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Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
Published on: January 21, 2020
Endogenous prolactin generated during peripheral inflammation contributes to thermal hyperalgesia.
Phoebe E Scotland1, Mayur Patil, Sergei Belugin
1Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
The European Journal of Neuroscience
|July 23, 2011
Summary
Inflammation releases prolactin (PRL) in rats, acting as a pain mediator differently in females and males. This study explores PRL
Area of Science:
- Neuroendocrinology
- Pain Research
- Inflammation Biology
Background:
- Prolactin (PRL) is a hormone and neuromodulator known to sensitize TRPV1 responses.
- The role of endogenous PRL in peripheral inflammation and its sex-dependent effects on pain are not well understood.
- PRL is found in peripheral tissues, including nerve fibers and immune cells, suggesting a local role.
Purpose of the Study:
- To investigate inflammation-induced release of endogenous PRL in female and male rats.
- To determine if endogenous PRL acts as a sex-dependent inflammatory mediator of thermal hyperalgesia.
Main Methods:
- Induction of peripheral inflammation using complete Freund's adjuvant (CFA) in female (OVX-E) and male rats.
- Measurement of PRL levels in hindpaws and plasma.
- Assessment of thermal hyperalgesia using a prolactin receptor (PRL-R) antagonist (Δ1-9-G129R-hPRL).
Main Results:
- CFA stimulated peripheral PRL release within 6-48 hours in both female and male rats, but not systemic release.
- The PRL-R antagonist partially reversed PRL-induced sensitization of capsaicin responses in sensory neurons.
- PRL contributed to inflammatory thermal hyperalgesia in females at 6 hours and in males at 24 hours post-CFA.
Conclusions:
- Inflammation causes the accumulation of endogenous PRL in peripheral tissues of both sexes.
- Endogenous PRL functions as an inflammatory mediator of thermal hyperalgesia in a sex- and time-dependent manner.
- These findings highlight a novel role for PRL in sex-specific inflammatory pain pathways.
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