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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
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Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
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G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
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GPR3 is an immediate-early gene-like GPCR regulating CREB-dependent neuronal differentiation.

Shigeru Tanaka1, Fumiaki Ikawa1, Hiroko Shiraki1

  • 1Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.

Iscience
|March 2, 2026
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Summary

G protein-coupled receptor 3 (GPR3) acts as an immediate-early gene during neuronal differentiation, rapidly responding to nerve growth factor (NGF) and cAMP. Its induction influences NR4A signaling and synaptic vesicle development.

Keywords:
biological sciencescellular neurosciencemolecular neurosciencesystems neuroscience

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • The transcriptional regulation of G protein-coupled receptor 3 (GPR3), a constitutively active Gs-coupled receptor, during neuronal differentiation is not well understood.
  • Understanding GPR3's role is crucial for deciphering neuronal development pathways.

Purpose of the Study:

  • To investigate the transcriptional regulation of GPR3 during neuronal differentiation.
  • To elucidate the role of GPR3 in downstream signaling pathways and synaptic development.

Main Methods:

  • Utilized PC12 cells and primary cortical neurons.
  • Employed native elongating transcript-cap analysis of gene expression (NET-CAGE) to map transcription.
  • Investigated cAMP response elements (CREs) and transcription factor binding (p-CREB).
  • Performed gene deletion studies in primary neurons.

Main Results:

  • Identified GPR3 as an immediate-early gene transcript rapidly induced by NGF and cAMP.
  • Demonstrated cooperative mediation of transcription by five CREs, with p-CREB enrichment at the proximal -34 CRE.
  • Showed that early GPR3 induction enhances NR4A1-3 expression and promotes Synapsin1 (Syn1) transcription via an NR4A1-dependent mechanism.
  • Observed diminished NR4A1-3 and Syn1 upregulation and reduced SYN1-positive vesicle density in GPR3-deleted primary neurons.

Conclusions:

  • GPR3 functions as an activity-dependent cAMP amplifier.
  • GPR3 couples early CREB activation to transcriptional programs involving NR4A signaling.
  • GPR3 plays a significant role in presynaptic maturation during neuronal differentiation.