brain circuitry
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Haim Sompolinsky, Kenneth Blum
The Swartz Program at Harvard University seeks applicants for a postdoctoral fellow in theoretical and computational neuroscience. Based on a grant from the Swartz Foundation, a Swartz postdoctoral fellowship is available at Harvard University with a start date in the summer or fall of 2024. Postdocs join a vibrant group of theoretical and experimental neuroscientists plus theorists in allied fields at Harvard’s Center for Brain Science. The Center for Brain Science includes faculty doing research on a wide variety of topics, including neural mechanisms of rodent learning, decision-making, and sex-specific and social behaviors; reinforcement learning in rodents and humans; human motor control; behavioral and fMRI studies of human cognition; circuit mechanisms of learning and behavior in worms, larval flies, and larval zebrafish; circuit mechanisms of individual differences in flies and humans; rodent and fly olfaction; inhibitory circuit development; retinal circuits; and large-scale reconstruction of detailed brain circuitry.
Mapping learning and decision-making algorithms onto brain circuitry
In the first half of my talk, I will discuss our recent work on the midbrain dopamine system. The hypothesis that midbrain dopamine neurons broadcast an error signal for the prediction of reward is among the great successes of computational neuroscience. However, our recent results contradict a core aspect of this theory: that the neurons uniformly convey a scalar, global signal. I will review this work, as well as our new efforts to update models of the neural basis of reinforcement learning with our data. In the second half of my talk, I will discuss our recent findings of state-dependent decision-making mechanisms in the striatum.
Sympathetic nerve remodeling in adipose tissue
Sympathetic nerve activation of adrenergic receptors on fat is the major pathway the brain uses to drive non-shivering thermogenesis in brown adipose tissue and lipolysis in white fat. There is accumulating evidence that the peripheral nerve architecture inside of organs is plastic (can be remodeled) but the factors and conditions that regulate or result in remodeling are largely unknown. Particularly for fat, it remains unclear if nerves in fat can be remodeled in step with hyperplasia/trophy of adipose tissue as result of a prolonged energy surfeit. This talk will discuss our recent work identifying the sympathetic nerve architecture in adipose tissue as highly plastic in response to the adipose hormone leptin, the brain circuitry leptin acts on to regulate this and the physiological effects remodeling of innervation has on fat tissue function.
Neuro-Immune Coupling: How the Immune System Sculpts Brain Circuitry
In this lecture, Dr Stevens will discuss recent work that implicates brain immune cells, called microglia, in sculpting of synaptic connections during development and their relevance to autism, schizophrenia and other brain disorders. Her recent work revealed a key role for microglia and a group of immune related molecules called complement in normal developmental synaptic pruning, a normal process required to establish precise brain wiring. Emerging evidence suggests aberrant regulation of this pruning pathway may contribute to synaptic and cognitive dysfunction in a host of brain disorders, including schizophrenia. Recent research has revealed that a person’s risk of schizophrenia is increased if they inherit specific variants in complement C4, gene plays a well-known role in the immune system but also helps sculpt developing synapses in the mouse visual system (Sekar et al., 2016). Together these findings may help explain known features of schizophrenia, including reduced numbers of synapses in key cortical regions and an adolescent age of onset that corresponds with developmentally timed waves of synaptic pruning in these regions. Stevens will discuss this and ongoing work to understand the mechanisms by which complement and microglia prune specific synapses in the brain. A deeper understanding of how these immune mechanisms mediate synaptic pruning may provide novel insight into how to protect synapses in autism and other brain disorders, including Alzheimer’s and Huntington’s Disease.
The role of orexin/hypocretin in social behaviour
My lab is focused on how brain encodes and modulates social interactions. Intraspecific social interactions are integral for survival and maintenance of society among all mammalian species. Despite the importance of social interactions, we lack a complete understanding of the brain circuitry involved in processing social behaviour. My lab investigates how the hypothalamic orexin (hypocretin) neurons and their downstream circuits participate in social interaction behaviours. These neurons are located exclusively in the hypothalamus that regulates complex and goal-directed behaviours. We recently identified that orexin neurons differentially encode interaction between familiar and novel animals. We are currently investigating how chronic social isolation, a risk factor for the development of social-anxiety like behaviours, affects orexin neuron activity and how we can manipulate the activity of these neurons to mitigate isolation-induced social deficits.
Adaptive plasticity in adult brain circuitry during naturally occurring regeneration of sensory inputs
FENS Forum 2024
An atopic dermatitis mouse model reveals potential utility for atopic dermatitis-generated comorbid depression brain circuitry studies
FENS Forum 2024
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