How sensory experience changes inhibitory brain cells in the sensory cortex
Sensory regulation of interneuron intrinsic excitability in sensorycortex
This project looks at how brief changes in sensory input alter key inhibitory brain cells, to help explain circuit problems seen in autism.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California Berkeley NIH-funded |
| Lab location | 1 site (Berkeley, United States) |
| Project ID | NIH-11286785 on NIH RePORTER |
What this research studies
From my perspective, researchers are using mouse models to see how short periods of sensory change (for example, reduced touch) rapidly change the excitability of inhibitory interneurons in the brain’s sensory cortex. They focus on two classes of interneurons (parvalbumin/PV and somatostatin/SST cells) and examine how changes in ion channel activity, especially Kv1 potassium currents, affect those cells' firing. The team combines protein and gene-mapping methods (immunohistochemistry, qHCR-FISH, and single-nucleus RNA sequencing) with pharmacological and genetic tools to identify the signaling pathways involved. They will test whether failures in this rapid intrinsic plasticity contribute to inhibitory circuit problems linked to autistic disorder.
Who could benefit from this research
Good fit: People with autistic disorder and their caregivers are the population most likely to benefit conceptually, though the project uses animal models rather than enrolling patients.
Not a fit: People without autism or whose conditions do not involve cortical inhibitory circuit dysfunction are unlikely to receive direct benefit from this specific project.
Why it matters
Potential benefit: If successful, the work could identify molecular targets to help restore inhibitory circuit balance and guide new therapies for autism.
How similar studies have performed: Prior animal studies have shown rapid intrinsic plasticity in PV and SST interneurons and implicated Kv1 channels, but applying these mechanisms to explain autism-related circuit dysfunction is a newer direction.
Where this research is happening
Berkeley, United States
- University of California Berkeley — Berkeley, United States (Active)
Researchers
- Principal investigator: Feldman, Daniel — University of California Berkeley
- Study coordinator: Feldman, Daniel
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.