Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the rat, unilateral intrastriatal injection of monoclonal antibodies to acetylcholinesterase (AChE) produced ipsilateral disappearance of AChE-positive nerve terminals within striatum and adjacent cortex. No alterations in striatal staining patterns were observed for tyrosine hydroxylase, somatostatin, neuropeptide Y, substance P, or neurotensin. Ultrastructural studies demonstrated the presence of degenerating AChE-positive boutons ipsilaterally, while tyrosine hydroxylase positive terminals seemed unaffected. Apomorphine administration to rats which had received unilateral antibody injection resulted in ipsilateral rotational behavior. These data suggest that selective effects on cholinergic terminals with functional deficits can be produced within the central nervous system by intracerebral injection of AChE antibodies.
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PMID:Effect of intracerebral injection of monoclonal acetylcholinesterase antibodies on cholinergic nerve terminals in the rat central nervous system. 168 80

The effects of adrenergic receptor agonists on GH secretion were studied in adult, male rats pretreated with reserpine and somatostatin antiserum. Frequent blood samples were obtained from intra-aortic cannulae. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg i.p.) caused a complete suppression of the normal, pulsatile secretion of GH in all animals. Administration of somatostatin antiserum resulted in rapid elevations of plasma GH in reserpine-pretreated rats with peak levels at 30 min. GH levels then fell but remained slightly elevated for the duration of the sampling period (8 h). Apomorphine (0.5 mg/kg i.p.) had no effect on plasma GH levels, whereas clonidine (0.5 mg/kg i.p.) induced release of GH in both antiserum treated and control rats. The results indicate that the alpha-adrenergic influence on the secretion of GH is mediated not by inhibition of somatostatin release but rather by effects on the release of a GHRF.
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PMID:Evidence for a growth hormone releasing factor mediating alpha-adrenergic influence on growth hormone secretion in the rat. 611 46

Drug addicts abusing heroin substitutes contaminated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and perhaps those who work with this substance, may develop symptoms similar to those seen in Parkinson's disease [7, 12, 13]. We describe the results of a study in which rats were given daily injections of MPTP for two weeks. A progressive suppression of activity was seen, but the subjects rapidly recovered when treatment ceased. The animals were then injected with D-amphetamine or apomorphine; the former drug enhanced activity, to levels seen in control (non-MPTP treated) subjects. Apomorphine had no effect, either on control or MPTP-treated subjects. The effects of acute (0, 2.5, 5.0 and 10.0 mg per rat) administration of MPTP were also studied. The two lower doses significantly decreased activity, but the highest dose did not. Histological examination showed that 2 weeks' treatment with MPTP did not produce neuronal degeneration in the pars compacta of the substantia nigra (SN). In these animals, there were no changes in levels of dopamine, 5-hydroxytryptamine, or their metabolites in either the SN or the caudate nucleus. MPTP had no effect on the levels of neurotensin, somatostatin and substance P in several brain areas. It is concluded that MPTP has reliable effects on locomotor activity in rats without producing measurable histological or neurochemical changes in the nigrostriatal dopaminergic system.
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PMID:N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) affects locomotor activity without producing a nigrostriatal lesion in the rat. 633 3

The effects of salmon gonadotropin-releasing hormone (sGnRH) and the superactive agonist [D-Arg6, Pro9NEt]-sGnRH (sGnRH-A) on growth hormone (GH) and gonadotropin (GtH) release were examined using a perifusion system for pituitary fragments of the common carp (Cyprinus carpio). Perifusion of 2-min pulses of different concentrations of sGnRH or sGnRH-A stimulated a rapid and dose-dependent increase in GH release: ED50 values for sGnRH and sGnRH-A in stimulating GH release were 2.8 +/- 0.7 and 0.5 +/- 0.1 nM, respectively, indicating that the superactivity of sGnRH-A for stimulation of GtH release also applies in induction of GH release. Exposure of the pituitary fragments to 10 nM sGnRH or sGnRH-A alone resulted in increases in GH and GtH release on a similar temporal course. Apomorphine (10, 100, and 1000 nM) significantly inhibited basal and GnRH-induced GtH release in a dose-dependent manner and significantly stimulated basal GH release; however, APO did not enhance GnRH-induced GH release. Somatostatin (100 nM) significantly blocked basal release and 10 nM sGnRH- and sGnRH-A-induced GH release, but was ineffective on GtH release. Treatment with somatostatin (100 nM) in combination with apomorphine (100 nM) caused an increase in sGnRH-induced GH release compared to treatment with somatostatin alone; whereas, on GtH there was a significant decrease in basal and GnRH-induced levels, compared to treatment with somatostatin alone. These results indicate that GH release in common carp is regulated by somatostatin as GH release inhibitor. sGnRH and sGnRH-A act as GH-releasing factors; the mechanisms by which GnRH stimulates GH and GtH secretion are independent. The dopamine agonist apomorphine stimulates GH release and inhibits GtH release directly at the pituitary level.
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PMID:Growth hormone and gonadotropin secretion in the common carp (Cyprinus carpio L.): in vitro interactions of gonadotropin-releasing hormone, somatostatin, and the dopamine agonist apomorphine. 809 60

We have previously demonstrated that dopamine (DA) and the DA D1 agonist SKF 38393 stimulate growth hormone (GH) release from perifused pituitary fragments of the goldfish, suggesting an involvement of DA D1 receptors in GH regulation. In the present study, the role of DA on GH release and body growth of the goldfish was further investigated both in vivo and in vitro. DA consistently stimulated GH release in a dose-dependent manner from perifused goldfish pituitary fragments. The GH-releasing action of DA was seasonal, being the highest in sexually regressed fish, intermediate in recrudescent fish, and the lowest in sexually mature (prespawning) fish. Somatostatin, a known GH-release inhibitor in the goldfish, suppressed basal GH release and abolished the GH response to DA in perifused pituitary fragments as well as pituitary cells under static incubation. Intraperitoneal administration of the nonselective DA agonist apomorphine and the D1 agonist SKF 82958 increased the plasma GH levels in the goldfish. These GH responses were blocked by simultaneous treatment with the D1 antagonist Sch 23390 but not the D2 antagonist pimozide. Apomorphine administered orally also induced a similar elevation in plasma GH levels. Long-term feeding with apomorphine was found to be stimulatory to the body growth of goldfish. These results provide evidence that the neurotransmitter DA, by acting through DA D1 receptors in the pituitary, also functions as a GH-releasing factor in the goldfish.
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PMID:In vitro and in vivo evidence that dopamine exerts growth hormone-releasing activity in goldfish. 810 29

Somatostatin (SRIF) influences the release of two important neuromodulators of retinal circuitry, dopamine (DA) and nitric oxide (NO). The aim of the present study was to examine whether DA and NO modulate SRIF release in rat retina, and the mechanisms involved in their actions. Retinas of adult female Sprague--Dawley rats (250--300 g) were mechanically detached from the eyecup and ex vivo experiments were performed. Retinal explants were incubated in the presence of dopaminergic [DA (10 microM, 100 microM and 200 microM), apomorphine (nonselective D1/D2 agonist, 0.50 mM, 1.0 microM and 10 microM), A68930 (D1 selective agonist, 0.50 microM, 1.0 microM and 10 microM), quinpirole (D2 selective agonist, 0.50 microM, 1.0 microM and 10 microM), SCH 23390 (D1 selective antagonist, 250 nM and 500 nM) and sulpiride (D2 selective antagonist, 100 microM and 200 microM)], and nitrinergic agents [arginine (62.5 microM--5mM), SIN-1 (50 microM, 100 microM and 500 microM) and 8-Br-cGMP (50 microM, 250 microM and 500 microM)]. SRIF levels were quantified using radioimmunoassay (RIA). Dopamine had no effect on SRIF levels. Apomorphine produced a concentration dependent decrease and increase in SRIF levels, suggestive of pre- and postsynaptic effects. A68930 (10 microM) and SCH 23390 (250 nM and 500 nM) mimicked and reversed apomorphine's postsynaptic actions, respectively. Quinpirole had no effect, but blockade of D2 autoreceptors by sulpiride (200 microM) afforded an increase in SRIF levels. Arginine and SIN-1 increased, and 8-Br-cGMP attenuated SRIF levels. These results show that dopamine D1 receptors, and NO/peroxynitrite agents modulate SRIF release in the retina suggesting that the triad SRIF--DA--NO have reciprocal interactions via which they regulate retinal circuitry and vision transduction.
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PMID:Dopamine (D1) receptor activation and nitrinergic agents influence somatostatin levels in rat retina. 1796 53