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Kastanenka, K. V.

Publications and source records attributed to Kastanenka, K. V..

2 recordsLinked to original sources

Building Transformers from Neurons and Astrocytes

Glial cells account for roughly 90% of all human brain cells, and serve a variety of important developmental, structural, and metabolic functions. Recent experimental efforts suggest that astrocytes, a type of glial cell, are also directly involved in core cognitive processes such as learning and memory. While it is well-established that astrocytes and neurons are connected to one another in feedback loops across many time scales and spatial scales, there is a gap in understanding the computational role of neuron-astrocyte interactions. To help bridge this gap, we draw on recent advances in artificial intelligence (AI) and astrocyte imaging technology. In particular, we show that neuron-astrocyte networks can naturally perform the core computation of a Transformer, a particularly successful type of AI architecture. In doing so, we provide a concrete and experimentally testable account of neuron-astrocyte communication. Because Transformers are so successful across a wide variety of task domains, such as language, vision, and audition, our analysis may help explain the ubiquity, flexibility, and power of the brains neuron-astrocyte networks. Significance StatementTransformers have become the default choice of neural architecture for many machine learning applications. Their success across multiple domains such as language, vision, and speech raises the question: how can one build Transformers using biological computational units? At the same time, in the glial community there is a gradually accumulating evidence that astrocytes, formerly believed to be passive house-keeping cells in the brain, in fact play important role in brains information processing and computation. In this work we hypothesize that neuron-astrocyte networks can naturally implement the core computation performed by the Transformer block in AI. The omnipresence of astrocytes in almost any brain area may explain the success of Transformers across a diverse set of information domains and computational tasks.

neuroscience↗

Hyperactive somatostatin interneurons near amyloid plaque and cell-type-specific firing deficits in a mouse model of Alzheimer's disease

Alzheimers disease (AD) is characterized by synaptic loss and neuronal network dysfunction. These network deficits are mediated by early alterations in neuronal firing rates that coincide with amyloid plaque accumulation. Mounting evidence supports that inhibitory networks are impaired in AD, but the mechanisms driving these inhibitory deficits are poorly understood. Here we use in vivo multiphoton calcium imaging to determine the relationship between amyloid accumulation and the spontaneous activity of excitatory neurons and inhibitory interneurons in an APP/PS1 mouse model of Alzheimers disease. We show that somatostatin-expressing (SOM) interneurons are hyperactive, while parvalbumin-expressing interneurons are hypoactive in APP/PS1 mice. Only SOM interneuron hyperactivity correlated with proximity to amyloid plaque. These inhibitory deficits were accompanied by decreased excitatory neurons activity and decreased pairwise activity correlations in APP/PS1 mice. Our study identifies cell-specific interneuronal firing deficits driven by amyloid pathology in APP/PS1 mice and provides new insights for targeting inhibitory circuits in Alzheimers disease.

neuroscience↗