# Shared Mechanisms of Absence Epilepsy and Selective Attention

> **NIH NIH F32** · STANFORD UNIVERSITY · 2021 · $35,229

## Abstract

PROJECT SUMMARY
The reticular thalamus (RT) is a thin shell of GABAergic neurons that provides a lateral border around the
dorsal thalamus. Its axons synapse into primary thalamic relay nuclei supplying both feedforward and feedback
inhibition from the cortex and thalamus respectively. The RT is topographically organized such that it primarily
receives inputs of specific sensory modalities (e.g., vision, somatosensation, and audition) and can regulate
the activity of the thalamic neurons within that same relay. In particular, the somatosensory RT has been
implicated in the generation of absence seizures, brief periods of unconsciousness accompanied by a lapse in
motor function. Interestingly, other RT regions have been linked to selective attention, an important feature of
cognitive flexibility that is often disrupted in epileptic individuals. Under normal conditions, RT output
suppresses incoming distracting information by selectively inhibiting thalamic subregions that represent
information irrelevant in the current context for guiding appropriate behavior. Importantly, changes in top-down
regulation of the RT can disrupt normal RT activation patterns and impair the sensory gating necessary for
selective attention tasks. This suggests that changes in synaptic regulation of RT neurons can interrupt normal
RT activity on which selective attention depends. Our lab has recently shown that in mice with disrupted
expression of the voltage gated sodium channel, Nav1.6 (Scn8a+/-), reductions in somatosensory intra-RT
synaptic inhibition lead to pathological thalamocortical (TC) oscillations and frequent absence seizures. We
hypothesize that this same loss of intra-RT inhibition may occur broadly throughout the RT and lead to
attentional deficits in the Scn8a+/- model of absence epilepsy. A loss of RT-RT inhibition would reduce local
inhibition of RT cells, thus increasing overall RT activity, and decreasing the sensory throughput of inhibited
thalamic neurons. Using a multi-level approach including behavior, circuit, and single-cell analysis we will
address the fundamental question of whether there is widespread dysregulation of the RT in absence epilepsy.
Further, our results will enable us to determine whether a common set of RT cells is responsible for both
absence seizure generation and attentional impairments, highlighting shared mechanisms in both pathologies.

## Key facts

- **NIH application ID:** 10410036
- **Project number:** 3F32NS112764-02S1
- **Recipient organization:** STANFORD UNIVERSITY
- **Principal Investigator:** Brielle Ferguson
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $35,229
- **Award type:** 3
- **Project period:** 2021-06-01 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10410036

## Citation

> US National Institutes of Health, RePORTER application 10410036, Shared Mechanisms of Absence Epilepsy and Selective Attention (3F32NS112764-02S1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10410036. Licensed CC0.

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