Specificin vivo binding of3H-spiperone to individual lobes of the pituitary gland of the rat. Evidence for the labelling of dopamine receptors

Køhler, Christer; Fahlberg, Karin

doi:10.1007/bf01249583

Cited by 11 publications

(2 citation statements)

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“…D, dopamine (DA) receptors are positively coupled to adenylate cyclase (Stoof and Kebabian, 1984), widely distributed in the CNS (Boyson et al, 1986;Dawson et al, 1986;Dubois et al, 1986;Bouthenet et al, 1987;Wamsley et al, 1989), and abundant in the parathyroid gland (Attie et al, 1980). D, DA receptors, on the other hand, are either not coupled to adenylate cyclase (Memo et al, 1986) or negatively coupled (Onali et al, 1985) and are densely distributed in the basal ganglia (Martres et al, 1985;Charuchinda et al, 1987;Joyce and Marshall, 1987;Richfield et al, 1987) and pituitary gland (Kohler and Fahlberg, 1985;Pazos et al, 1985;DeSouza, 1986).…”

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Localization of dopamine D2 receptor mRNA and D1 and D2 receptor binding in the rat brain and pituitary: an in situ hybridization- receptor autoradiographic analysis

et al. 1990

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Several lines of evidence suggest the existence of multiple dopamine receptor subtypes, referred to as D1 and D2. The present study examines the distribution of these dopamine binding sites in the rat brain and pituitary in relation to the distribution of D2 receptor mRNA using a combination of in vitro receptor autoradiographic and in situ hybridization techniques. 3H-Raclopride and 3H-SCH23390 (in the presence of 1 microM ketanserin) were used to label D2 and D1 receptor binding sites, respectively, while a 495 bp cRNA probe synthesized from the Sac I-Bgl II fragment of a rat D2 receptor cDNA was used to visualize the D2 receptor mRNA. Analysis of adjacent tissue sections in which receptor autoradiography and in situ hybridization had been performed revealed several brain regions where the D2 binding site and corresponding mRNA appear to be similarly distributed, including the caudate-putamen, nucleus accumbens, olfactory tubercle, globus pallidus, substantia nigra, and ventral tegmental area. In the pituitary gland, D2 binding sites and mRNA appear to be codistributed with very dense levels in the intermediate lobe and individually labeled cells in the anterior lobe. Brain regions demonstrating a lack of correspondence between the distribution of the D2 binding site and D2 receptor mRNA include the olfactory bulb, neocortex, paleocortex, hippocampus, and zona incerta. Several hypotheses are discussed to explain the lack of correspondence in certain brain regions; these include the localization of receptor binding sites on both fibers and cell bodies and receptor transport. These studies provide a better understanding of the anatomical distribution of the D2 receptor and serve as a framework for future regulatory and anatomical mapping studies. By focusing on specific brain regions, such as the nigrostriatal system, hippocampus, and olfactory bulb, they provide insights into D2 receptor synthesis, transport, and insertion into cell membranes.

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Localization of dopamine D2 receptor mRNA and D1 and D2 receptor binding in the rat brain and pituitary: an in situ hybridization- receptor autoradiographic analysis

et al. 1990

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“…However, the D2 DA receptor antagonist remoxipride showed inconsis tent results on serum prolactin levels. Remoxipride, unlike raclopride, has been shown to affect in the highest doses only 30% of the anterior pituitary D2 DA receptors in vivo [43] but exerts D2-DA-receptor-blocking activity in the brain [68]. The present results may suggest that remoxipride may be a partial agonist at some pituitary D2 DA receptors.…”

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confidence: 51%

Involvement of D1 Dopamine Receptors in the Nicotine-Induced Neuro-Endocrine Effects and Depletion of Diencephalic Catecholamine Stores in the Male Rat

et al. 1988

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Male rats were treated acutely with nicotine (4 × 2 mg/kg, 30-min time intervals, total treatment time 2 h) or exposed to cigarette smoke from 4 × 1 cigarette (30-min time intervals, total treatment time 2 h). Some rats were pretreated with the Dl dopamine (DA) receptor antagonist SCH 23390 (0.1–3.0 mg/kg, i.p.), or with the D2 DA receptor antagonists remoxipride and raclopride (1 mg/kg, i.p.), or with the 5-hydroxytryptamine 2 (5-HT2) receptor antagonist ketanserin (0.3 mg/kg, i.p.) 5 min before nicotine treatment or the acute intermittent exposure to cigarette smoke. Some rats were treated with the Dl DA receptor agonist SK&F 38393 (1–10 mg/kg, i.p.) 15 min, 30 min or 2 h before decapitation. Hypo-thalamic and pre-optic catecholamine (CA) levels were measured by quantitative histofluorimetry in discrete DA and noradrenaline (NA) nerve terminal systems. Serum thyroid-stimulating hormone (TSH), prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), vasopressin, corticosterone and testosterone levels were determined by radio-immunoassay procedures. Nicotine treatment and to a minor degree also acute intermittent exposure to cigarette smoke produced a reduction in serum prolactin, LH and TSH but not in serum FSH, vasopressin and testosterone levels. Nicotine treatment also increased serum corticosterone levels. Pretreatment with the Dl DA receptor antagonist SCH 23390 (1–3 mg/kg) counteracted the lowering of serum LH, but not of prolactin and TSH levels induced by nicotine or exposure to cigarette smoke. SCH 23390 alone (1–3 mg/kg) increased serum TSH levels. Remoxipride, raclopride or ketanserin did not counteract any of the neuro-endocrine actions induced by nicotine treatment. However, ketanserin alone lowered serum prolactin levels. SK&F 38393 increased serum TSH, prolactin and LH levels. It was found that nicotine treatment and exposure to cigarette smoke with few exceptions produced a depletion of CA stores in NA and DA nerve terminals of the hypothalamus, pre-optic area and median eminence which was counteracted by SCH 23390 (1 mg/kg) but not by remoxipride, raclopride (1 mg/kg) or ketanserin (0.3 mg/kg). The results indicate that Dl but not D2 DA or 5-HT2 receptors may modulate the NA and DA release in the median eminence, the hypothalamus and the pre-optic area induced by nicotinic cholinoceptor activation. Furthermore, Dl DA receptors in the median eminence may at least in part mediate the inhibitory effects of nicotine on LH but not on TSH and prolactin secretion, although there appears to exist a Dl DA receptor in the median eminence which inhibits TSH secretion. The results are in line with our hypothesis that activation of the tubero-infundibular DA neurons via Dl DA receptors mediates the inhibition of LH secretion caused by nicotine treatment or exposure to cigarette smoke. Finally, the facilitatory serotonergic mechanism on prolactin secretion is probably mediated via 5-HT2 receptors.

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In vivo labelling of rat brain dopamine D-2 receptors

Køhler¹,

Karlsson-Boethius²

1988

J. Neural Transmission

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The stereospecific blockade by raclopride and FLB472 (the R enantiomer of raclopride) of the specific in vivo binding of [3H]-spiperone, [3H]-N,N-propylnorapomorphine (NPA) and [3H]-raclopride was studied in seven brain regions (e.g., caudate nucleus, olfactory tubercle, septum, hippocampus, frontal cortex, substantia nigra, pituitary gland) of the male albino rat. The binding of all three ligands was dose-dependently blocked by raclopride and FLB472. The blockade by FLB472 occurred at doses 50-100 times higher than that obtained by raclopride. The maximal blockade by raclopride of [3H]-spiperone binding differed between brain areas. Thus, the largest blockade was obtained in the substantia nigra (95%), septum (90%), caudate nucleus (60%) and olfactory tubercle (60%), while the blockade of [3H]-spiperone binding in the frontal cortex and pituitary gland did not exceed 30% and 50%, respectively. In contrast to [3H]-spiperone, the in vivo binding of [3H]-NPA and [3H]-raclopride was prevented by 90-100% in all brain areas examined. Taken together, the present findings indicate that the in vivo binding of three radioactive ligands to a central dopamine D-2 receptor can be stereoselectively blocked by the enantiomers of raclopride. The findings suggest that, under in vivo conditions, [3H]-raclopride and [3H]-NPA may label a closely related receptor site. However only some of the [3H]-spiperone binding sites may be identical to the [3H]-raclopride binding sites. The findings indicate furthermore that the relative overlap of D-2 sites shared by [3H]-spiperone and [3H]-raclopride may vary between brain regions.

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Specificin vivo binding of3H-spiperone to individual lobes of the pituitary gland of the rat. Evidence for the labelling of dopamine receptors

Cited by 11 publications

References 29 publications

Localization of dopamine D2 receptor mRNA and D1 and D2 receptor binding in the rat brain and pituitary: an in situ hybridization- receptor autoradiographic analysis

Localization of dopamine D2 receptor mRNA and D1 and D2 receptor binding in the rat brain and pituitary: an in situ hybridization- receptor autoradiographic analysis

Involvement of D1 Dopamine Receptors in the Nicotine-Induced Neuro-Endocrine Effects and Depletion of Diencephalic Catecholamine Stores in the Male Rat

In vivo labelling of rat brain dopamine D-2 receptors

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