Biochemical and Physiological Studies of the Beta-Adrenoceptor and the D-2 Dopamine Receptor in the Intermediate Lobe of the Rat Pituitary Gland: A Review

Côté, Thomas E.; Eskay, Robert L.; Frey, Elizabeth A.; Grewe, C. W.; Munemura, Masahide; Stoof, Johannes C.; Tsuruta, K.; Kebabian, J. W.

doi:10.1159/000123384

Cited by 136 publications

(39 citation statements)

References 30 publications

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“…With regard to the molecular mechanisms underlying the phenomena described here, it is very likely that the modulatory receptor-mediated interactions occur at the level of adenylate cyclase, since it has been shown that on activation both opioid receptors (Abood et al, 1985;Cooper et al, 1982;Frey and Kebabian, 1984;Gentleman et al, 1983;Kurose et al, 1983;Law et al, 198 1;West and Miller, 1983) and dopamine receptors (Cote et al, 1982;Creese et al, 1983;Kuno et al, 1983;Rodbell, 1980) may be coupled to the enzyme through guanine nucleotide regulatory proteins. It has been suggested that the opioid binding sites-designated as II-, 6-, and K-opioid receptors-correspond to seperate biochemical entities (Cho et al, 1983;Zajac and Roques, 1985) with different primary structures (Howard et al, 1985).…”

Section: Discussionmentioning

confidence: 97%

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

Schoffelmeer¹,

Hansen²,

Stoof³

et al. 1986

J. Neurosci.

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The interactions between dopamine receptors and opioid recep tors coupled to adenylate cyclase in rat neostriatum were investigated. CAMP efflux from neostriatal slices induced by simultaneous activation of (stimulatory) D-l and (inhibitory) D-2 dopamine receptors with 30 PM dopamine was inhibited by the preferential &opioid receptor agonist [r+Ala*-D-LeuS] enkephalin (DADLE) and the cc-opioid receptor agonist morphine with an EC, of 100 and 800 nM, respectively. On selective D-l receptor activation (i.e., with D-2 receptors blocked by 10 e(~ (-)sulpiride), the EC, of DADLE was strongly reduced to 3 nM, whereas that of morphine was unaffected. When D-l and D-2 receptors were activated simultaneously, the inhibitory effects of DADLE (0.3 PC(M) and morphine (3 PM) on CAMP efflux were antagonized equally well by naloxone, a p-opioid receptor antagonist. In contrast, on selective D-l receptor activation, naloxone was about 20 times more potent in antagonizing the inhibitory effect of morphine than DADLE. Moreover, the &opioid receptor antagonist ICI 174864 (0.75 PM) did not affect the inhibitory effect of morphine but antagonized that of DADLE, provided that D-2 receptors were blocked. The highly selective b-opioid receptor agonist [D-Pen*+-Pens] enkephalin (DPDPE) inhibited dopamine-stimulated CAMP efflux only when D-2 receptors were blocked. Similar results were obtained when the agonists SKF 38393 and LY 141865 were used to activate D-l and D-2 receptors, respectively.These data indicate that blockade of D-2 receptors in the neostriatum elicits the coupling of bopioid receptors to dopamine-sensitive adenylate cyclase, thereby making it considerably more sensitive to inhibition by the enkephalins.Opioid receptors in peripheral tissues and in the CNS can be distinguished pharmacologically in at least 3 different typesviz., p(morphine), G(enkephalin), and K(benzomorphan/dynorphin) receptors-but the functional implications of this receptor multiplicity are still largely unknown (Chang et al., 198 1;Gillan and Kosterlitz, 1982;Lord et al., 1977;Martin, 1984; Mulder et al., 1984;Paterson et al., 1983;Wood, 1982; Wiister et al., 198 1). The neostriatum, the major target region for information transmitted by dopaminergic neurons arising from the substantia nigra (Dray, 1979), contains a large number of enkephalinergic neurons (Cuello, 1983;Hughes et al., 1977;Yang et al., 1977), as well as a high density of opioid receptors, particularly those of the 6-and p-types (Atweh and Kuhar, 1983; Wamsley, Received Sept. 30, 1985; revised Jan. 23, 1986; accepted Jan. 24, 1986. Correspondence should be addressed to Anton N. Iwamato and Way, 1979; Mulderet al., 1984;Wood, 1983) and may, in fact, also be one of the functional consequences of release of endogenous opioid peptides. In the neostriatum, 2 pharmacologically and functionally different types ofdopamine receptors have been demonstrated, i.e., D-1 and D-2 (Creese et al., 1983;Kebabian and Calne, 1979;Seeman, 1980; Stoof and Kebabian, 198 1). Activation of D-l receptor...

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Section: Discussionmentioning

confidence: 97%

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

Schoffelmeer¹,

Hansen²,

Stoof³

et al. 1986

J. Neurosci.

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“…[38][39][40][41]. Indeed, inhibitory dopaminergic control represents the major influence on POMC-derived peptide secretion in the NIL (32) and is thought to be mediated via D 2 receptors that are negatively coupled to adenylate cyclase (42).…”

Section: Discussionmentioning

confidence: 99%

Mortality in 7B2 null mice can be rescued by adrenalectomy: Involvement of dopamine in ACTH hypersecretion

Laurent

Kimble

Peng

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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(1999) Cell 96, 689). Here, we have compared the 7B2 and PC2 null mouse models to determine why the 7B2 null, but not the PC2 null, exhibits a lethal disease state. Both 7B2 and PC2 nulls contained highly elevated pituitary adrenocorticotropic hormone (ACTH); the neurointermediate lobe content of ACTH in 7B2 nulls was 13-fold higher than in WT mice; that of the PC2 null was 65-fold higher. However, circulating ACTH levels were much higher in the 7B2 null than in the PC2 null. Because hypothalamic inhibitory dopaminergic control represents the major influence on intermediate lobe proopiomelanocortin-derived peptide secretion, dopamine levels were measured, and they revealed that 7B2 null pituitaries contained only one-fourth of WT pituitary dopamine. Adrenalectomized 7B2 null animals survived past the usual time of death at 5 weeks; a month after adrenalectomy, they exhibited normal levels of pituitary dopamine, circulating ACTH, and corticosterone. Elevated corticosterone, therefore, seems to play a central role in the lethal phenotype of the 7B2 null, whereas a 7B2-mediated dopaminergic deficiency state may be involved in the actual ACTH hypersecretion phenomenon. Interestingly, adrenalectomized 7B2 nulls also developed unexpectedly severe obesity.

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“…These effects on POMC-derived peptide secretion from the IP appear to be mediated through a D2 dopamine receptor on the IP melanotroph (for a review, see ref. 5). Dopamine-containing synaptic endings had been identified directly in the rat IP, suggesting direct neural control of IP POMC secretion (6).…”

mentioning

confidence: 99%

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

Chen¹,

Dionne²,

Roberts³

1983

Proc. Natl. Acad. Sci. U.S.A.

136

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Dopamine-containing neurons directly innervate the intermediate lobe of the pituitary and dopaminergic compounds exert inhibitory effects on the secretion and the content of a-melanocyte-stimulating hormone and P-endorphin in this tis-sue. In this study, we have investigated the effects of dopamine receptor agonists and antagonists on the level of pro-opiomelanocortin (POMG) mRNA in rat pituitary. RNAs isolated from neurointermediate pituitary (NIP) or anterior pituitary were spotted on nitrocellulose filters and the levels of POMC mRNA were quantified by hybridization to a POMC-specific complementary DNA probe coupled with autoradiography and densitometry. Administration of a dopamine receptor antagonist, haloperidol (2 mg/kg per day), to adult female rats resulted in a 3-to 5-fold increase in POMC mRNA level in the NIP. Treatment with the dopamine agonist 2-Br-a-ergocryptine (1 mg/kg per day) decreased significantly the content of POMC mRNA in the NIP. These drugs had no apparent effect on the POMC mRNA levels in the anterior pituitary. The effect of haloperidol and ergocryptine on POMC mRNA in the NIP is time-and dose-dependent. The elevation of POMC mRNA content in the NIP by haloperidol can be observed as early as 6 hr after treatment. These effects of dopaminergic compounds can also be demonstrated in adult male and ovariectomized female rats. The (-endorphin content of the NIP, as measured by radioimmunoassay, and the de novo synthesis of POMC, as determined by radioactive amino acid labeling and two-dimensional gel electrophoresis analysis, also show negative regulation by dopaminergic compounds.The monoamine neurotransmitter dopamine and its agonists have been shown to inhibit the release of ca-melanocyte-stimulating hormone (a-MSH) and ,B-endorphin, two pro-opiomelanocortin (POMC)-derived peptides, from the intermediate lobe (IP) of the rat pituitary (1-3). Dopamine antagonists, such as haloperidol, stimulate the release of a-MSH and ,B-endorphin (3,4). These effects on POMC-derived peptide secretion from the IP appear to be mediated through a D2 dopamine receptor on the IP melanotroph (for a review, see ref. 5). Dopamine-containing synaptic endings had been identified directly in the rat IP, suggesting direct neural control of IP POMC secretion (6). In the rat pituitary anterior lobe (AP), a tissue that also synthesizes and secretes POMC-derived peptides, dopaminergic agonists and antagonists have not been shown to have similar effects on POMC peptide secretion (1,7,8).Recently, it has been shown that in addition to having effects on POMC peptide secretion, dopaminergic compounds can also change IP content of POMC peptides (3, 9). Chronic treatment of the rat with dopamine agonists or antagonists either decreases or increases, respectively, the amount of radioimmunoactive ,3endorphin or a-MSH in the IP. Such observations would suggest.that these drugs have effects on POMC synthesis parallel to their effects on secretion. Indeed, a very recent study by Hollt et al. showed that chronic (7 day) ...

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Biochemical and Physiological Studies of the Beta-Adrenoceptor and the D-2 Dopamine Receptor in the Intermediate Lobe of the Rat Pituitary Gland: A Review

Cited by 136 publications

References 30 publications

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

Mortality in 7B2 null mice can be rescued by adrenalectomy: Involvement of dopamine in ACTH hypersecretion

Regulation of the pro-opiomelanocortin mRNA levels in rat pituitary by dopaminergic compounds.

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