Camundongos Transgênicos , Estimulação Luminosa/métodos , Ácido gama-Aminobutírico/metabolismoRESUMO
Alzheimer's disease (AD) is the most common and devastating neurodegenerative condition worldwide, characterized by the aggregation of amyloid-ß and phosphorylated tau protein, and is accompanied by a progressive loss of learning and memory. A healthy nervous system is endowed with synaptic plasticity, among others neural plasticity mechanisms, allowing structural and physiological adaptations to changes in the environment. This neural plasticity modification sustains learning and memory, and behavioral changes and is severely affected by pathological and aging conditions, leading to cognitive deterioration. This article reviews critical aspects of AD neurodegeneration as well as therapeutic approaches that restore neural plasticity to provide functional recoveries, including environmental enrichment, physical exercise, transcranial stimulation, neurotrophin involvement, and direct electrical stimulation of the amygdala. In addition, we report recent behavioral results in Octodon degus, a promising natural model for the study of AD that naturally reproduces the neuropathological alterations observed in AD patients during normal aging, including neuronal toxicity, deterioration of neural plasticity, and the decline of learning and memory.
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Atividades Cotidianas/psicologia , Doença de Alzheimer/psicologia , Doença de Alzheimer/terapia , Plasticidade Neuronal/fisiologia , Neurônios/fisiologia , Recuperação de Função Fisiológica/fisiologia , Doença de Alzheimer/fisiopatologia , Animais , Exercício Físico/fisiologia , Exercício Físico/psicologia , Humanos , Estimulação Transcraniana por Corrente Contínua/métodos , Estimulação Transcraniana por Corrente Contínua/psicologiaRESUMO
The role of Pannexin (PANX) channels during collective and single cell migration is increasingly recognized. Amongst many functions that are relevant to cell migration, here we focus on the role of PANX-mediated adenine nucleotide release and associated autocrine and paracrine signaling. We also summarize the contribution of PANXs with the cytoskeleton, which is also key regulator of cell migration. PANXs, as mechanosensitive ATP releasing channels, provide a unique link between cell migration and purinergic communication. The functional association with several purinergic receptors, together with a plethora of signals that modulate their opening, allows PANX channels to integrate physical and chemical cues during inflammation. Ubiquitously expressed in almost all immune cells, PANX1 opening has been reported in different immunological contexts. Immune activation is the epitome coordination between cell communication and migration, as leukocytes (i.e., T cells, dendritic cells) exchange information while migrating towards the injury site. In the current review, we summarized the contribution of PANX channels during immune cell migration and recruitment; although we also compile the available evidence for non-immune cells (including fibroblasts, keratinocytes, astrocytes, and cancer cells). Finally, we discuss the current evidence of PANX1 and PANX3 channels as a both positive and/or negative regulator in different inflammatory conditions, proposing a general mechanism of these channels contribution during cell migration.
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Movimento Celular/fisiologia , Conexinas/fisiologia , Células Dendríticas/fisiologia , Leucócitos/fisiologia , Fagócitos/fisiologia , Nucleotídeos de Adenina/fisiologia , Envelhecimento/imunologia , Envelhecimento/fisiologia , Animais , Astrócitos/fisiologia , Polaridade Celular , Quimiotaxia de Leucócito/fisiologia , Citoesqueleto/fisiologia , Fibroblastos/fisiologia , Humanos , Inflamação/imunologia , Inflamação/fisiopatologia , Queratinócitos/fisiologia , Mecanotransdução Celular/fisiologia , Neoplasias/imunologia , Degeneração Neural/imunologia , Degeneração Neural/fisiopatologia , Proteínas do Tecido Nervoso/fisiologia , Receptores Purinérgicos/fisiologiaRESUMO
Motion detection represents one of the critical tasks of the visual system and has motivated a large body of research. However, it remains unclear precisely why the response of retinal ganglion cells (RGCs) to simple artificial stimuli does not predict their response to complex, naturalistic stimuli. To explore this topic, we use Motion Clouds (MC), which are synthetic textures that preserve properties of natural images and are merely parameterized, in particular by modulating the spatiotemporal spectrum complexity of the stimulus by adjusting the frequency bandwidths. By stimulating the retina of the diurnal rodent, Octodon degus with MC we show that the RGCs respond to increasingly complex stimuli by narrowing their adjustment curves in response to movement. At the level of the population, complex stimuli produce a sparser code while preserving movement information; therefore, the stimuli are encoded more efficiently. Interestingly, these properties were observed throughout different populations of RGCs. Thus, our results reveal that the response at the level of RGCs is modulated by the naturalness of the stimulus - in particular for motion - which suggests that the tuning to the statistics of natural images already emerges at the level of the retina.
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Ritmo Circadiano/fisiologia , Percepção de Movimento/fisiologia , Movimento (Física) , Octodon/fisiologia , Retina/fisiologia , Células Ganglionares da Retina/fisiologia , Algoritmos , Animais , Potenciais Pós-Sinápticos Inibidores/fisiologia , Modelos Neurológicos , Movimento/fisiologia , Rede Nervosa/fisiologia , Estimulação Luminosa/métodos , Retina/citologia , Transmissão Sináptica/fisiologiaRESUMO
Although the properties of the neurons of the visual system that process central and peripheral regions of the visual field have been widely researched in the visual cortex and the LGN, they have scarcely been documented for the retina. The retina is the first step in integrating optical signals, and despite considerable efforts to functionally characterize the different types of retinal ganglion cells (RGCs), a clear account of the particular functionality of cells with central vs. peripheral fields is still wanting. Here, we use electrophysiological recordings, gathered from retinas of the diurnal rodent Octodon degus, to show that RGCs with peripheral receptive fields (RF) are larger, faster, and have shorter transient responses. This translates into higher sensitivity at high temporal frequencies and a full frequency bandwidth when compared to RGCs with more central RF. We also observed that imbalances between ON and OFF cell populations are preserved with eccentricity. Finally, the high diversity of functional types of RGCs highlights the complexity of the computational strategies implemented in the early stages of visual processing, which could inspire the development of bio-inspired artificial systems.
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A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
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A17 amacrine cells are an important part of the scotopic pathway. Their synaptic varicosities receive glutamatergic inputs from rod bipolar cells (RBC) and release GABA onto the same RBC terminal, forming a reciprocal feedback that shapes RBC depolarization. Here, using patch-clamp recordings, we characterized electrical coupling between A17 cells of the rat retina and report the presence of strongly interconnected and non-coupled A17 cells. In coupled A17 cells, evoked currents preferentially flow out of the cell through GJs and cross-synchronization of presynaptic signals in a pair of A17 cells is correlated to their coupling degree. Moreover, we demonstrate that stimulation of one A17 cell can induce electrical and calcium transients in neighboring A17 cells, thus confirming a functional flow of information through electrical synapses in the A17 coupled network. Finally, blocking GJs caused a strong decrease in the amplitude of the inhibitory feedback onto RBCs. We therefore propose that electrical coupling between A17 cells enhances feedback onto RBCs by synchronizing and facilitating GABA release from inhibitory varicosities surrounding each RBC axon terminal. GJs between A17 cells are therefore critical in shaping the visual flow through the scotopic pathway.
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Células Amácrinas/fisiologia , Células Bipolares da Retina/metabolismo , Animais , Cálcio/metabolismo , Adaptação à Escuridão/fisiologia , Retroalimentação , Feminino , Junções Comunicantes/fisiologia , Masculino , Potenciais da Membrana/efeitos dos fármacos , Visão Noturna/fisiologia , Técnicas de Patch-Clamp , Ratos , Ratos Sprague-Dawley , Receptores de AMPA/metabolismo , Receptores de GABA/metabolismo , Retina/metabolismo , Retina/fisiologia , Células Bipolares da Retina/fisiologia , Células Fotorreceptoras Retinianas Bastonetes/fisiologia , Sinapses/metabolismo , Transmissão Sináptica/fisiologia , Ácido gama-Aminobutírico/metabolismoRESUMO
Altered proteostasis is a salient feature of Alzheimer's disease (AD), highlighting the occurrence of endoplasmic reticulum (ER) stress and abnormal protein aggregation. ER stress triggers the activation of the unfolded protein response (UPR), a signaling pathway that enforces adaptive programs to sustain proteostasis or eliminate terminally damaged cells. IRE1 is an ER-located kinase and endoribonuclease that operates as a major stress transducer, mediating both adaptive and proapoptotic programs under ER stress. IRE1 signaling controls the expression of the transcription factor XBP1, in addition to degrade several RNAs. Importantly, a polymorphism in the XBP1 promoter was suggested as a risk factor to develop AD. Here, we demonstrate a positive correlation between the progression of AD histopathology and the activation of IRE1 in human brain tissue. To define the significance of the UPR to AD, we targeted IRE1 expression in a transgenic mouse model of AD. Despite initial expectations that IRE1 signaling may protect against AD, genetic ablation of the RNase domain of IRE1 in the nervous system significantly reduced amyloid deposition, the content of amyloid ß oligomers, and astrocyte activation. IRE1 deficiency fully restored the learning and memory capacity of AD mice, associated with improved synaptic function and improved long-term potentiation (LTP). At the molecular level, IRE1 deletion reduced the expression of amyloid precursor protein (APP) in cortical and hippocampal areas of AD mice. In vitro experiments demonstrated that inhibition of IRE1 downstream signaling reduces APP steady-state levels, associated with its retention at the ER followed by proteasome-mediated degradation. Our findings uncovered an unanticipated role of IRE1 in the pathogenesis of AD, offering a novel target for disease intervention.
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Doença de Alzheimer/metabolismo , Hipocampo/metabolismo , Proteínas de Membrana/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Transdução de Sinais/fisiologia , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Peptídeos beta-Amiloides/metabolismo , Precursor de Proteína beta-Amiloide/metabolismo , Animais , Modelos Animais de Doenças , Progressão da Doença , Estresse do Retículo Endoplasmático/fisiologia , Hipocampo/patologia , Humanos , Potenciação de Longa Duração/fisiologia , Proteínas de Membrana/genética , Camundongos , Camundongos Transgênicos , Neurônios/metabolismo , Neurônios/patologia , Proteínas Serina-Treonina Quinases/genética , Memória Espacial/fisiologia , Resposta a Proteínas não Dobradas/fisiologiaRESUMO
The use of transgenic models for the study of neurodegenerative diseases has made valuable contributions to the field. However, some important limitations, including protein overexpression and general systemic compensation for the missing genes, has caused researchers to seek natural models that show the main biomarkers of neurodegenerative diseases during aging. Here we review some of these models-most of them rodents, focusing especially on the genetic variations in biomarkers for Alzheimer diseases, in order to explain their relationships with variants associated with the occurrence of the disease in humans.
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Doença de Alzheimer/genética , Modelos Animais de Doenças , Variação Genética , Envelhecimento/genética , Animais , Animais Geneticamente Modificados , Código de Barras de DNA Taxonômico , Cobaias , Humanos , Camundongos , Ratos , Análise de Sequência de ProteínaRESUMO
The use of transgenic models for the study of neurodegenerative diseases has made valuable contributions to the field. However, some important limitations, including protein overexpression and general systemic compensation for the missing genes, has caused researchers to seek natural models that show the main biomarkers of neurodegenerative diseases during aging. Here we review some of these models-most of them rodents, focusing especially on the genetic variations in biomarkers for Alzheimer diseases, in order to explain their relationships with variants associated with the occurrence of the disease in humans.
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Humanos , Animais , Cobaias , Camundongos , Ratos , Variação Genética , Modelos Animais de Doenças , Doença de Alzheimer/genética , Envelhecimento/genética , Animais Geneticamente Modificados , Análise de Sequência de Proteína , Código de Barras de DNA TaxonômicoRESUMO
Alzheimer's disease (AD) is the most common neurodegenerative disorder and the leading cause of age-related dementia worldwide. Several models for AD have been developed to provide information regarding the initial changes that lead to degeneration. Transgenic mouse models recapitulate many, but not all, of the features of AD, most likely because of the high complexity of the pathology. In this context, the validation of a wild-type animal model of AD that mimics the neuropathological and behavioral abnormalities is necessary. In previous studies, we have reported that the Chilean rodent Octodon degus could represent a natural model for AD. In the present work, we further describe the age-related neurodegeneration observed in the O. degus brain. We report some histopathological markers associated with the onset progression of AD, such as glial activation, increase in oxidative stress markers, neuronal apoptosis and the expression of the peroxisome proliferative-activated receptor γ coactivator-1α (PGC-1α). With these results, we suggest that the O. degus could represent a new model for AD research and a powerful tool in the search for therapeutic strategies against AD.
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Envelhecimento/patologia , Doença de Alzheimer/patologia , Doença de Alzheimer/fisiopatologia , Encéfalo/patologia , Adenilato Quinase/metabolismo , Envelhecimento/fisiologia , Animais , Apoptose/fisiologia , Astrócitos/patologia , Astrócitos/fisiologia , Comportamento Animal , Encéfalo/fisiopatologia , Modelos Animais de Doenças , Interleucina-6/metabolismo , Microglia/patologia , Microglia/fisiologia , Neurônios/patologia , Neurônios/fisiologia , Octodon , Estresse Oxidativo/fisiologia , Fatores de Transcrição/metabolismoRESUMO
Nitric oxide (NO) is involved in retinal signal processing, but its cellular actions are only partly understood. An established source of retinal NO are NOACs, a group of nNOS-expressing amacrine cells which signal onto bipolar, other amacrine and ganglion cells in the inner plexiform layer. Here, we report that NO regulates glutamate responses in morphologically and electrophysiologically identified type 4 OFF cone bipolar cells through activation of the soluble guanylyl cyclase-cGMP-PKG pathway. The glutamate response of these cells consists of two components, a fast phasic current sensitive to kainate receptor agonists, and a secondary component with slow kinetics, inhibited by AMPA receptor antagonists. NO shortened the duration of the AMPA receptor-dependent component of the glutamate response, while the kainate receptor-dependent component remained unchanged. Application of 8-Br-cGMP mimicked this effect, while inhibition of soluble guanylate cyclase or protein kinase G prevented it, supporting a mechanism involving a cGMP signaling pathway. Notably, perfusion with a NOS-inhibitor prolonged the duration of the glutamate response, while the NO precursor L-arginine shortened it, in agreement with a modulation by endogenous NO. Furthermore, NO accelerated the response recovery during repeated stimulation of type 4 cone bipolar cells, suggesting that the temporal response properties of this OFF bipolar cell type are regulated by NO. These results reveal a novel cellular mechanism of NO signaling in the retina, and represent the first functional evidence of NO modulating OFF cone bipolar cells.
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Ácido Glutâmico/metabolismo , Óxido Nítrico/fisiologia , Células Fotorreceptoras Retinianas Cones/metabolismo , Animais , Ratos , Ratos Sprague-Dawley , Receptores de AMPA/metabolismo , Células Fotorreceptoras Retinianas Cones/citologiaRESUMO
The threshold for bidirectional modification of synaptic plasticity is known to be controlled by several factors, including the balance between protein phosphorylation and dephosphorylation, postsynaptic free Ca(2+) concentration and NMDA receptor (NMDAR) composition of GluN2 subunits. Pannexin 1 (Panx1), a member of the integral membrane protein family, has been shown to form non-selective channels and to regulate the induction of synaptic plasticity as well as hippocampal-dependent learning. Although Panx1 channels have been suggested to play a role in excitatory long-term potentiation (LTP), it remains unknown whether these channels also modulate long-term depression (LTD) or the balance between both types of synaptic plasticity. To study how Panx1 contributes to excitatory synaptic efficacy, we examined the age-dependent effects of eliminating or blocking Panx1 channels on excitatory synaptic plasticity within the CA1 region of the mouse hippocampus. By using different protocols to induce bidirectional synaptic plasticity, Panx1 channel blockade or lack of Panx1 were found to enhance LTP, whereas both conditions precluded the induction of LTD in adults, but not in young animals. These findings suggest that Panx1 channels restrain the sliding threshold for the induction of synaptic plasticity and underlying brain mechanisms of learning and memory.
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Several studies have shown that connexin channels play an important role in retinal neural coding in nocturnal rodents. However, the contribution of these channels to signal processing in the retina of diurnal rodents remains unclear. To gain insight into this problem, we studied connexin expression and the contribution of connexin channels to the retinal light response in the diurnal rodent Octodon degus (degu) compared to rat, using in vivo ERG recording under scotopic and photopic light adaptation. Analysis of the degu genome showed that the common retinal connexins present a high degree of homology to orthologs expressed in other mammals, and expression of Cx36 and Cx43 was confirmed in degu retina. Cx36 localized mainly to the outer and inner plexiform layers (IPLs), while Cx43 was expressed mostly in cells of the retinal pigment epithelium. Under scotopic conditions, the b-wave response amplitude was strongly reduced by 18-ß-glycyrrhetinic acid (ß-GA) (-45.1% in degu, compared to -52.2% in rat), suggesting that connexins are modulating this response. Remarkably, under photopic adaptation, ß-GA increased the ERG b-wave amplitude in degu (+107.2%) while reducing it in rat (-62.3%). Moreover, ß-GA diminished the spontaneous action potential firing rate in ganglion cells (GCs) and increased the response latency of ON and OFF GCs. Our results support the notion that connexins exert a fine-tuning control of the retinal light response and have an important role in retinal neural coding.
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STUDY OBJECTIVES: To determine rapid eye movement (REM) sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. DESIGN: We have investigated REM sleep rebound, recovery, and documented REM sleep propensity measures during and after diurnal and nocturnal selective REM sleep deprivations. SUBJECTS: Nine male wild-captured O. degus prepared for polysomnographic recordings. INTERVENTIONS: Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). MEASUREMENTS AND RESULTS: Diurnal and nocturnal REM sleep deprivations provoked equivalent amounts of REM sleep debt, but a consistent REM sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM sleep associated with an augment in REM/total sleep time ratio and enhancement in REM sleep episode consolidation. CONCLUSIONS: Our results support the notion that the circadian system actively promotes REM sleep. We propose that the sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM sleep
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Octodon/fisiologia , Privação do Sono/fisiopatologia , Sono REM/fisiologia , Animais , Ritmo Circadiano/fisiologia , Masculino , Polissonografia , Fatores de TempoRESUMO
One major goal of integrative and comparative biology is to understand and explain the interaction between the performance and behavior of animals in their natural environment. The Caviomorph, Octodon degu, is a native rodent species from Chile, and represents a unique model to study physiological and behavioral traits, including cognitive and sensory abilities. Degus live in colonies and have a well-structured social organization, with a mostly diurnal-crepuscular circadian activity pattern. More notable is the fact that in captivity, they reproduce and live between 5 and 7 yr and show hallmarks of neurodegenerative diseases (including Alzheimer's disease), diabetes, and cancer.