# Investigating a mammalian inhibitory circuit for distractor suppression

> **NIH NIH F32** · JOHNS HOPKINS UNIVERSITY · 2021 · $66,390

## Abstract

Project Summary
Operating in complex environments, animals selectively process the most important (highest ‘priority’) stimulus
to guide behavior, while ignoring distracting stimuli at all other spatial locations. This ability, called spatial
selective attention, is critical for behavior and even survival. Converging evidence from primates and birds has
implicated the midbrain superior colliculus (SC in mammals; optic tectum – OT in birds)2,3 as a critical node for
the control of spatial attention when multiple competing targets are present. Studies also show that competitive
interactions among stimuli are encoded in the intermediate and deep layers of the SC (SCid; OTid in birds), with
stimulus competition manifesting as the suppression of the responses of each stimulus by competing stimuli.
Additionally, recent work in birds (by the Mysore Lab and others) has revealed that such competitive interactions
within the OTid are controlled by a group of parvalbumin positive (PV+) inhibitory neurons in the avian midbrain
tegmentum called nucleus isthmi pars magnocellularis (Imc). The Imc connects with the OT in a specialized
manner and drives long-range suppression of OTid responses by competing stimuli 4-6, leading to the suggestion
that, in birds, the Imc may serve to suppress distracters and facilitate the selection of the target of spatial
attention1,5,7. However, not only is the inhibitory source for similar long-range competitive interactions in the
mammalian SCid unknown, but also the specific circuit mechanisms underlying distractor suppression and target
selection for spatial selective attention in any animal are yet to be discovered11. Here, I will address these
questions in mice by investigating the function of the peri-parabigeminal lateral tegmental nucleus (pLTN), which
is thought to be mammalian homolog of the Imc1,12,13. Specifically, in Aim 1, I will use focal cell type-specific
optogenetic manipulations of the PV+ pLTN, coupled with SCid electrophysiology in head-fixed, passive-viewing
mice to test if pLTN neurons are responsible for controlling competitive interactions in the SCid. I predict that
silencing pLTN neurons will abolish stimulus competition within SCid. Next, in Aim 2, I will leverage a new
behavioral paradigm developed in the lab for the study of primate-like visuospatial selective attention in freely
behaving mice14, and using cell-type specific optogenetic manipulation, investigate the causal role of pLTN in
distractor suppression and target selection. I predict that optogenetic activation of the portion of pLTN encoding
the target will cause hyper-attention (resistance to distractibility), whereas optogenetic inactivation of the portion
of the pLTN encoding the target with cause hyper-distractibility. These results will reveal, for the first time, neural
circuit mechanisms for the control of distracter suppression for spatial attention, and can shed light on the circuit
basis of the debilitating attentional dysfunctio...

## Key facts

- **NIH application ID:** 10235659
- **Project number:** 1F32EY032776-01
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Ninad B Kothari
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $66,390
- **Award type:** 1
- **Project period:** 2021-05-01 → 2023-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10235659

## Citation

> US National Institutes of Health, RePORTER application 10235659, Investigating a mammalian inhibitory circuit for distractor suppression (1F32EY032776-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10235659. Licensed CC0.

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