# The role of Brain-specific angiogenesis inhibitor 2 (BAI2) in synaptic structural organization and functional dynamics

> **NIH NIH F99** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2024 · $42,972

## Abstract

PROJECT SUMMARY
Excitatory ionotropic synapses and their associated dendritic spines play critical roles in fundamental
information processing within the brain. The development and morphology of these synapses are highly
functionally relevant; previous studies have established that patients with many different neurodevelopmental,
neurodegenerative, and neuropsychiatric conditions are clinically defined by synaptopathies. Synaptopathies,
or disease at the level of the synapse, includes inappropriate loss of synapses and spines, enhanced or
lowered synapse and spine development, and aberrations to the synaptic structure that leads to dysfunctional
signaling. The Brain-specific angiogenesis inhibitor (BAI) subfamily of neuronal adhesion G-protein coupled
receptors (aGPCRs) are a three-member postsynaptic family of receptors predicted to form trans-synaptic
complexes to direct synaptogenesis and synapse structural development. BAI2 is the least studied of these
proteins, with no established role in neuronal or synaptic development. BAI2 also appears to be the most
functionally non-redundant member of the BAI family. Though whole exome data from human patients with
autism spectrum disorder, schizophrenia, and bipolar disorder suggests all BAI proteins are implicated in these
conditions, BAI2 does not bind the same presynaptic proteins as BAI1 and BAI3. Furthermore, a gain-of-
function mutation to BAI2 is the putative cause of a rare spastic paraparesis condition in humans, and loss-of-
function mutations are associated with hyperactive behavior in mice. Addressing the fundamental role and
molecular mechanism of BAI2 thus can help us understand both basic synapse development, and potentially
inform future studies into treatments of psychiatric and central nervous system-derived motor disorders. To this
end, my data on BAI2 suggests that the protein localizes to the PSD and promotes both pre- and postsynaptic
development. I propose to further define the role of BAI2 in synapse and spine development by delineating the
functional domains that regulate synapse development (Aim 1.1), quantifying nanostructural changes to
synaptic structures (Aim 1.2), and describing functional deficits (Aim 1.3) induced by loss of BAI2. In the future,
I plan to pursue a postdoctoral position investigating real-time changes to excitatory and inhibitory synaptic
nanodomains and signaling in baseline, plasticity, and disease conditions (Aim 2).

## Key facts

- **NIH application ID:** 11075686
- **Project number:** 1F99NS141387-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Christina Meyer
- **Activity code:** F99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $42,972
- **Award type:** 1
- **Project period:** 2024-09-15 → 2026-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11075686

## Citation

> US National Institutes of Health, RePORTER application 11075686, The role of Brain-specific angiogenesis inhibitor 2 (BAI2) in synaptic structural organization and functional dynamics (1F99NS141387-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/11075686. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*