Publication

The activation of D-2 and D-3 receptor subtypes inhibits pathways mediating primary afferent depolarization (PAD) in the mouse spinal cord

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Last modified
  • 09/11/2025
Type of Material
Authors
    Jonathan J Milla-Cruz, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico NacionalElvia Mena-Avila, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico NacionalJorge R Calvo, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico NacionalShawn Hochman, Emory UniversityCarlos M Villalon, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico NacionalJorge N Quevedo, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional
Language
  • English
Date
  • 2020-09-25
Publisher
  • ELSEVIER IRELAND LTD
Publication Version
Copyright Statement
  • © 2020 Elsevier B.V. All rights reserved.
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 736
Start Page
  • 135257
End Page
  • 135257
Grant/Funding Information
  • This work was supported by the following grants: CONACyT 59873 (J.Q.), México (http://conacyt.gob.mx) and National Institutes of Health (NIH) NS-065949 (S.H), USA (http://nih.gov)
Abstract
  • Somatosensory information can be modulated at the spinal cord level by primary afferent depolarization (PAD), known to produce presynaptic inhibition (PSI) by decreasing neurotransmitter release through the activation of presynaptic ionotropic receptors. Descending monoaminergic systems also modulate somatosensory processing. We investigated the role of D1-like and D2-like receptors on pathways mediating PAD in the hemisected spinal cord of neonatal mice. We recorded low-threshold evoked dorsal root potentials (DRPs) and population monosynaptic responses as extracellular field potentials (EFPs). We used a paired-pulse conditioning-test protocol to assess homosynaptic and heterosynaptic depression of evoked EFPs to discriminate between dopaminergic effects on afferent synaptic efficacy and/or on pathways mediating PAD, respectively. DA (10 μM) depressed low-threshold evoked DRPs by 43 %, with no effect on EFPs. These depressant effects on DRPs were mimicked by the D2-like receptor agonist quinpirole (35 %). Moreover, by using selective antagonists at D2-like receptors (encompassing the D2, D3, and D4 subtypes), we found that the D2 and D3 receptor subtypes participate in the quinpirole depressant inhibitory effects of pathways mediating PAD.
Author Notes
  • Jorge N. Quevedo, Departamento de Fisiología, Biofísica y Neurociencias, CINVESTAV del IPN, Av. IPN, 2508, Col. San Pedro Zacatenco, C.P. 07300, Mexico City, Mexico., Email: jquevedo@fisio.cinvestav.mx
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