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Vergara, R. C.

Publications and source records attributed to Vergara, R. C..

4 recordsLinked to original sources

Extending the integrate-and-fire model to account for metabolic dependencies

It is widely accepted that the brain, like any other physical system, is subjected to physical constraints restricting its operation. The brains metabolic demands are particularly critical for proper neuronal function, but the impact of these constraints is still poorly understood. Detailed single-neuron models are recently integrating metabolic constraints, but the computational resources these models need, make it difficult to explore the dynamics of extended neural networks imposed by such constraints. Thus, there is a need for a simple-enough neuron model that incorporates metabolic activity and allows us to explore neural network dynamics. This work introduces an energy-dependent leaky integrate-and-fire (LIF) neuronal model extension to account for the effects of metabolic constraints on the single-neuron behavior (EDLIF). This simple energy-dependent model shows better performance predicting real spikes trains -in spike coincidence measure sense-than the classical leaky integrate-and-fire model. It can describe the relationship between the average firing rate and the ATP cost, and replicate a neurons behavior under a clinical setting such as amyotrophic lateral sclerosis. The simplicity of the energy-dependent model presented here, makes it computationally efficient and thus, suitable to study the dynamics of large neural networks. Author summaryAny physical system or biological tissue is restricted by physical constraints bounding their behavior, and the brain is not free from these constraints. Energetic disorders in the brain have been linked to several neurodegenerative diseases, highlighting the relevance of maintaining a critical balance between energy production and consumption in neurons. These observations motivate the development of mathematical tools that can help to understand the dependence of the brains behavior in metabolism. One of the essential building blocks to achieve this task is the mathematical representation of neurons through models, allowing computational simulations of single-neurons and neural networks. Here we construct a simple and computational cheap energy-dependent neuron model that allows the study of neurons behavior under an energetic perspective. The introduced neuron model is contrasted with one of the widest-used neuron models and shows better prediction capabilities when real neuron recordings are used. Our model is suitable for replicating neurons behavior under a specific neurodegenerative disease, which cannot be achieved by the abovementioned popular model. Our simple model is promising because it allows the simulation and study of neuronal networks under a metabolic-dependent perspective.

neuroscience↗

Agency improves working memory and accelerates visual and attentional processing

Agency, understood as the ability of an organism to control stimuli onset, modulates perceptual and attentional functions. Since stimulus encoding is an essential component of working memory (WM), we conjectured that the perceptual processs agency would positively modulate WM. To corroborate this proposition, we tested twenty-five healthy subjects in a modified-Sternberg WM task under three stimuli presentation conditions: an unpredictable presentation of encoding stimulus, self-initiated presentation of the stimulus, and self-initiation presentation with random-delay stimulus onset. Concurrently, we recorded the subjects electroencephalographic signals during WM encoding. We found that the self-initiation condition was associated with better WM accuracy, and earlier latencies of N100 and P200 evoked potential components representing visual and attentional processes, respectively. Our work demonstrates that agency enhances WM performance and accelerates early visual and attentional processes deployed during WM encoding. We also found that self-initiation presentation correlates with an increased attentional state compared to the other two conditions, suggesting a role for temporal stimuli predictability. Our study remarks on the relevance of agency in sensory and attentional processing for WM.

neuroscience↗

Reduced Suprathreshold Auditory Nerve Responses are Associated with Thinner Temporal Cortex and Slower Processing Speed in Presbycusis

Epidemiological evidence shows an association between hearing loss and dementia in elderly people. However, the mechanisms that connect hearing impairments and cognitive decline are still unknown. Here we propose that a suprathreshold auditory-nerve impairment is associated with cognitive decline and brain atrophy. Methods: audiological, neuropsychological, and brain structural 3-Tesla MRI data were obtained from elders with different levels of hearing loss recruited in the ANDES cohort. The amplitude of waves I (auditory nerve) and V (midbrain) from auditory brainstem responses were measured at 80 dB nHL. We also calculated the ratio between wave V and I as a proxy of a suprathreshold brainstem function. Results: we included a total of 101 subjects (age: 73.5 {+/-} 5.2 years (mean {+/-} SD), mean education: 9.5 {+/-} 4.2 years, and mean audiogram thresholds (0.5-4 kHz): 25.5 {+/-} 12.0 dB HL). We obtained reliable suprathreshold waves V in all subjects (n=101), while replicable waves I were obtained in 92 subjects (91.1%). Partial Spearman correlations (corrected by age, gender, education and hearing thresholds) showed that reduced suprathreshold wave I responses were associated with thinner bilateral medial and inferior temporal cortex and, with slower processing speed as evidenced by the Trail-Making Test-A and digit symbol tests. Non-significant correlations were obtained between wave I amplitudes and other cognitive domains. Conclusions: These results evidence that reduced suprathreshold auditory nerve responses in presbycusis are associated with slower processing speed and brain structural changes in the temporal cortex.

neuroscience↗

Cingulate Cortex Atrophy is Associated with Hearing Loss in Presbycusis with Cochlear Amplifier Dysfunction

Age-related hearing loss is associated with cognitive decline and has been proposed as a risk factor for dementia. However, the mechanisms that relate hearing loss to cognitive decline remain elusive. Here, we propose that the impairment of the cochlear amplifier mechanism is associated with structural brain changes and cognitive impairment. Ninety-six subjects aged over 65 years old (63 female and 33 male) were evaluated using brain magnetic resonance imaging, neuropsychological and audiological assessments, including distortion product otoacoustic emissions as a measure of the cochlear amplifier function. All the analyses were adjusted by age, gender and education. The group with cochlear amplifier dysfunction showed greater brain atrophy in the cingulate cortex and in the parahippocampus. In addition, the atrophy of the cingulate cortex was associated with cognitive impairment in episodic and working memories and in language and visuoconstructive abilities. We conclude that the neural abnormalities observed in presbycusis subjects with cochlear amplifier dysfunction extend beyond core auditory network and are associated with cognitive decline in multiple domains. These results suggest that a cochlear amplifier dysfunction in presbycusis is an important mechanism relating hearing impairments to brain atrophy in the extended network of effortful hearing.

neuroscience↗