SCH 23390, but not raclopride, decreases intake of intraorally infused 10% sucrose

Appetite ◽  
1992 ◽  
Vol 19 (2) ◽  
pp. 223 ◽  
Author(s):  
A. Tyrka ◽  
G.P. Smith
Keyword(s):  
Sch 23390

The relaxing effect of SCH 23390 in the molluscan smooth muscle

1989 ◽  
Vol 94 (1) ◽  
pp. 341-344
Author(s):  
Hajime Murakami ◽  
Masakazu Sano ◽  
Takashi Tsukimura ◽  
Akira Yamazaki
Keyword(s):  
Smooth Muscle ◽  
Sch 23390 ◽  
Molluscan Smooth Muscle ◽  
Relaxing Effect

scholarly journals Altered heparan sulfate metabolism during development triggers dopamine-dependent autistic-behaviours in models of lysosomal storage disorders

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria De Risi ◽  
Michele Tufano ◽  
Filomena Grazia Alvino ◽  
Maria Grazia Ferraro ◽  
Giulia Torromino ◽  
...  
Keyword(s):  
Heparan Sulfate ◽  
Sch 23390 ◽  
Lysosomal Storage Disorders ◽  
Dopamine Neurons ◽  
Therapeutic Effects ◽  
Lysosomal Storage ◽  
Cellular Models ◽  
Mps Ii ◽  
Mps Iiia ◽  
Storage Disorders

AbstractLysosomal storage disorders characterized by altered metabolism of heparan sulfate, including Mucopolysaccharidosis (MPS) III and MPS-II, exhibit lysosomal dysfunctions leading to neurodegeneration and dementia in children. In lysosomal storage disorders, dementia is preceded by severe and therapy-resistant autistic-like symptoms of unknown cause. Using mouse and cellular models of MPS-IIIA, we discovered that autistic-like behaviours are due to increased proliferation of mesencephalic dopamine neurons originating during embryogenesis, which is not due to lysosomal dysfunction, but to altered HS function. Hyperdopaminergia and autistic-like behaviours are corrected by the dopamine D1-like receptor antagonist SCH-23390, providing a potential alternative strategy to the D2-like antagonist haloperidol that has only minimal therapeutic effects in MPS-IIIA. These findings identify embryonic dopaminergic neurodevelopmental defects due to altered function of HS leading to autistic-like behaviours in MPS-II and MPS-IIIA and support evidence showing that altered HS-related gene function is causative of autism.

DA1 dopamine receptors in renal cortical collecting duct

1991 ◽  
Vol 261 (5) ◽  
pp. F890-F895 ◽  
Author(s):  
K. Ohbu ◽  
R. A. Felder
Keyword(s):  
Adenylate Cyclase ◽  
Specific Binding ◽  
Collecting Duct ◽  
Sch 23390 ◽  
Receptor Density ◽  
Cortical Collecting Duct ◽  
Tightly Coupled ◽  
Renal Dopamine ◽  
Dissociation Constant Kd ◽  
Stimulation Of

Renal dopamine DA1 receptors are linked to the regulation of sodium transport. We have previously reported the presence of DA1 receptors in the proximal convoluted tubule (PCT) but not in the distal convoluted tubule. However, the DA1 receptor in the collecting duct, the final determinant of electrolyte transport, has not been studied. DA1 receptors were studied in the microdissected cortical collecting duct (CCD) of rats by autoradiography with use of the selective DA1 radioligand 125I-Sch 23982 and by measurement of adenylate cyclase (AC) activity. Specific binding of 125I-Sch 23982 to CCD was saturable with radioligand concentration. The dissociation constant (Kd) was 0.46 +/- 0.08 nM (n = 5), and the maximum receptor density (Bmax) was 1.41 +/- 0.43 fmol/mg protein (n = 5). The DA1 antagonist Sch 23390 was more effective than the DA1 agonist fenoldopam in competing for specific 125I-Sch 23982 binding. Fenoldopam stimulated AC activity in CCD in a concentration-dependent (10(-9)-10(-6) M) manner. The ability of fenoldopam to stimulate AC activity was similar in CCD and PCT even though DA1 receptor density was 1,000 times greater in the CCD than in the PCT. In additional studies, fenoldopam stimulation of AC activity did not influence vasopressin-stimulated AC activity. We conclude that the DA1 receptor in rat CCD is tightly coupled to AC stimulation and that there is no interaction between DA1 agonist-stimulated and vasopressin-stimulated AC activity in the CCD.

Effects of acute thioridazine, metoclopramide and SCH 23390 on the basal activity of A9 and A10 dopamine cells

1987 ◽  
Vol 137 (2-3) ◽  
pp. 251-255 ◽  
Author(s):  
Timothy H. Hand ◽  
Richard J. Kasser ◽  
Rex Y. Wang
Keyword(s):  
Sch 23390 ◽  
Basal Activity

[3H]SCH 23390 identifies D-1 binding sites in rat striatum and other brain areas

1986 ◽  
Vol 38 (12) ◽  
pp. 907-912 ◽  
Author(s):  
GAVIN J. KILPATRICK ◽  
PETER JENNER ◽  
C. DAVID MARSDEN
Keyword(s):  
Binding Sites ◽  
Sch 23390 ◽  
Rat Striatum ◽  
Brain Areas

Dopaminergic control of angiotensin II-induced vasopressin secretion in vitro

1998 ◽  
Vol 275 (4) ◽  
pp. E687-E693 ◽  
Author(s):  
Noreen F. Rossi
Keyword(s):  
Angiotensin Ii ◽  
Sch 23390 ◽  
Receptor Activation ◽  
Significant Rise ◽  
Skf 38393 ◽  
Receptor Subtype ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist ◽  
Vasopressin Secretion

Because dopamine influences arginine vasopressin (AVP) release, the present studies were designed to ascertain the dopamine receptor subtype that potentiates angiotensin II-induced AVP secretion in cultured hypothalamo-neurohypophysial explants. Dopamine (a nonselective D1/D2 agonist), apomorphine (a D2 ≫ D1 agonist), and SKF-38393 (a selective D1 agonist) dose dependently increased AVP secretion. Maximal AVP release was observed with 5 μM dopamine, 307 ± 66% ⋅ explant−1 ⋅ h−1, 1 μM SKF-38393, 369 ± 41% ⋅ explant−1 ⋅ h−1, and 0.1 μM apomorphine, 374 ± 67% ⋅ explant−1 ⋅ h−1. Selective D1 antagonism with 1 μM SCH-23390 blocked AVP secretion to values no different from basal. Domperidone (D2 antagonist), phenoxybenzamine (nonselective adrenergic antagonist), and prazosin (α1-antagonist) failed to prevent release. D1 antagonism also prevented AVP secretion to 1 μM angiotensin II [angiotensin II, 422 ± 87% ⋅ explant−1 ⋅ h−1vs. angiotensin II plus SCH-23390, 169 ± 28% ⋅ explant−1 ⋅ h−1( P < 0.05)], but D2 and α1-adrenergic blockade did not. In contrast, AT1 receptor inhibition with 0.5 μM losartan blocked angiotensin II- but not dopamine-induced AVP release. AT2antagonism had no effect. Although subthreshold doses of the agonists did not increase AVP secretion (0.05 μM dopamine, 133 ± 44% ⋅ explant−1 ⋅ h−1; 0.01 μM SKF-38393, 116 ± 26% ⋅ explant−1 ⋅ h−1;and 0.001 μM angiotensin II, 104 ± 29% ⋅ explant−1 ⋅ h−1), the combination of dopamine and angiotensin II provoked a significant rise in AVP [420 ± 83% ⋅ explant−1 ⋅ h−1( P < 0.01)]. Similar results were observed with SKF-38393 and angiotensin II, and the AVP response was blocked to basal levels by either D1 or AT1 antagonism. These findings support a role for D1 receptor activation to increase AVP release and mediate angiotensin II-induced AVP release within the hypothalamo-neurohypophysial system. The data also suggest that the combined subthreshold stimulation of receptors that use distinct intracellular pathways can prompt substantial AVP release.

scholarly journals Effects of costimulation of dopamine D1- and D2-like receptors on renal function

1998 ◽  
Vol 275 (4) ◽  
pp. R986-R994 ◽  
Author(s):  
Pedro A. Jose ◽  
Laureano D. Asico ◽  
Gilbert M. Eisner ◽  
Felice Pocchiari ◽  
Claudio Semeraro ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
Sodium Transport ◽  
Sodium Excretion ◽  
Rank Order ◽  
Sch 23390 ◽  
Urine Flow ◽  
Dopamine Receptor Agonist ◽  
Vasodilatory Effect

In vitro studies have suggested that dopamine D1- and D2-like receptors interact to inhibit renal sodium transport. We used Z-1046, a dopamine receptor agonist with the rank-order potency D3 ≥ D4 > D2 > D5 > D1, to test the hypothesis that D1- and D2-like receptors interact to inhibit renal sodium transport in vivo in anesthetized rats. Increasing doses of Z-1046, administered via the right renal artery, increased renal blood flow (RBF), urine flow, and absolute and fractional sodium excretion without affecting glomerular filtration rate. For determination of the dopamine receptor involved in the renal functional effects of Z-1046, another group of rats received Z-1046 at 2 μg ⋅ kg−1 ⋅ min−1( n = 10) in the presence or absence of the D2-like receptor antagonist domperidone and/or the D1-like antagonist SCH-23390. Domperidone alone had no effect but blocked the Z-1046-mediated increase in urine flow and sodium excretion; it enhanced the increase in RBF after Z-1046. SCH-23390 by itself decreased urine flow and sodium excretion without affecting RBF and blocked the diuretic, natriuretic, and renal vasodilatory effect of Z-1046. We conclude that the renal vasodilatory effect of Z-1046 is D1-like receptor dependent, whereas the diuretic and natriuretic effects are both D1- and D2-like receptor dependent.

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