ArticleThe international journal of neuropsychopharmacology2015
Dysfunctional inhibitory mechanisms in locus coeruleus neurons of the wistar kyoto rat.
Article in The international journal of neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- The Wistar-Kyoto rat as a model relevant to inattentive ADHD: substrain variability and affective comorbidity.Pharmacological reports : PR · 2026Review
- A Diet Enriched withInternational journal of molecular sciences · 2023Article
- Opioid Activity in the Locus Coeruleus Is Modulated by Chronic Neuropathic Pain.Molecular neurobiology · 2019Article
- Differential behavioral sensitivity to carbon dioxide (CONeuroscience · 2017Article
- Neuronal correlates of depression.Cellular and molecular life sciences : CMLS · 2015Review
- The role of the locus coeruleus in the generation of pathological anxiety.Brain and neuroscience advancesReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe noradrenergic nucleus locus coeruleus (LC) has functional relevance in several psychopathologies such as stress, anxiety, and depression. In addition to glutamatergic and GABAergic synaptic inputs, the activation of somatodendritic α2-adrenoceptors is the main responsible for LC activity regulation. The Wistar Kyoto (WKY) rat exhibits depressive- and anxiety-like behaviors and hyperresponse to stressors. Thus, the goal of the present study was to investigate in vitro the sensitivity of α2-adrenoceptors, as well as the glutamatergic and GABAergic synaptic activity on LC neurons of the WKY strain.
methodsFor that purpose patch-clamp whole-cell recordings were done in LC slices.
resultsThe α2-adrenoceptors of LC neurons from WKY rats were less sensitive to the effect induced by the agonist UK 14 304 as compared to that recorded in the Wistar (Wis) control strain. In addition, the GABAergic input to LC neurons of WKY rats was significantly modified compared to that in Wis rats, since the amplitude of spontaneous GABAergic postsynaptic currents was reduced and the half-width increased. On the contrary, no significant alterations were detected regarding glutamatergic input to LC neurons between rat strains.
conclusionsThese results point out that in WKY rats the inhibitory control exerted by α2-adrenoceptors and GABAergic input onto LC neurons is dysregulated. Overall, this study supports in this animal model the hypothesis that claims an imbalance between the glutamatergic-GABAergic systems as a key factor in the pathophysiology of depression.
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