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)

We have measured somatostatin-like immunoreactivity SLI in cerebroventricular fluid of patients with Parkinson's disease (PD) and other extrapyramidal disorders with hyperkinesia. Patients with PD showed a significantly lower concentration of SLI when compared with levels in control patients with chronic stable multiple sclerosis or temporal lobe epilepsy. Less markedly decreased levels of SLI were also noted in patients with torsion dystonia. Of two patients with Huntington's disease one showed a high and one a medium concentration of SLI. According to the site of the stereotactic cannula, verified by ventriculopathy, SLI concentrations in CSF specimen obtained from the foramen Monro tended to be higher than in specimen from a supraforaminal level. Of 5 other patients with lateral and third ventricle being accessible during the passage of the stereotactic cannula, 4 showed higher SLI concentrations in the third ventricle compared to the lateral ventricle. High performance liquid chromatographic analysis combined with radioimmunoassay showed molecular heterogeneity of SLI in CSF. The ratio of SST-14 to SST-28 was higher in the third ventricle than in the lateral ventricle.
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PMID:Ventricular fluid neuropeptides in Parkinson's disease. I. Levels and distribution of somatostatin-like immunoreactivity. 197 61

Changes in the cholinergic, serotonergic, noradrenergic, dopaminergic, GABAergic and somatostatinergic neurons were investigated to determine their roles in Alzheimer's disease (AD). Markers for these systems were analyzed in postmortem brain samples from 20 patients with AD and 14 controls. In the CSF study, markers for the cholinergic neurons (choline esterase, ChE) and for the somatostatinergic neurons (somatostatin-like immunoreactivity, SLI) were assayed for 93 and 75 probable AD patients and 29 and 19 controls, respectively. Activity of choline acetyltransferase (CAT) was decreased by 50-85% in four cortical areas and hippocampus in patients with AD, but not in other areas of the brain, indicating a profound deficit in the function of cholinergic projections ascending from the nucleus basalis to the cerebral cortex and hippocampus in AD. Muscarinic receptor binding was reduced by 18% in the frontal cortex but not in other areas of the brain in AD. Serotonin (5HT) concentrations were reduced (by 21-37%) in hippocampal cortex, hippocampus and striatum; and 5HT metabolite levels were lowered (by 39-54%) in three cortical areas, thalamus and putamen in AD patients. Concentrations of noradrenaline (NA) were reduced (18-36%) in frontal and temporal cortex and putamen. These data imply that serotonergic and noradrenergic projections are also affected in AD but less than the cholinergic neurons. Dopamine (DA) concentrations in AD patients were reduced by 18-27% in temporal and hippocampal cortex and hippocampus, while HVA, the metabolite of DA, was unaltered. Glutamic acid decarboxylase activity was not altered in AD. SLI was decreased (28-42%) in frontal, temporal and parietal cortex, but not in thalamus and putamen in patients with AD. Frontal tangle scores correlated most strongly with cortical CAT activity reduction and less so with decreases of 5HT, NA and DA, indicating a closer correlation with the cholinergic changes and severity of AD than with other neurotransmitter deficiencies. ChE activity and SLI were reduced by 20% and 35%, respectively, in CSF of the whole group of AD patients as compared to the controls. Comparison of CSF findings between four subgroups of dementia severity indicated that the SLI was already reduced in the group of mildest AD (-31%), while ChE activity was not. Although ChE activity in CSF declined in relation to dementia severity, however, the maximal reduction was only modest (-30%). On the other hand, SLI in CSF showed only a slight further reduction (up to -41%) as the dementia become more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. 198 17

The level of cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 11 chronic schizophrenic patients with moderate cognitive impairment and for 8 controls. The CSF SLI was significantly reduced (37%) in schizophrenic patients, but this decrease did not correlate with the degree of cognitive decline measured by the Mini-Mental State Examination, with psychotic symptoms estimated by the Brief Psychiatric Rating Scale, or with the neuroleptic dose. Although a reducing effect of long-term neuroleptic treatment cannot be totally excluded, the present study suggests that the CSF SLI level is decreased in cognitively impaired schizophrenic patients, as in many other disorders with cognitive impairment.
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PMID:Decreased somatostatin-like immunoreactivity in the cerebrospinal fluid of chronic schizophrenic patients with cognitive impairment. 224 5

Cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 9 patients with chronic alcohol ingestion and dementia associated with alcoholism and for 8 age-equivalent controls. The CSF SLI was significantly reduced (32%) in the alcoholics with dementia as compared to the controls. This finding is in accordance with previous observations on the relationship between reduced CSF SLI and cognitive impairment in various neuropsychiatric disorders, and extends this finding to patients with dementia associated with alcoholism.
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PMID:Somatostatin-like immunoreactivity in the CSF of patients with dementia associated with alcoholism. 228 44

Calcitonin gene-related peptide (CGRP) was found to potently inhibit a substance P endopeptidase isolated from human CSF. CGRP potentiated substance P irritant actions; a possible mechanism is interaction for a common metabolic step. Somatostatin is another peptide capable of competing with substance P endopeptidase.
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PMID:Calcitonin gene-related peptide is a potent inhibitor of substance P degradation. 241 71

The concentrations of arginine vasopressin (AVP), somatostatin (SS), and the primary brain metabolites of norepinephrine (MHPG), serotonin (5-HIAA), and dopamine (HVA) were measured in samples of lumbar CSF obtained from ten amnesics with Korsakoff's psychosis, four patients with a history of Korsakoff's psychosis who had recovered from the amnesic symptoms of this disease, and control subjects. Significant deficits were observed in the amnesic group for AVP and MHPG, but not for the other substances measured. Subjects who had recovered from the amnesic symptoms of Korsakoff's psychosis had increased concentrations of AVP and MHPG, but not of SS or the other monoamine metabolites.
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PMID:Reduced concentrations of arginine vasopressin and MHPG in lumbar CSF of patients with Korsakoff's psychosis. 242 5

Improved knowledge about biochemical mechanisms underlying pain suppression by CNS electric stimulation is one condition for the further advancement of this form of treatment. In 6 patients treated with PVG stimulation and in 14 with spinal cord stimulation the concentration of substance P-like immunoreactivity in lumbar CSF increased significantly following stimulation. However, these changes may be unspecific and not directly related to the suppression of pain. Measurements of somatostatin, cholecystokinin, vasoactive intestinal polypeptide, neurotensin and monoamine metabolites in CSF showed no changes related to stimulation and the ensuing pain relief. Possible reasons for these negative findings are discussed.
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PMID:Possible neurohumoral mechanisms in CNS stimulation for pain suppression. 242 25

Acetylcholinesterase, somatostatin-like immunoreactivity, and homovanillic acid levels were measured in the cerebrospinal fluid of 36 patients with early stages of Parkinson's disease and in 19 control patients. In patients with Parkinson's disease the levels of somatostatin-like immunoreactivity were lower than in the controls (p less than 0.01); these values were lowest in the demented Parkinsonian patients. Concentrations of homovanillic acid were also significantly lower in Parkinsonian patients (p less than 0.05). In contrast, no changes were observed in the acetylcholinesterase activity of patients with Parkinson's disease. The reduced somatostatin-like immunoreactivity in CSF agrees with previous post-mortem studies and indicates that Parkinson's disease and Alzheimer's disease may have some neurochemical features in common.
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PMID:Somatostatin-like immunoreactivity in the cerebrospinal fluid of patients with Parkinson's disease and its relation to dementia. 243 3

CSF samples from ten healthy volunteers and 22 patients with major depression were collected by lumbar puncture at 9 a.m. and the content of monoamine metabolites, corticotropin releasing factor (CRF) and somatostatin (SRIF) was analyzed. Plasma concentrations of TSH following a TRH challenge test (200 micrograms) and plasma cortisol following dexamethasone (1 mg; DST) were also analyzed. No relationships were observed between the CRF or SRIF concentrations and either basal or post-dexamethasone cortisol concentrations. Fourteen of 21 depressed patients were DST nonsuppressors using a plasma cortisol concentration cut off point greater than or equal to 138 nmol/l. If a more conservative cut off point was used (greater than 290 nmol/l) seven out of 21 patients revealed a severity-related cortisol nonsuppression. No significant difference was observed between healthy volunteers and depressed patients with regard to TSH response to TRH. The CSF content of CRF was elevated and the content of SRIF reduced in the depressed patients. In the healthy volunteers an inverse relationship was observed between CSF concentrations of CRF and MHPG (r = -0.72; P = 0.019); no relationship was observed between the concentrations of CRF and 5-HIAA or HVA. In the depressed patients positive correlations were found between CSF concentrations of CRF and 5-HIAA (r = 0.59; P = 0.004) and between CRF and HVA (r = 0.44; P = 0.042). These data are concordant with the view that norepinephrine and serotonin may be involved in the regulation of CRF secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monoamine metabolites, corticotropin releasing factor and somatostatin as CSF markers in depressed patients. 245 42

The present study examines the effects of intrathecal administration of selected peptides on nociceptive responses in the rat. Each peptide was delivered via a chronically implanted catheter to the L5 vertebral level. In the tail flick test, VIP (0.65-6.5 nmoles) produced a dose-dependent decrease in reaction time (RT) from 1 to 6-16 min after injection; 6.5 nmoles decreased RT to 37% of control value at 1 min after injection. Galanin (0.65-6.5 nmoles) produced a dose-dependent increase in reaction time at 1 and 6 min; at high doses, many of the rats failed to flick the tail. CGRP (6.5 nmoles) produced a small, transient decrease in RT to 73% of control values at 1 min; 3.25 nmoles were without effect. CSF and 6.5 nmoles of somatostatin, TRH and angiotensin II were without effect. At high doses of galanin and CGRP, rats vocalized to innocuous touch of the tail, as reported for substance P. Von Frey hairs were thus applied to the tail after 6.5 nmoles of VIP, galanin, CGRP or substance P. Vocalization in response to a previously innocuous pressure stimulus was observed at 30 s after injection in all rats given galanin and some rats given CGRP or substance P; the effect lasted 4-8 min. VIP and CSF had no effect. These results suggest that VIP, galanin, CGRP and substance P may act as excitatory agents in nociceptive pathways and that specific peptides may function in the different types of pain modalities; VIP in thermal, galanin in mechanical and substance P and CGRP in both.
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PMID:Effects of intrathecal administration of neuropeptides on a spinal nociceptive reflex in the rat: VIP, galanin, CGRP, TRH, somatostatin and angiotensin II. 245 92


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