ArticleFrontiers in cellular neuroscience2017
Dichotomous Effects of Mu Opioid Receptor Activation on Striatal Low-Threshold Spike Interneurons.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Ventral tegmental area glutamate neurons establish a mu-opioid receptor gated circuit to mesolimbic dopamine neurons and regulate opioid-seeking behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Characterization and mu opioid receptor sensitivity of neuropeptide Y interneurons in the mouse nucleus accumbens.Neuropharmacology · 2022Article
- Chronic stress increases susceptibility to food addiction by increasing the levels of DR2 and MOR in the nucleus accumbens.Neuropsychiatric disease and treatment · 2019Article
- Merging the Pathophysiology and Pharmacotherapy of Tics.Tremor and other hyperkinetic movements (New York, N.Y.) · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Striatal low-threshold spike interneurons (LTSIs) are tonically active neurons that express GABA and nitric oxide synthase and are involved in information processing as well as neurovascular coupling. While mu opioid receptors (MORs) and their ligand encephalin are prominent in the striatum, their action on LTSIs has not been investigated. We addressed this issue carrying out whole-cell recordings in transgenic mice in which the NPY-expressing neurons are marked with green fluorescent protein (GFP). The MOR agonist (D-Ala(2), N-MePhe(4), Gly-ol)-enkephalin (DAMGO) produced dual effects on subpopulations of LTSIs. DAMGO caused inhibitory effects, accompanied by decreases of spontaneous firing, in 62% of LTSIs, while depolarizing effects (accompanied by an increase in spontaneous firing) were observed in 23% of LTSIs tested. The dual effects of DAMGO persisted in the presence of tetrodotoxin (TTX), a sodium channel blocker or in the presence of the nicotinic acetylcholine receptor antagonist mecamylamine. However, in the presence of either the GABA
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