ArticleeNeuro
Neuregulin and Dopamine D4 Receptors Contribute Independently to Depotentiation of Schaffer Collateral LTP by Temperoammonic Path Stimulation.
Article in eNeuro. 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, 7 citations in OpenAlex.
- Inhibitory Neural Network's Impairments at Hippocampal CA1 LTP in an Aged Transgenic Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- On the Modulatory Roles of Neuregulins/ErbB Signaling on Synaptic Plasticity.International journal of molecular sciences · 2019Review
- Temperoammonic Stimulation Depotentiates Schaffer Collateral LTP via p38 MAPK Downstream of Adenosine A1 Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Cannabinoid disruption of learning mechanisms involved in reward processing.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
- Bidirectional modulation of hippocampal synaptic plasticity by Dopaminergic D4-receptors in the CA1 area of hippocampus.Scientific reports · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Prior studies have found that dopamine (DA), acting at D4 receptors, and neuregulin (NRG), likely acting at ErbB4 receptors, are involved in a form of depotentiation of long-term potentiation (LTP) at Schaffer collateral (SC) synapses in the hippocampus. Furthermore, DA and NRG actions are intertwined in that NRG induces DA release. We previously found that low-frequency stimulation (LFS) of temperoammonic (TA) inputs to area CA1 also depotentiates previously established SC LTP through a complex signaling pathway involving endocannabinoids, GABA, adenosine, and mitogen-activated protein kinases (MAPKs), but not glutamate. In the present studies, we found that TA-induced SC depotentiation in hippocampal slices from Sprague-Dawley albino rats also involves activation of both D4 receptors and NRG-activated ErbB receptors, but that the roles of these two modulator systems are independent with D4 receptor antagonism failing to alter chemical depotentiation by NRG1β. Furthermore, a selective D4 receptor agonist was unable to depotentiate SC LTP when administered alone, suggesting that D4 receptor activation is necessary but not sufficient for TA-induced SC depotentiation. Chemical depotentiation by NRG1β was inhibited by a Pan-ErbB antagonist and by picrotoxin (PTX), an antagonist of GABA-A receptors (GABA
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.