Barna Dudok
Baylor College of Medicine, TX·Neuroscience·Early-career
Epilepsy affects 50 million people worldwide. In 40% of people with temporal lobe epilepsy (TLE), drugs fail to stop seizures, raising the risk of injury, cognitive decline, and death.
- Fields
Neuroscience
Physiology
- Topics
epilepsy
seizures
GABAergic interneurons
- Grants
- 1 known grant, through Mar 2027
What they work on
- Test whether CCK and PV basket cells, two types of inhibitory neurons, are active in different brain states in a kainate mouse model of temporal lobe epilepsy, using two-photon calcium imaging with hippocampal field recordings.
- Test whether excitatory inputs and mutual inhibition between the cell types explain why PV and CCK interneurons are recruited differently, using in vitro electrophysiology in brain slices.
- Test whether activating CCK interneurons dampens epileptic network activity in the hippocampus without disrupting how neurons represent spatial location.
More about the research
A key cause of epilepsy is weakened inhibition, the brain's braking system. This braking comes from inhibitory neurons (interneurons) that release the chemical GABA. There are many types of interneurons, and how each type works in brain circuits is poorly understood. That gap makes it hard to design treatments.
Why it matters
Many people with temporal lobe epilepsy do not respond to current drugs. This work could show whether targeting CCK basket cells dampens seizure-related brain activity without disrupting how the brain encodes spatial information. It may point to strategies that prevent seizures without harming memory and thinking.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ivan Soltesz
Stanford University, CA·Neuroscience
Identify non-invasive behavioral biomarkers that predict chronic seizures and death, using MoSeq AI analysis of 3D video in mouse models of temporal lobe epilepsy and Dravet syndrome.
Shelley J Russek
Boston University, MA·Neuroscience
Test whether STAT3 signaling in excitatory neurons drives epilepsy progression by silencing synaptic plasticity and neuroinflammation genes, using mice with neuron-specific STAT3 knockout in the intrahippocampal kainate model.
Martha Streng
University of Minnesota, MN·Neuroscience·Early-career
Use mesoscale calcium imaging of the cerebellar cortex in mice to determine how chronic, spontaneous seizures from the hippocampus alter cerebellar activity.
The school
Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.
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