Mary Sommer

ORCID: 0000-0001-8339-6159
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Ion channel regulation and function
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neural dynamics and brain function
  • Genetics and Neurodevelopmental Disorders
  • Functional Brain Connectivity Studies
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Epilepsy research and treatment
  • Mitochondrial Function and Pathology
  • Neonatal and fetal brain pathology
  • Traumatic Brain Injury Research
  • Memory and Neural Mechanisms

Tufts University
2019-2025

Developing cortical GABAergic interneurons rely on genetic programs, neuronal activity, and environmental cues to construct inhibitory circuits during early postnatal development. Disruption of these events can cause long-term changes in inhibition may be involved neurological disorders associated with circuit dysfunction. We hypothesized that tonic glutamate signaling the neonatal cortex contributes to, is necessary for, maturation interneurons. To test this hypothesis, we used mice both...

10.1523/jneurosci.1392-18.2019 article EN cc-by-nc-sa Journal of Neuroscience 2019-03-07

Abstract Glutamate, the primary excitatory neurotransmitter in central nervous system (CNS), is regulated by amino acid transporters glutamate transporter 1 (GLT-1) and aspartate (GLAST). Following traumatic brain injury, extracellular levels increase, contributing to excitotoxicity, circuit dysfunction, morbidity. Increased neuronal release compromised astrocyte-mediated uptake contribute elevated glutamate, but mechanistic spatiotemporal underpinnings of these changes are not well...

10.1093/cercor/bhaf031 article EN Cerebral Cortex 2025-02-01

Traumatic brain injury (TBI) causes cortical dysfunction and can lead to posttraumatic epilepsy. Multiple studies demonstrate that GABAergic inhibitory network function is compromised following TBI, which may contribute hyperexcitability motor, behavioral, cognitive deficits. Preserving the of interneurons, therefore, a rational therapeutic strategy preserve after TBI prevent long-term clinical complications. Here, we explored an approach based on ketogenic diet, neuroprotective...

10.1172/jci.insight.126506 article EN JCI Insight 2019-04-30

Traumatic brain injury (TBI) is the leading cause of death in young people and can cognitive motor dysfunction disruptions functional connectivity between regions. In human TBI patients rodent models TBI, decreased after injury. Recovery associated with improved cognition memory, suggesting an important link outcome. We examined widespread alterations following using simultaneous widefield mesoscale GCaMP7c calcium imaging electrocorticography (ECoG) mice injured controlled cortical impact...

10.1093/cercor/bhae038 article EN Cerebral Cortex 2024-01-31

Infantile and epileptic spasms syndrome (IESS) is a childhood epilepsy characterized by infantile or late-onset spasms, abnormal neonatal EEG, epilepsy. Few treatments exist for IESS, clinical outcomes are poor, the molecular circuit-level etiologies of IESS not well understood. Multiple human risk genes linked to Wnt/β-catenin signaling, pathway that controls developmental transcriptional programs promotes glutamatergic excitation via β-catenin's role as synaptic scaffold. We previously...

10.1523/jneurosci.0572-22.2022 article EN cc-by-nc-sa Journal of Neuroscience 2023-01-30

Glutamate, the primary excitatory neurotransmitter in CNS, is regulated by amino acid transporters (EAATs) GLT-1 and GLAST. Following traumatic brain injury (TBI), extracellular glutamate levels increase, contributing to excitotoxicity, circuit dysfunction, morbidity. Increased neuronal release compromised astrocyte-mediated uptake contribute elevated glutamate, but mechanistic spatiotemporal underpinnings of these changes are not well established. Using controlled cortical impact (CCI)...

10.1101/2024.08.28.610143 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-08-29

Abstract Astrocytes are glial cells that interact with neuronal synapses via their distal processes, where they remove glutamate and potassium (K + ) from the extracellular space following activity. Astrocyte clearance of both K is voltage-dependent, but astrocyte membrane potential (V m has been thought to be largely invariant. As a result, these voltage-dependencies have not considered relevant function. Using genetically encoded voltage indicators enabling measurement V at processes...

10.1101/2021.07.03.450922 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-07-04

ABSTRACT Traumatic brain injury (TBI) is the leading cause of death in young people and can cognitive motor dysfunction disruptions functional connectivity between regions. In human TBI patients rodent models TBI, decreased after injury. Recovery associated with improved cognition memory, suggesting an important link outcome. We examined widespread alterations following using simultaneous widefield mesoscale GCaMP7c calcium imaging electrocorticography (ECoG) mice injured controlled cortical...

10.1101/2023.10.06.560776 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-10-06

Abstract Infantile Spasms syndrome (ISS) is a childhood epilepsy characterized by infantile or late onset spasms, abnormal neonatal EEG, and epilepsy. Few treatments exist for IS, clinical outcomes are poor, the molecular circuit-level etiologies of IS not well understood. Multiple human ISS risk genes linked to Wnt/β-catenin signaling, pathway which controls developmental transcriptional programs promotes glutamatergic excitation via β-catenin’s role as synaptic scaffold. We previously...

10.1101/2022.07.06.499046 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-07-06
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