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

After pointing out the reasons for undertaking the study of the regulation of prolactin secretion, the neuroendocrine mechanisms implicated in such secretion are discussed. Special attention is dedicated to the participation of chemical agents. Thus, the principal effects dealt with are: the net inhibition produced by dopamine and the less generalized inhibition effects of nicotine and somatostatin; the facilitatory action of serotoninergic pathways, TRH, histamine and endorphins. The dual effect described for GABA and noradrenaline, as well as some paradoxical actions, e.g., the antiserotoninergic and antihistaminergic H2 drugs which liberate prolactin in basal conditions but abolish the prolactin releasing effect of the respective agonist, or the immediate blocking effect of muscarinic agonists and antagonists are discussed. Finally, the possibility of a new mechanism of control at anterior pituitary receptors level is postulated.
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PMID:[Neurotransmitters, neurohormones and prolactin]. 615 45

High concentrations of K+ increase the release of substance P (SP) and somatostatin (SRIF) from superfused slices of rat spinal cord. This increase is Ca-dependent. Baclofen (100-500 microM) does not significantly alter the K+-evoked release of SP or SRIF. Stereoisomers of baclofen and GABA, similarly, are without effect. The spinal analgesic action of baclofen does not appear to be due to alterations in the release of SP or SRIF.
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PMID:Lack of effect of baclofen on substance P and somatostatin release from the spinal cord in vitro. 618 Mar 29

Homogenates of rat dorsal or ventral spinal cord were subjected to centrifugation on a continuous density gradient. The gradient was generated according to a new method with the aid of a microprocessor-controlled HPLC pump. The distribution of substance P-like immunoreactivity (SPI) and somatostatin-like immunoreactivity (SRIFI) across the gradient showed two peaks. The SPI peak seen at lower density was found only in dorsal spinal cord tissue. No peak of SPI was seen at this position in homogenates prepared from the spinal cords of capsaicin-pretreated rats. The second peak of SPI, found at a higher density, was accompanied by peaks in the levels of endogenous 5-hydroxytryptamine (5-HT), [14C]glycine, and [3H]norepinephrine uptake. This peak was seen at the same density in the dorsal and the ventral spinal cord. Tissue derived from capsaicin-pretreated rats exhibited one peak of SPI, accompanied by a maximum of [14C]glycine uptake. The uptake of [3H]gamma-aminobutyric acid ( [3H]GABA) was found to have a maximum at a somewhat lower density than that of [14C]glycine. It is concluded that the peak of SPI found at lower density in the dorsal spinal cord is associated with nerve endings belonging to capsaicin-sensitive primary afferents, while other endings, including those also containing 5-HT, are probably associated with the peak of SPI found at higher density.
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PMID:Distribution of spinal cord nerve endings containing various neurotransmitters on a continuous density gradient. 619 68

Classical and 'new' neurotransmitters appear in a certain sequence which seem to be similar in rat and man. Serotonin is one of the earliest transmitter which can be detected at a gestational age of 8 days in the rat. A couple of days later noradrenergic and dopaminergic fluorescence can be detected. The development of neurons with gamma-aminobutyric acid and acetylcholine lags behind the monoaminergic neurons. Endorphin is found in high concentrations at an early stage, while substance P, enkephalin and hypothalamic peptides like thyrotropin releasing hormone appear later in development. Inhibitory transmitters like GABA, somatostatin and endorphins reach their maximal concentrations in CNS during infancy, which might have some functional implications. The classical neurotransmitter noradrenaline might have certain unique functions during fetal and perinatal life. It seems to be important for the development of the cerebral cortex. It is released in high quantities at birth and might be of importance for the neonatal adaptation such as inducing arousal. The function of all the newly detected neuropeptides is far from elucidated even in adult life. Some of them seem to have important functions during perinatal life, while perhaps they occur in the adult organism only as evolutionary residues. For example endorphins seem to affect respiratory control in the fetus and the newborn in ways not seen in the adult. So called neuromodulators, for example adenosine, might also have particular functions during perinatal life.
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PMID:Classical and 'new' neurotransmitters during development--some examples from control of respiration. 620 44

We studied the acute effects of pharmacologic stimulation of neurotransmitter systems implicated in growth hormone and prolactin regulation in eight patients with Huntington's disease and matched control subjects. Both apomorphine, a dopamine agonist, and muscimol, a GABA agonist, produced an exaggerated rise in plasma growth hormone levels in the Huntington patients. Neither the growth hormone response to a muscarinic agonist, arecoline, nor the prolactin response to any of these drugs differed in the patients and controls. Loss of somatostatin activity in the hypothalamic-pituitary axis in Huntington's disease could account for these endocrinologic changes.
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PMID:Plasma growth hormone and prolactin response to dopaminergic GABAmimetic and cholinergic stimulation in Huntington's disease. 622 34

A gate control exists by which peripheral afferents and descending pathways can modulate sensory transmission. Evidence is presented that the mechanism may exist in the substantia gelatinosa laminae II and III. This area receives all known types of peripheral afferent from skin, from viscera and from high-threshold muscle afferents. The chemistry of the region is unique. Peripheral afferent terminals contain substance P, somatostatin, and fluoride-resistant acid phosphatase. Cells in the region contain enkephalin and GABA. At least three descending systems from the brainstem terminate in the area. The anatomical substrate exists by which cells in laminae II and III can receive afferents and descending axons and intrude onto cells of laminae I, IV, and V. Stimuli limited to the axons of laminae II and III cells in the Lissauer tract produce dorsal root potential and change the excitability of mono- and polysynaptic reflexes. They also change the excitability and receptive fields of cells in laminae IV and V. Recording from single units in laminae II and III reveals cells with many unusual properties not seen in the large dorsal horn cells. These unusual properties include small receptive fields, very prolonged responses to single stimuli, prolonged habituation, and shifting receptive fields. The action of the gate control shows it to be subtle and far beyond a simple control of overall excitability. Excitations and inhibitions are independently controlled. Different types of convergent afferent may be turned on and off. There are signs of both short-and long-lasting actions. It seems that a good case has been made for the cells of substantia gelatinosa taking part in the gate control mechanism.
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PMID:The role of substantia gelatinosa as a gate control. 624 35

3-Mercaptopropionic acid (3MP) (1 mM) inhibited the potassium-evoked release of endogenous GABA from slices of rat hippocampus and cerebral cortex in vitro. This did not appear to be due to an inhibition of GABA biosynthesis, since 3MP failed to affect the basal rate of GABA release or to accelerate the decline in the GABA content of tissue slices during prolonged exposure to 3MP (up to 120 min). 3MP, furthermore, inhibited the potassium-evoked release of [3H]GABA from preloaded brain slices, suggesting a direct inhibitory effect on GABA release. The threshold concentration was approximately 0.1 mM. 3MP at 1 mM failed to inhibit the potassium-evoked release of [3H]5-hydroxytryptamine, [3H]noradrenaline or somatostatin under similar conditions. The ability of 3MP to inhibit GABA release may contribute to the convulsant properties of this substance in vivo.
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PMID:3-mercaptopropionic acid inhibits GABA release from rat brain slices in vitro. 627 39

gamma-Aminobutyric acid (GABA; 50 or 500 microgram/10 microliter) was injected into the right lateral ventricle of urethane- or pentobarbital-anesthetized male rats. The animals were decapitated 15 min after injection. Serum GH and hypothalamic somatostatin (SRIF) concentration were measured by specific RIAs. Intraventricular GABA caused a dose-related increase in GH and SRIF. In another study, aminooxyacetic acid (5 or 20 mg) was injected ip into urethane-anesthetized rats. Aminooxyacetic acid at 20 mg produced a significant increase in both serum GH and hypothalamic SRIF. Furthermore, 12.5 mg gamma-hydroxybutyric acid (GHB) injected ip into urethane- or pentobarbital-anesthetized rats elicited a significant increase in both serum GH and hypothalamic SRIF. Pretreatment with 20 mg L-dopa produced decreases in the GHB-induced serum GH increase and in hypothalamic SRIF in pentobarbital-anesthetized rats. These results show that GABA and GHB stimulated GH secretion, which was accompanied by increased hypothalamic SRIF. Thus, the GH release induced by GABA or GHB may be partly involved in inhibiting the release of hypothalamic SRIF. As the GHB-induced GH release was inhibited by L-dopa, the stimulatory effect of GHB on GH secretion might be mediated by inhibition of the dopaminergic mechanism.
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PMID:Concomitant increases in serum growth hormone and hypothalamic somatostatin in rats after injection of gamma-aminobutyric acid, aminooxyacetic acid, or gamma-hydroxybutyric acid. 734 64

The serotoninergic neuronal systems of the brain stem are involved in several processes, like sleep, anxiety and depression. Because of this, these systems have received a great deal of attention during the last few years. As a result, the raphe nuclei have been shown to contain a variety of substances in addition to serotonin. For example they were shown to contain GABA, noradrenaline, enkephalin, somatostatin, substance P and cholecystokinin. Additionally, neuropeptide Y and tirotrophine releasing factor have been found to colocalize with serotonin in the dorsal raphe nuclei. All these results have expanded our knowledge on the raphe nuclei and suggest that many other substances, apart from serotonin, could be involved in the regulation of processes such as sleep, anxiety and depression. Further experiments are necessary to test if this hypothesis is correct.
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PMID:[New concepts relating to histochemistry of the serotonergic neural systems of the raphe nucleus]. 748 82

Following a previous study in which we showed ameliorative effects of basic fibroblast growth factor (FGF-2) locally applied to the nigrostriatal system in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mice, we investigated FGF-2 actions at different time intervals after the lesion and effects on non-dopaminergic striatal transmitter systems. A triple intraperitoneal injection of 30 mg/kg MPTP at 24 h intervals caused a reduction of striatal dopamine to 23% of control levels that lasted for at least 4 weeks. Four micrograms FGF-2 soaked into gel foam and placed onto the right striatum partially and bilaterally restored dopamine levels and tyrosine hydroxylase activity after 2 weeks, when the treatment started simultaneously or 1 day after the toxin lesion. FGF-2 was ineffective, if administration commenced with a delay of 7 days. Striatal neurotransmitters that are known to be linked to the dopaminergic system were also altered by the MPTP treatment. GABA was significantly increased, while somatostatin levels were reduced. Upon FGF-2 administration both GABA and somatostatin levels were partially normalized. Our data are consistent with the notion that FGF-2 protects and rescues acutely and subacutely MPTP-lesioned nigrostriatal neurons and that its effects must be mainly indirect. Likewise, positive effects of FGF-2 on non-dopaminergic neurons may be due to the partial restoration of striatal dopamine.
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PMID:FGF-2 modulates dopamine and dopamine-related striatal transmitter systems in the intact and MPTP-lesioned mouse. 750 15


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