Gq-DREADD Selectively Initiates Glial Glutamate Release and Inhibits Cue-induced Cocaine Seeking
Open accessAbstract
Background Glial cells of the central nervous system directly influence neuronal activity by releasing neuroactive small molecules, including glutamate. Long-lasting cocaine-induced reductions in extracellular glutamate in the nucleus accumbens core (NAcore) affect synaptic plasticity responsible for relapse vulnerability.Methods We transduced NAcore astrocytes with an adeno-associated virus vector expressing hM3D designer receptor exclusively activated by a designer drug (DREADD) under control of the glial fibrillary acidic protein promoter in 62 male Sprague Dawley rats, 4 dominant-negative soluble N-ethylmaleimide-sensitive factor attachment protein receptor mice, and 4 wild-type littermates. Using glutamate biosensors, we measured NAcore glutamate levels following intracranial or systemic administration of clozapine N-oxide (CNO) and tested the ability of systemic CNO to inhibit reinstated cocaine or sucrose seeking following self-administration and extinction training.Results Administration of CNO in glial fibrillary acidic protein-hM3D-DREADD transfected animals increased NAcore extracellular glutamate levels in vivo. The glial origin of released glutamate was validated by an absence of CNO-mediated release in mice expressing a dominant-negative soluble N-ethylmaleimide-sensitive factor attachment protein receptor variant in glia. Also, CNO-mediated release was relatively insensitive to N-type calcium channel blockade. Systemic administration of CNO inhibited cue-induced reinstatement of cocaine seeking in rats extinguished from cocaine but not sucrose self-administration. The capacity to inhibit reinstated cocaine seeking was prevented by systemic administration of the group II metabotropic glutamate receptor antagonist LY341495.Conclusions DREADD-mediated glutamate gliotransmission inhibited cue-induced reinstatement of cocaine seeking by stimulating release-regulating group II metabotropic glutamate receptor autoreceptors to inhibit cue-induced synaptic glutamate spillover.
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Gq-DREADD expression remained restricted to astrocytes based on co-localization with GFAP and morphology consistent with astrocytic immunoreactivity patterns.
“Histological visualization with the fluorescent reporter mCherry confirmed that Gq-DREADD expression remained restricted to astrocytes based on their co-localization with the astrocyte marker GFAP (Figure 1C) and morphology consistent with astrocytic immunoreactivity patterns (Benediktsson et al., 2005;Bushong et al., 2002;Scofield et al., 2015).”
From Single-cell resolution analysis of the crosstalk between chemogenically activated astrocytes and microglia (2020) · cites this paper as Scofield et al., 2015
The Results section ('Astrocyte-specific Expression of Gq-DREADD') describes astrocyte-like morphology and apparent co-localization of viral HA with GFAP, supporting the basis for identifying astrocytic expression. It calls astrocyte-specific expression 'very likely,' however, and the Discussion says a minor neuronal contribution cannot be ruled out. The source therefore does not establish that expression was strictly restricted to astrocytes. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPrevious studies have expressed the Gq-DREADD specifically in astrocytes using the GFAP promotor and showed an increase in intracellular Ca2+ after activation with CNO.
“Previous studies have expressed the Gq-DREADD specifically in astrocytes using the GFAP promotor and showed an increase in intracellular Ca 2+ after activation with CNO (Agulhon et al., 2013;Bull et al., 2014;Scofield et al., 2015).”
From Single-cell resolution analysis of the crosstalk between chemogenically activated astrocytes and microglia (2020) · cites this paper as Scofield et al., 2015
The Results section, “Astrocyte-specific Expression of Gq-DREADD” (page unavailable), reports GFAP-driven Gq-DREADD expression in astrocytes. The paper measured CNO-induced glutamate release, not an increase in intracellular Ca2+; its calcium discussion cites a separate report and infers a role for internal calcium stores. Thus, this study does not itself show the claimed calcium increase. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThis is the first study to show transcriptional changes in glia that occur after long-term activation of astrocytes with the Gq-DREADD in an in vivo model.
“To the best of our knowledge, this is the first study to show transcriptional changes in glia that occur after long-term activation of astrocytes with the Gq-DREADD in an in vivo model.”
From Single-cell resolution analysis of the crosstalk between chemogenically activated astrocytes and microglia (2020) · cites this paper as Scofield et al., 2015
The Results sections on astrocyte-specific expression and Gq-DREADD activation describe an in vivo model in which Gq-DREADD was expressed and activated in astrocytes. They report glutamate release, not transcriptional changes after long-term activation. The 'first study' wording is the citing authors’ characterization of their own study, not a finding established by this source. (LLM, conf=0.85)
Experimental — accuracy not yet measuredNone of these previous studies looked at the effect of long-term Gq-DREADD-mediated activation on the transcriptome of astrocytes or other neighboring brain cells.
“However, none of these studies looked at the effect of long-term Gq-DREADD-mediated activation on the transcriptome of astrocytes or other neighboring brain cells.”
From Single-cell resolution analysis of the crosstalk between chemogenically activated astrocytes and microglia (2020) · cites this paper as Scofield et al., 2015
Because astrocytes influence glutamatergic transmission in the NAc, they could participate in cocaine-induced changes.
“As astrocytes influence glutamatergic transmission in the NAc 118, 119 , they could participate in these changes.”
From Astrocyte function from information processing to cognition and cognitive impairment (2019) · cites this paper as [119]
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“Previous studies have expressed the Gq-DREADD specifically in astrocytes using the GFAP promotor and showed an increase in intracellular Ca2+ after activation with CNO (Agulhon et al., 2013; Bull et al., 2014; Scofield et al., 2015).”
Background
- Authors
- Scofield, M. D., Boger, H. A., Smith, R. J., Li, H., Haydon, P. G., & Kalivas, P. W.
- Affiliations
- Medical University of South Carolina (US)
- Tufts University (US)
- Corresponding author
- Scofield, Michael D.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 78
- Issue
- 7
- Pages
- 441-451
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC4547911
- OpenAlex
- W2040937016
- Cited by
- 197
- References
- 65
- Citations by year
- 2026: 6 · 2025: 18 · 2024: 19 · 2023: 16 · 2022: 24 · 2021: 16 · 2020: 17 · 2019: 23 · 2018: 18 · 2017: 16 · 2016: 20 · 2015: 3
- FWCI
- 8.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R015369, DA003906)
- National Institute on Drug Abuse Training (T32 DA 7288-22)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cocaine seeking, cocaine reinstatement, nucleus accumbens core, astrocytes, clozapine-N-oxide, group II metabotropic glutamate receptors, LY341495, glutamate spillover, relapse vulnerability, glutamate biosensor
- MeSH terms
- Animals, Astrocytes, Central Nervous System Agents, Clozapine, Cocaine, Cues, Disease Models, Animal, Extinction, Psychological, Male, Mice, Transgenic, Nucleus Accumbens, Self Administration, Genetic Therapy, Rats, Sprague-Dawley, Receptors, Metabotropic Glutamate, Glutamic Acid, Dopamine Uptake Inhibitors, Dietary Sucrose, Cocaine-Related Disorders, Calcium Channels, N-Type, Receptors, G-Protein-Coupled, SNARE Proteins, Drug-Seeking Behavior
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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