Multiple Opioid Binding Sites

Itzhak, Yossef

doi:10.1007/978-1-60761-990-1_4

Cited by 20 publications

(13 citation statements)

References 134 publications

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“…A number of factors may account for the failure of beta-FNA to attenuate morphine-induced hypothermia. For example, social separation can induce hyperthermia in domestic fowl (Frohm & Wallnau, 1983;Sufka & Hughes, 1990b) (Goodman, Adler, & Pasternak, 1988;Itzhak, 1988;Tarn, 1989). Previous research demonstrated that delta receptors are only minimally involved in nociceptive processes (Tam, 1989).…”

Section: Methodsmentioning

confidence: 99%

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

Sufka

Hughes

Giordano

1991

Pharmacology Biochemistry and Behavior

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Sufka, Kenneth Joseph, "Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl " (1990 INFORMATION TO USERSThe most advanced technology has been used to photograph and reproduce this manuscript from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer.The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction.In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion.Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand corner and continuing from left to right in equal sections with small overlaps. Each original is also photographed in one exposure and is included in reduced form at the back of the book.Photographs included in the original manuscript have been reproduced xerographically in this copy. Higher quality 6" x 9" black and white photographic prints are available for any photographs or illustrations appearing in this copy for an additional charge. Contact UMI directly to order.

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Section: Methodsmentioning

confidence: 99%

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

Sufka

Hughes

Giordano

1991

Pharmacology Biochemistry and Behavior

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“…The binding characteristics of /I-cndorphin indicate that this peptide has affinity for all of thc well charactcrizcd reccptor subtypes (i.e. p, 6. ti) (14). In addition, autoradiographic studies support the concept that this peptidc binds to a unique receptor subtype.…”

Section: Discussionmentioning

confidence: 78%

“…The most widely accepted and best characterizcd receptor subtypes are the p, 6 and K sites (review in 14). Pasternak and colleagues have proposed two different subtypes of the p receptor termed pl and p2 (9,10,(15)(16)(17).…”

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confidence: 99%

The Role of the Mu₁ Opioid Receptor Subtype in the Regulation of Prolactin and Growth Hormone Secretion by Beta‐Endorphin in Female Rats: Studies with Naloxonazine

Janik

Callahan

Rabii

1992

J Neuroendocrinology

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The μ opioid receptor subtype has been reported to mediate the prolactin secretory response to opioids. This receptor subtype has been implicated in the morphine-induced prolactin increase, as well as the prolactin response to μ-specific opioid peptides. Subtypes of the μ receptor have been proposed and the μ(1) , site has been postulated as the receptor subtype involved in the morphine-induced prolactin secretory response. However, the role of this receptor subtype in mediating the endocrine effects of the endogenous opioid peptides has not been characterized. In order to determine the physiological significance of this receptor subtype, animals were pretreated with saline, WIN 44,441-3 (a μ, δ and κ antagonist) or naloxonazine (a μ(1) antagonist) followed by a stimulatory dose of morphine or β-endorphin. A dose response study for β-endorphin was conducted to determine the minimal stimulatory dose of β-endorphin on the prolactin and growth hormone (GH) secretory response. The dose response study indicated that β-endorphin is a more potent stimulus for prolactin release than for GH. A dose as low as 25 ng increased prolactin levels as much as 100-fold in both lactating and diestrous female rats. In contrast, 2.5 μg β-endorphin was required in order to consistently and significantly increase circulating levels of GH by 2- to 3-fold. WIN 44,441-3 antagonized the stimulatory effects of β-endorphin on both prolactin and GH secretion. Naloxonazine pretreatment abolished the morphine-induced prolactin secretory response, without affecting the GH increase in diestrous females. Naloxonazine also antagonized the prolactin response to β-endorphin in both lactating and diestrous females. In addition, it attenuated the GH secretory response but did not totally abolish it. These data indicate that β-endorphin elicits an increase in prolactin release through an opioid specific receptor which appears to be the μ(1) opioid receptor subtype. They further suggest that β-endorphin may increase GH levels, at least partially, via its action at this μ(1) site.

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“…We are confident that we are antagonizing 8-mediated effects in this dose range. The possibility that morphine increases prolactin secre tion through 8-sites as well as u-sites must be considered since morphine does have some affinity for the 8-site [ 15], K-sites also appear to be involved in the stimulatory effects of |l-endorphin on prolactin secretion. norBNI has been shown to be a specific K-receptor antagonist [31,46].…”

Section: Discussionmentioning

confidence: 99%

Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

Kehoe

Parman²,

Janik³

et al. 1993

Neuroendocrinology

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The prolactin secretory response to β-endorphin and the involvement of opiate receptor subtypes in this response was determined in both diestrous and postpartum, lactating female rats. The involvement of the µ-, δ- and/or ĸ-site was determined by administering specific antagonists for each of these sites prior to β-endorphin. β-Funaltrexamine (β-FNA, 1 or 5 µg) was administered to block µ-sites, ICI 154,129 (5,10 or 25 µg) blocked δ-sites and nor-binaltor-phimine (norBNI, 8 µg) blocked ĸ-sites. The ability of β-FNA and ICI 154, 129 to block prolactin secretion following morphine administration was also determined. A dose response study for β-endorphin indicated that β-endorphin, at doses as low as 25 ng, was a potent stimulus for prolactin release producing an increase in prolactin that mimicked the suckling-induced prolactin increase. In addition, all three antagonists were capable of antagonizing the stimulatory effect of β-endorphin in both diestrous and postpartum female rats. These results indicate that β-endorphin is a potent stimulus for prolactin secretion and that these three opiate receptor subtypes interact to produce its stimulatory effect on prolactin release.

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Multiple Opioid Binding Sites

Cited by 20 publications

References 134 publications

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

The Role of the Mu₁ Opioid Receptor Subtype in the Regulation of Prolactin and Growth Hormone Secretion by Beta‐Endorphin in Female Rats: Studies with Naloxonazine

Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

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Multiple Opioid Binding Sites

Cited by 20 publications

References 134 publications

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

Effects of selective opiate antagonists on morphine-induced hyperalgesia in domestic fowl

The Role of the Mu1 Opioid Receptor Subtype in the Regulation of Prolactin and Growth Hormone Secretion by Beta‐Endorphin in Female Rats: Studies with Naloxonazine

Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

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The Role of the Mu₁ Opioid Receptor Subtype in the Regulation of Prolactin and Growth Hormone Secretion by Beta‐Endorphin in Female Rats: Studies with Naloxonazine