A5090241864- Neuroscience and Neuropharmacology Research
- Amino Acid Enzymes and Metabolism
- Metabolism and Genetic Disorders
- Neural dynamics and brain function
- Axon Guidance and Neuronal Signaling
- Tryptophan and brain disorders
- Plant-based Medicinal Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Traumatic Brain Injury and Neurovascular Disturbances
University of Miami
2017-2022
Neurological Surgery
2022
Max Planck Florida Institute for Neuroscience
2017
After traumatic brain injury (TBI), glial cells have both beneficial and deleterious roles in progression recovery. However, few studies examined the influence of reactive astrocytes tripartite synapse following TBI. Here, we demonstrated that hippocampal synaptic damage caused by controlled cortical impact (CCI) mice results a switch from neuronal to astrocytic d-serine release. Under nonpathological conditions, functions as neurotransmitter coagonist for NMDA receptors is involved...
Abstract Synaptic damage is one of the most prevalent pathophysiological responses to traumatic CNS injury and underlies much associated cognitive dysfunction; however, it poorly understood. The D‐amino acid, D‐serine, serves as primary co‐agonist at synaptic NMDA receptors (NDMARs) a critical mediator NMDAR‐dependent transmission plasticity. In physiological conditions, D‐serine produced released by neurons from enzymatic conversion L‐serine serine racemase (SRR). However, under...
Diverse types of cortical interneurons (INs) mediate various kinds inhibitory control mechanisms to balance and shape network activity. Distinct IN subtypes develop uniquely organized axonal arbors that innervate different subcellular compartments excitatory principal neurons (PNs), which critically contribute determining their output properties. However, it remains poorly understood how they establish this peculiar organization synaptic connectivity during development. Here, taking...
Abstract Clinical trials examining neuroprotective strategies after brain injury, including those targeting cell death mechanisms, have been underwhelming. This may be in part due to an incomplete understanding of the signalling mechanisms that induce traumatic injury. The recent identification a new family receptors initiate pro-cell signals absence their ligand, called dependence receptors, provides insight into factors contribute Here, we show blocking receptor EphB3 improves...