ArticleEpilepsia2017
Inherent vulnerabilities in monoaminergic pathways predict the emergence of depressive impairments in an animal model of chronic epilepsy.
Article in Epilepsia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- Sex differences in resilience at puberty depend upon divergent effects of a stress steroid at α4βδ GABABrain research · 2025Article
- Impaired Response to Mismatch Novelty in the LiBiomedicines · 2024Article
- Reduced serum neurotrophic factors and monoamine neurotransmitters in epilepsy patients with comorbid depression.Frontiers in neurology · 2024Article
- Stress and Epilepsy: Towards Understanding of Neurobiological Mechanisms for Better Management.eNeuro · 2023Review
- The diverse role of the raphe 5-HTergic systems in epilepsy.Acta pharmacologica Sinica · 2022Review
- Impact of Melatonin Deficit on Emotional Status and Oxidative Stress-Induced Changes in Sphingomyelin and Cholesterol Level in Young Adult, Mature, and Aged Rats.International journal of molecular sciences · 2022Article
- Depression and Anxiety in the Epilepsies: from Bench to Bedside.Current neurology and neuroscience reports · 2020Review
- Abnormal Hippocampal Melatoninergic System: A Potential Link between Absence Epilepsy and Depression-Like Behavior in WAG/Rij Rats?International journal of molecular sciences · 2018Article
- Review
- Article
Corrections and comments
- Erratum issuedErratum.2018
Authors and funding
4 authors.
Funding
Abstract
The objective was to determine whether the depression comorbid with epilepsy could be predicted based on inherent premorbid patterns of monoaminergic transmission. In male Wistar rats, despair-like and anhedonia-like behaviors were examined using forced swimming and taste preference tests, respectively. Serotonergic raphe nucleus (RN)-prefrontal cortex (PFC) and dopaminergic ventral tegmental area (VTA)-nucleus accumbens (NAcc) pathways were interrogated by fast scan cyclic voltammetry (FSCV). The assays were performed before and 2 months after pilocarpine status epilepticus. In a subset of naive rats, FSCV, coupled with the intensity-dependent stimulation paradigm, detected specific deviations in each pathway (six rats for RN-PFC and seven rats for VTA-NAcc, with overlap in two, of 19 total subjects) in the absence of behavioral impairments. During epilepsy, animals with preexisting deviations in RN-PFC invariably developed despair, and rats with deviations in VTA-NAcc developed anhedonia. Serotonergic and dopaminergic pathways, respectively, showed signs of explicit deterioration. We suggest that epilepsy triggers decompensations in the already vulnerable depression-relevant neuronal circuits, which culminate in depression. The established connection between the identified specific signatures in monoamine transmission in naive rats and specific symptoms of epilepsy-associated depression may help in understanding causes of comorbidity and in developing its early biomarkers.
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Registered trials
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