title: Prolactin response to formalin is related to the acute nociceptive response and it is attenuated by combined application of different stressors.
abstract: Subcutaneous injection of diluted formalin (0.2 ml of 4% solution/100 g BW) can influence the increase of plasma epinephrine levels in rats exposed to exteroceptive (handling, immobilization), as well as to interoceptive stressors (insulin-induced hypoglycemia), without having any effect on norepinephrine release. In the present studies, the effect of the above-mentioned stressors has been investigated on formalin-induced prolactin (PRL) and corticosterone secretion. Administrations of formalin via chronically implanted subcutaneous cannula into the hind limb without handling induce an immediate increase in both plasma PRL and corticosterone levels. While PRL concentration reaches its peak value within 5 min then returns to the basal level by the end of the 30th min, corticosterone level also starts to rise immediately after formalin administration reaching its highest concentration within 15-30 min, but it remains at this high level during the next 60 min, then it declines and returns to the pre-injection level. Application of formalin to animals exposed to different heterotypic stressors (like handling or insulin-induced hypoglycemia) produces an attenuated PRL response, while plasma corticosterone levels induced by the same nociceptive component remained unchanged. Combinations of formalin injection with immobilization also show an attenuated PRL response. The present data indicate that plasma PRL response to formalin is related to its acute nociceptive phase, and application of different stressors prior to formalin injection significantly attenuate plasma PRL levels, while it does not influence corticosterone responses.
authors.affiliation: Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.
authors.forename: Boris
authors.initials: B
authors.lastname: Mravec
authors.forename: Ibolya
authors.initials: I
authors.lastname: Bodnár
authors.forename: Andrej
authors.initials: A
authors.lastname: Tillinger
authors.forename: Gabriella
authors.initials: G
authors.lastname: Uhereczky
authors.forename: Richard
authors.initials: R
authors.lastname: Kvetnansky
authors.forename: Miklós
authors.initials: M
authors.lastname: Palkovits
authors.forename: György M
authors.initials: GM
authors.lastname: Nagy
mesh_terms: D000208:Acute Disease; D000818:Animals; D003345:Corticosterone / Q000097:blood; D005557:Formaldehyde / Q000494:pharmacology; D006234:Handling, Psychological; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced; D007004:Hypoglycemic Agents; D007279:Injections, Subcutaneous; D007328:Insulin; D008297:Male; D009619:Nociceptors / Q000502:physiology*; D010146:Pain / Q000097:blood* / Q000503:physiopathology; D010147:Pain Measurement; D011388:Prolactin / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000097:blood* / Q000503:physiopathology
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D005557:Formaldehyde; D011388:Prolactin; D003345:Corticosterone