Twice-exceptional learners face a unique set of challenges arising from the intersection of extraordinary talent and disability. Neurobiology research has the capacity to complement pedagogical research and provide support for twice-exceptional learners. Very few studies have attempted to specifically address the neurobiological underpinnings of twice-exceptionality. However, neurobiologists have built a broad base of knowledge in nervous system function spanning from the level of neural circuits to the molecular basis of behavior. It is known that distinct neural circuits mediate different neural functions, which suggests that 2e learning may result from enhancement in one circuit and disruption in another. Neural circuits are known to adapt and change in response to experience, a cellular process known as neuroplasticity. Plasticity is controlled by a bidirectional connection between the synapse, where neural signals are received, and the nucleus, where regulated gene expression can return to alter synaptic function. Complex molecular mechanisms compose this connection in distinct neural circuits, and genetic alterations in these mechanisms are associated with both memory enhancements and psychiatric disorder. Understanding the consequences of these changes at the molecular, cellular, and circuit levels will provide critical insights into the neurobiological bases of twice-exceptionality.
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http://dx.doi.org/10.1016/j.nlm.2022.107684 | DOI Listing |
Brain
January 2025
Department of Neurology, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
Epilepsy is a network disorder, involving neural circuits at both the micro- and macroscale. While local excitatory-inhibitory imbalances are recognized as a hallmark at the microscale, the dynamic role of distinct neuron types during seizures remain poorly understood. At the macroscale, interactions between key nodes within the epileptic network, such as the central median thalamic nucleus (CMT), are critical to the, hippocampal epileptic process.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Ernst Strüngmann Institute, Frankfurt am Main 60528, Germany.
The dynamics of neuronal systems are characterized by hallmark features such as oscillations and synchrony. However, it has remained unclear whether these characteristics are epiphenomena or are exploited for computation. Due to the challenge of selectively interfering with oscillatory network dynamics in neuronal systems, we simulated recurrent networks of damped harmonic oscillators in which oscillatory activity is enforced in each node, a choice well supported by experimental findings.
View Article and Find Full Text PDFVision (Basel)
January 2025
Centre for the Study of Perceptual Experience, Department of Philosophy, University of Glasgow, Glasgow G12 8QQ, UK.
Mental imagery is claimed to underlie a host of abilities, such as episodic memory, working memory, and decision-making. A popular view holds that mental imagery relies on the perceptual system and that it can be said to be 'vision in reverse'. Whereas vision exploits the bottom-up neural pathways of the visual system, mental imagery exploits the top-down neural pathways.
View Article and Find Full Text PDFACS Nano
January 2025
Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha 410078, Hunan, China.
Spinal cord injury (SCI) remains a formidable challenge in biomedical research, as the silencing of intrinsic regenerative signals in most spinal neurons results in an inability to reestablish neural circuits. In this study, we found that neurons with low axonal regeneration after SCI showed decreased extracellular signal-regulated kinase (ERK) phosphorylation levels. However, the expression of dual specificity phosphatase 26 (DUSP26)─which negatively regulates ERK phosphorylation─was reduced considerably in neurons undergoing spontaneous axonal regeneration.
View Article and Find Full Text PDFFront Neural Circuits
January 2025
Department of Neurobiology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
A strong repetitive stimulus can occasionally enhance axonal excitability, leading to the generation of afterdischarge. This afterdischarge outlasts the stimulus period and originates either from the physiological spike initiation site, typically the axon initial segment, or from ectopic sites for spike generation. One of the possible mechanisms underlying the stimulus-induced ectopic afterdischarge is the local depolarization due to accumulated potassium ions surrounding the axonal membranes of the distal portion.
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