Blockade of Astrocytic Glutamate Uptake in the Prefrontal Cortex Induces Anhedonia
Open accessAbstract
Major depression is associated with both dysregulated glutamatergic neurotransmission and fewer astrocytes in limbic areas including the prefrontal cortex (PFC). These deficits may be functionally related. Notably, astrocytes regulate glutamate levels by removing glutamate from the synapse via the glutamate transporter (GLT-1). Previously, we demonstrated that central blockade of GLT-1 induces anhedonia and c-Fos expression in the PFC. Given the role of the PFC in regulating mood, we hypothesized that GLT-1 blockade in the PFC alone would be sufficient to induce anhedonia in rats. We microinjected the GLT-1 inhibitor, dihydrokainic acid (DHK), into the PFC and examined the effects on mood using intracranial self-stimulation (ICSS). At lower doses, intra-PFC DHK produced modest increases in ICSS thresholds, reflecting a depressive-like effect. At higher doses, intra-PFC DHK resulted in cessation of responding. We conducted further tests to clarify whether this total cessation of responding was related to an anhedonic state (tested by sucrose intake), a nonspecific result of motor impairment (measured by the tape test), or seizure activity (measured with electroencephalogram (EEG)). The highest dose of DHK increased latency to begin drinking without altering total sucrose intake. Furthermore, neither motor impairment nor evidence of seizure activity was observed in the tape test or EEG recordings. A decrease in reward value followed by complete cessation of ICSS responding suggests an anhedonic-like effect of intra-PFC DHK; a conclusion that was substantiated by an increased latency to begin sucrose drinking. Overall, these results suggest that blockade of astrocytic glutamate uptake in the PFC is sufficient to produce anhedonia, a core symptom of depression.
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Increasing the excitability of ILc by blockade of the glutamate transporter (GLT1) had an anhedonia-like effect, including an increase in the latency to drink sucrose and an increased threshold for intracranial self-stimulation.
“For example, increasing the excitability of ILc by blockade of the glutamate transporter (GLT1) had an anhedonia-like effect, including an increase in the latency to drink sucrose and an increased threshold for intracranial self-stimulation [140].”
From Prefrontal cortex and depression (2022) · cites this paper as [140]
The Discussion reports that intra-PFC GLT-1 blockade increased ICSS thresholds and latency to begin drinking sucrose, consistent with an anhedonic-like effect. Figure 1 places the injections in the infralimbic PFC. The paper suggests that increased infralimbic activity could produce such effects, but it does not establish that the blockade increased ILc excitability. (LLM, conf=0.84)
Experimental — accuracy not yet measuredReduced glutamate clearance, leading to greater glutamate accumulation in the medial prefrontal cortex, has been shown to produce anhedonic behaviors.
“reduced glutamate clearance (and thus enhanced accumulation of glutamate in the mPFC) has been shown to produce anhedonic behaviors (126).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [126]
In rodents, acute exposure to stress via restraint or swimming test procedures increases glutamate production, particularly in hippocampus and prefrontal cortex.
“In rodents, acute exposure to stress via restraint or swimming test procedures, increases glutamate production, particularly in hippocampus and prefrontal cortex153-155.”
From Dysregulation of adult hippocampal neuroplasticity in major depression: Pathogenesis and therapeutic implications (2022) · cites this paper as [154]
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- Authors
- John, C. S., Smith, K. L., Van'T Veer, A., Gompf, H. S., Carlezon, W. A., Cohen, B. M., Öngür, D., & Bechtholt-Gompf, A. J.
- Affiliations
- Harvard University (US)
- Venue
- Neuropsychopharmacology
- Published
- 2012-06-27
- Volume
- 37
- Issue
- 11
- Pages
- 2467-2475
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3442341
- OpenAlex
- W1993860176
- Cited by
- 136
- References
- 62
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 10 · 2023: 8 · 2022: 14 · 2021: 7 · 2020: 8 · 2019: 12 · 2018: 7 · 2017: 8 · 2016: 8 · 2015: 18 · 2014: 11 · 2013: 7 · 2012: 1
- FWCI
- 4.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression (MH063266)
- National Institutes of Health (5r01mh063266-25)
- National Institute of Mental Health (MH063266, R01-MH063266, R03MH087695, MH087695, T32MH020017)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- anhedonia, major depressive disorder, astrocytes, glutamate uptake, GLT-1, dihydrokainic acid, prefrontal cortex, glutamatergic neurotransmission, intracranial self-stimulation, reward value, sucrose intake, c-fos
- MeSH terms
- Analysis of Variance, Animals, Astrocytes, Disease Models, Animal, Dose-Response Relationship, Drug, Electric Stimulation, Electroencephalography, Electromyography, Food Preferences, Kainic Acid, Male, Psychomotor Performance, Self Stimulation, Sucrose, Rats, Sprague-Dawley, Prefrontal Cortex, Excitatory Amino Acid Agonists, Glutamic Acid, Rats, Brain Waves, Anhedonia
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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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