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)

The molecular size distribution of somatostatin-like immunoreactivity (SLI) in the cerebroventricular fluid of patients with Parkinson's disease, dystonic syndromes, multiple sclerosis, basal and midline tumors, epilepsy and pain syndromes was investigated by separation with a Sephadex G-50f column and subsequent radioimmunoassay of the eluate. Marked heterogeneity of SLI was observed in most of the pools investigated. The most conspicuous feature of the elution profiles was the preponderance of the peak coeluting with synthetic somatostatin-14, whereas the peaks comigrating with synthetic somatostatin-28 and attributable to precursor-like SLI represented only minor or trace amounts of total immunoreactivity. These findings are consistent with the greater biological activity of somatostatin-14 in the human central nervous system, whereas somatostatin-28 appears to represent the more active form in the pituitary and in the intestinal mucosa. Solely in the case of brain tumor patients, some differences could be seen, resulting in an approximately equal distribution of somatostatin-14 and somatostatin-28 in two pools of ventricular fluid and by the detection of a degradation product of somatostatin-14 in another one. These observations could be explained by a lowered barrier function as a consequence of increased intracranial pressure in case of brain tumors, which is well in accordance with a markedly elevated total protein content being a sign of a lowered barrier function.
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PMID:Molecular size distribution of somatostatin-like immunoreactivity in the cerebroventricular fluid of neurosurgical patients. 367 Jul 43

The finding of a number of peptides in the central nervous system and the discovery of the endogenous opiates represent major recent advances in the understanding of neural transmission. A number of these neuropeptides are found in the dorsal root entry zone and may play a role in pain. An analysis of changes in distribution of substance P, methionine-enkephalin, and somatostatin after simulated nerve root avulsion injury suggested a possible mechanism for deafferentation pain. A review of the localizations and actions of these peptides in the dorsal root entry zone is included.
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PMID:Neuropharmacology of the dorsal root entry zone. 608 4

The effects of neuroactive peptides on the release of 5-HT were studied. The 5-HT released from the spinal cord was significantly increased by somatostatin, substance P and peripheral pain stimulation (tail pinch), but not affected by neurotensin, beta-endorphin and met-enkephalin. The somatostatin-evoked 5-HT release was inhibited by baclofen and met-enkephalin in vivo but not in vitro. The substance P-evoked 5-HT release was strongly inhibited by baclofen, and slightly potentiated by met-enkephalin in vivo but not in vitro. The tail pinch-induced 5-HT release was inhibited by met-enkephalin and baclofen, but potentiated by naloxone. These findings provide further evidence on the important role of neuropeptides and suggest that the descending serotonergic neurones are modulated by neuropeptide interneurones in the spinal cord.
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PMID:Effect of neuroactive peptides on labeled 5-hydroxytryptamine release from rat spinal cord. 608 98

The pain relieving effect of somatostatin treatment during 72 attacks of cluster headache in 8 male patients was compared to treatment with ergotamine or placebo in a double-blind study. Infusion of somatostatin (25 micrograms/min for 20 min i.v.) reduced the maximal pain intensity and the duration of pain significantly compared to placebo treatment, and to a degree comparable to ergotamine tartrate treatment (250 micrograms i.m.). The results obtained provide new information concerning the possible mechanism of cluster headache attacks and suggest a new therapeutic approach.
Pain 1984 Apr
PMID:Pain relief by somatostatin in attacks of cluster headache. 614 38

When the dorsal hand vein (DHV) is locally injected with somatostatin (SS) it spasms visibly. These spasms can be measured using the computerized venospasm technique. Acute, complete long-lasting tolerance (tachyphylaxis) develops following 2-4 injections of somatostatin. A revival of sensitivity to SS is induced in the fatigued vein by the local injection of naloxone. This suggests that endogenous opioids could participate partially or totally in SS tachyphylaxis. The analgesic effect displayed by somatostatin on the dramatic pain of the cluster attack is quantitatively similar to that of ergotamine; the therapeutic mechanism of both drugs has until now remained undefined.
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PMID:Venospastic activity of somatostatin in vivo in man: naloxone reversible tachyphylaxis. 614 97

Release of immunoreactive somatostatin (I-SRIF) and immunoreactive substance P (I-SP) was studied from slices prepared from upper dorsal horn (UDH) and lower dorsal plus ventral horn (LDH-VH) of rat spinal cord. Superfusion with capsaicin (10 microM) led to release of I-SRIF and I-SP from UDH slices but not from LDH-VH slices. The capsaicin-evoked release of I-SP was 6 fold higher than that of I-SRIF. A pulse of 60 mM K+ applied after the capsaicin pulse caused release of I-SRIF and I-SP from UDH as well as LDH-VH slices. Pretreatment of rats with capsaicin (125 mg/kg, s.c.) led to a nearly 40% depletion of I-SP in slices from UDH only. Capsaicin-evoked release from these slices was reduced by 81% for I-SRIF and by 79% for I-SP. Release evoked by K+ remained unchanged. These results indicate that capsaicin causes release of both I-SRIF and-I-SP and that this release is most likely restricted to primary sensory neurons. The marked reduction of the release of I-SP after systemic capsaicin pretreatment may well represent one of the, or even the reason for the insensitivity of capsaicin pretreated rats towards chemogenic pain.
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PMID:Effect of capsaicin pretreatment on capsaicin-evoked release of immunoreactive somatostatin and substance P from primary sensory neurons. 616 21

Capsaicin was applied locally to the sciatic or saphenous nerve, and the effects on axoplasmic transport, neurogenic plasma extravasation, and thermal pain were studied. Capsaicin (10 mg/ml) led to a complete block of axoplasmic transport of immunoreactive substance P (I-SP) and somatostatin (I-SRIF) in rat sciatic nerve without affecting the transport of noradrenaline or acetylcholinesterase. Inhibition of I-SP transport was also found in sciatic nerves of guinea-pig, cat and rabbit. In contrast, one or two weeks after systemic capsaicin treatment (125 mg/kg s.c.), orthograde transport of I-SP was the same in control and capsaicin-treated rats. After local capsaicin application to the sciatic nerve, a decrease of I-SP was found not only in skin and sciatic nerve distal to the site of application, but also in dorsal root ganglia, dorsal roots and the dorsal half of the spinal cord segments L 4-5. This was accompanied by a loss of acid phosphatase activity in the substantia gelatinosa supplied by sciatic nerve afferents. Plasma extravasation by mustard oil was reduced in the skin of the hind paw with a time course identical to the I-SP depletion. The response to noxious heat (hot plate test) was, however, abolished earlier. These results indicate that capsaicin applied to a peripheral nerve inhibits axoplasmic transport in sensory but not in adrenergic or cholinergic neurons, which leads to long-term biochemical and functional changes of the entire sensory neuron. In addition, capsaicin appears to inhibit impulse propagation in certain populations of sensory neurons.
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PMID:Capsaicin applied to peripheral nerve inhibits axoplasmic transport of substance P and somatostatin. 617 69

Substance P appears to be involved in the transmission of pain signals from the periphery to the spinal cord and brain stem. Substance P containing neurons are responsible for the neurogenic vasodilation identical to that obtained by substance P release evoked by antidromic stimulation of these fibres. Both endogenous opioids and somatostatin inhibit the release of substance P from central and peripheral endings. Present pharmacological investigations conclude that morphine and somatostatin are as effective as ergotamine in reducing the pain of CH. All three drugs are significantly more active than placebo. Somatostatin and opiates could act by inhibiting the release of substance P.
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PMID:Substance P and endogenous opioids: how and where they could play a role in cluster headache. 619 86

The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. Following the first injection, a rise of 108 +/- 66% in CSF somatostatin levels was observed in 7 out of 13 patients, and a rise of 87 +/- 26% in 4 out of the 5 patients undergoing a second injection. A rise of 179 +/- 99% in levels of Substance P in CSF was observed in 4 out of 8 patients after a single injection. No change in peptide concentration was detected in peripheral plasma. Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. The data are consistent with our previous experience that injection of alcohol into the pituitary fossa can cause destruction to nervous tissue, in addition to the obvious destruction of pituitary gland tissue. They do not support the suggestion that hypothalamic damage is necessary in order to obtain pain relief.
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PMID:Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. 620 18

Immunohistochemical studies on rats showed cysteamine to deplete immunoreactive somatostatin, but not substance P, in the substantia gelatinosa of the spinal trigeminal nucleus and spinal cord. The effect of cysteamine treatment on chemical pain was investigated using capsaicin as the pain-producing stimulus. Thermal pain was assessed with a hot plate test after cysteamine treatment. It was found that cysteamine did not alter the hind paw lick latency in the hot plate test or the number of forepaw wipes after application of a drop of capsaicin into the cornea, compared to normal animals. In capsaicin-treated animals a significantly lower number of forepaw wipes were seen after corneal capsaicin application. However, in cysteamine-treated animals slower wiping was observed compared to untreated and capsaicin-treated animals. This suggests that somatostatin may be of importance for the modulation of nociceptive information, although it is not a major pain transmitter.
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PMID:Effects of cysteamine on pain behaviour and on somatostatin- and substance P-like immunoreactivity in the substantia gelatinosa of the rat. 620 49


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