scholarly journals Serotonin Agonist

2020 ◽  
Author(s):  
Keyword(s):  

1986 ◽  
Vol 113 (4) ◽  
pp. 471-478 ◽  
Author(s):  
R. J. Kemppainen ◽  
J. L. Sartin

Abstract. In order to examine regulation of pituitary intermediate lobe secretion, plasma immunoreactive (i)ACTH, cortisol, and α-MSH responses to iv bolus injections of CRF, quipazine maleate (serotonin agonist), isoproterenol (β-adrenergic agonist) or haloperidol (dopamine antagonist) were determined in conscious, unrestrained dogs. Endocrine responses to these test substances were also determined in dogs pre-treated with dexamethasone. Administration of one or more doses of each test substance resulted in significant elevations in plasma iACTH and cortisol concentrations. Only haloperidol injection caused significant increases in plasma iα-MSH. Following dexamethasone pre-treatment, plasma iACTH and cortisol increases in response to all test substances were considerably reduced or abolished. Dexamethasone did not alter baseline or haloperidol-stimulated plasma ia-MSH concentrations. However, infusion of bromocriptine mesylate (dopamine agonist) in combination with dexamethasone pre-treatment reduced the plasma iα-MSH response to haloperidol. We conclude that a dopaminergic pathway is important in the in vivo regulation of pituitary intermediate lobe activity in dogs.



2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
D. Kontis ◽  
V. Boulougouris ◽  
S. Papadopoulos ◽  
V.-M. Papakosta ◽  
S. Kalogerakou ◽  
...  

Rationale:In the rewarded alternation model of obsessive compulsive disorder (OCD), the serotonin agonist m-chlorophenylpiperazine (mCPP) increases persistent behaviour, while chronic pretreatment with selective serotonin reuptake inhibitor (SSRI-fluoxetine) but not benzodiazepine or desipramine abolishes mCPP effects. However, we noted that acute SSRI administration also causes transient persistence increases, counteracted by mCPP pretreatment.Objectives:This studya.further explores the apparent cross-tolerance between fluoxetine and mCPP andb.extends the model by investigating its sensitivity to dopaminergic manipulations (D2,3 agonism - quinpirole).Methods:In both experiments, baseline and drug testing was carried out under daily T-maze alternation training.Exp.1:Matched group (n=8) pairs of rats received one of the following 20-day pretreatments (daily intraperitoneal administration):1.saline,2.low-dose fluoxetine (2.5mg/kg),3.low-dose mCPP (0.5mg/kg) or4.combined fluoxetine+mCPP.One group per pretreatment then received a 4-day challenge with high-dose fluoxetine (10mg/kg), the other with high-dose mCPP (2.5mg/kg).Exp.2:One group (n=12) of rats received 20-day treatment with saline, another with quinpirole (0.5 mg/kg).Results:Exp.1:Saline and low-dose mCPP- or fluoxetine-pretreated animals showed significant persistence increases under both challenges, while combined low-dose fluoxetine+mCPP pretreatment afforded full protection from either challenge.Exp.2:Quinpirole significantly increased directional persistence after 13 administration days.Conclusions:These results establish the sensitivity of the rewarded alternation OCD model to D2,3receptor activation, thereby extending its profile of pharmacological isomorphism with OCD. Furthermore, they suggest a common mechanism of action of an SSRI and a serotonin agonist in the control of directional persistence.



1982 ◽  
Vol 29 (3) ◽  
pp. 383-388 ◽  
Author(s):  
KOZO HASHIMOTO ◽  
NORIHITO OHNO ◽  
KAZUHARU MURAKAMI ◽  
JINGO KAGEYAMA ◽  
YOSHIYUKI AOKI ◽  
...  




Author(s):  
Wei Liu ◽  
Paweł Stachura ◽  
Haifeng C. Xu ◽  
Nikkitha Umesh Ganesh ◽  
Fiona Cox ◽  
...  


1989 ◽  
Vol 257 (6) ◽  
pp. R1441-R1449 ◽  
Author(s):  
W. D. Steers ◽  
W. C. de Groat

The effects of m-chlorophenylpiperazine (MCPP), a serotonin agonist, on spontaneous and evoked neural firing in nerves supplying the penis and bladder were examined in the urethan-anesthetized rat. MCPP (0.1-10 mg/kg iv) elicited, after a 2- to 4-min delay, an increase in spontaneous firing in cavernous nerves but no detectable firing in bladder nerves. The cavernous nerve firing was accompanied by an increase in intracavernous pressure and a depression of rhythmic bladder activity. Administration of ganglionic-blocking agents or transection of peripheral nerves revealed that the cavernous nerve discharge was mediated by activation of pre-ganglionic cholinergic pathways in the pelvic nerve. The effects of MCPP were noted in intact as well as in acute and chronic spinal rats and were prevented by the administration of the serotonin (5-HT) antagonist, metergoline (3 mg/kg im). These data indicate that pharmacological activation of 5-HT receptors, possibly of the 5-HT1B subtype, can facilitate the sacral preganglionic outflow to the penis and inhibit bladder activity.



2015 ◽  
Vol 46 (6) ◽  
pp. 1197-1209 ◽  
Author(s):  
C. O. Carlisi ◽  
K. Chantiluke ◽  
L. Norman ◽  
A. Christakou ◽  
N. Barrett ◽  
...  

BackgroundSerotonin is under-researched in attention deficit hyperactivity disorder (ADHD), despite accumulating evidence for its involvement in impulsiveness and the disorder. Serotonin further modulates temporal discounting (TD), which is typically abnormal in ADHD relative to healthy subjects, underpinned by reduced fronto-striato-limbic activation. This study tested whether a single acute dose of the selective serotonin reuptake inhibitor (SSRI) fluoxetine up-regulates and normalizes reduced fronto-striato-limbic neurofunctional activation in ADHD during TD.MethodTwelve boys with ADHD were scanned twice in a placebo-controlled randomized design under either fluoxetine (between 8 and 15 mg, titrated to weight) or placebo while performing an individually adjusted functional magnetic resonance imaging TD task. Twenty healthy controls were scanned once. Brain activation was compared in patients under either drug condition and compared to controls to test for normalization effects.ResultsRepeated-measures whole-brain analysis in patients revealed significant up-regulation with fluoxetine in a large cluster comprising right inferior frontal cortex, insula, premotor cortex and basal ganglia, which further correlated trend-wise with TD performance, which was impaired relative to controls under placebo, but normalized under fluoxetine. Fluoxetine further down-regulated default mode areas of posterior cingulate and precuneus. Comparisons between controls and patients under either drug condition revealed normalization with fluoxetine in right premotor-insular-parietal activation, which was reduced in patients under placebo.ConclusionsThe findings show that a serotonin agonist up-regulates activation in typical ADHD dysfunctional areas in right inferior frontal cortex, insula and striatum as well as down-regulating default mode network regions in the context of impulsivity and TD.





Sign in / Sign up

Export Citation Format

Share Document