GPCRs are notoriously low in abundance and can be difficult to detect at the protein level. Yet, they represent one of the most successfully targeted classes of cell-surface receptors in medicine, underscoring the importance of understanding which tissues and cell types express individual GPCRs.

We use transgenic mouse models with fluorescently tagged GPCRs to visualize receptor expression and localization in neurons. These models allow us to determine where GPCRs are expressed and to track dynamic changes in receptor localization and trafficking in neuronal preparations from these animals.

GPCRs are dynamically regulated by networks of proteins that control their delivery to and removal from the cell surface. Following activation by drugs or other signaling molecules, GPCRs can be removed from the plasma membrane and trafficked to distinct intracellular compartments, where they may continue to signal or be recycled or degraded.

The protein interactions that govern GPCR trafficking are therefore critical regulators of receptor function and cellular responses. By identifying the molecular mechanisms that control receptor delivery, removal, and intracellular trafficking, we aim to uncover new opportunities for selectively targeting GPCR signaling and developing improved therapeutic strategies.

Like most cells in the body, neurons possess a dynamic organelle known as the primary cilium. Although the primary cilium is well established as a specialized signaling compartment during development, its role in GPCR-mediated neuromodulation and signaling in mature neurons is an emerging area of research.

Our laboratory is actively investigating how primary cilia contribute to mature neuronal signaling, with a particular focus on GPCR-mediated signaling and the function of synaptic proteins localized to this unique and intriguing cellular compartment.