ArticleNeuropsychiatric disease and treatment2016
cAMP/PKA/CREB/GLT1 signaling involved in the antidepressant-like effects of phosphodiesterase 4D inhibitor (GEBR-7b) in rats.
Article in Neuropsychiatric disease and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 25 citations in OpenAlex.
- PDE4D: A Multipurpose Pharmacological Target.International journal of molecular sciences · 2024Review
- Astroglial Dysfunctions in Mood Disorders and Rodent Stress Models: Consequences on Behavior and Potential as Treatment Target.International journal of molecular sciences · 2024Review
- Astrocytic Calcium and cAMP in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- EAAT2 as a Research Target in Bipolar Disorder and Unipolar Depression: A Systematic Review.Molecular neuropsychiatry · 2020Review
- Understanding PDE4's function in Alzheimer's disease; a target for novel therapeutic approaches.Biochemical Society transactions · 2019Review
- Effects of opioids on the parental brain in health and disease.Frontiers in neuroendocrinology · 2019Review
- The Astrocytic cAMP Pathway in Health and Disease.International journal of molecular sciences · 2019Review
- Glibenclamide Enhances the Therapeutic Benefits of Early Hypothermia after Severe Stroke in Rats.Aging and disease · 2018Article
- Melatonin Promotes Brain-Derived Neurotrophic Factor (BDNF) Expression and Anti-Apoptotic Effects in Neonatal Hemolytic Hyperbilirubinemia via a Phospholipase (PLC)-Mediated Mechanism.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Neural Plasticity Associated with Hippocampal PKA-CREB and NMDA Signaling Is Involved in the Antidepressant Effect of Repeated Low Dose of Yueju Pill on Chronic Mouse Model of Learned Helplessness.Neural plasticity · 2017Article
- The cyclic AMP signaling pathway: Exploring targets for successful drug discovery (Review).Molecular medicine reports · 2016Review
- Transcriptional Regulation of Glutamate Transporters: From Extracellular Signals to Transcription Factors.Advances in pharmacology (San Diego, Calif.) · 2016Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesGEBR-7b, a potential phosphodiesterase 4D inhibitor, has been shown to have memory-enhancing effects in rodents. However, it is still unknown whether GEBR-7b also has the antidepressant-like effects in rats. Herein, we examined the potential of GEBR-7b to attenuate depression-like behaviors in the rat model of depression induced by chronic unpredictable stress (CUS). Next, we also investigated the alterations of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA) catalytic subunit (PKAca), cAMP response element-binding (CREB), and glutamate transporter 1 (GLT1) levels produced by GEBR-7b in the rats model of depression.
methodsEffects of GEBR-7b on CUS (35 days)-induced depression-like behaviors were examined by measuring immobility time in the forced swimming test (FST). Hippocampal cAMP levels were examined by enzyme-linked immunosorbent assay, whereas PKAca, phosphorylation of CREB (pCREB), CREB, and GLT1 in the hippocampus of rats were subjected to Western blot analysis.
resultsCUS exposure caused a depression-like behavior evidenced by the increased immobility time in FST. Depression-like behavior induced by CUS was accompanied by a significant increased GLT, decreased cAMP, PKAca, pCREB activities in hippocampus. However, repeated GEBR-7b administration significantly reversed CUS-induced depression-like behavior and changes of cAMP/PKA/CREB/GLT1 signaling. No alteration was observed in locomotor activity in open field test.
conclusionThese findings indicate that GEBR-7b reversed the depression-like behaviors induced by CUS in rats, which is at least in part mediated by modulating cAMP, PKAca, pCREB, and GLT1 levels in the hippocampus of rats, supporting its neuroprotective potential against behavioral and biochemical dysfunctions induced by CUS.
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