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Prolactin fractions from lactating rats elicit effects upon sensory spinal cord cells of male rats.

Authors :
Mena F
González-Hernández A
Navarro N
Castilla A
Morales T
Rojas-Piloni G
Martínez-Lorenzana G
Condés-Lara M
Source :
Neuroscience [Neuroscience] 2013 Sep 17; Vol. 248, pp. 552-61. Date of Electronic Publication: 2013 Jul 02.
Publication Year :
2013

Abstract

Recently it has been suggested that the neurohormone prolactin (PRL) could act on the afferent nociceptive neurons. Indeed, PRL sensitizes transient receptor potential vanilloid 1 (TRPV1) channels present in nociceptive C-fibers and consequently reduces the pain threshold in a model of inflammatory pain. Accordingly, high plasma PRL levels in non-lactating females have been associated with several painful conditions (e.g. migraine). Paradoxically, an increase of PRL secretion during lactation induced a reduction in pain sensitivity. This difference could be attributed to the fact that PRL secreted from the adenopituitary (AP) is transformed into several molecular variants by the suckling stimulation. In order to test this hypothesis, the present study set out to investigate whether PRL from AP of suckled (S) or non-suckled (NS) lactating rats affects the activity of the male Wistar wide dynamic range (WDR) neurons. The WDR neurons are located in the dorsal horn of the spinal cord and receive input from the first-order neurons (Ab-, Ad- and C-fibers). Spinal administration of prolactin variant from NS rats (NS-PRL) or prolactin variant from S rats (S-PRL) had no effect on the neuronal activity of non-nociceptive Ab-fibers. However, the activities of nociceptive Ad-fibers and C-fibers were: (i) increased by NS-PRL and (ii) diminished by S-PRL. Either NS-PRL or S-PRL enhanced the post-discharge activity. Taken together, these results suggest that PRL from S or NS lactating rats could either facilitate or depress the nociceptive responses of spinal dorsal horn cells, depending on the physiological state of the rats.<br /> (Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.)

Details

Language :
English
ISSN :
1873-7544
Volume :
248
Database :
MEDLINE
Journal :
Neuroscience
Publication Type :
Academic Journal
Accession number :
23830906
Full Text :
https://doi.org/10.1016/j.neuroscience.2013.06.052