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)

Multiple neuroreceptor changes are present in Alzheimer disease. These observations are based upon analysis from autopsy brain tissue or more seldom from neurosurgical biopsies. The drawback of information from autopsy material is that the receptor changes represent the final stage of the dementia disorder. It might therefore be somewhat misleading to base therapeutic strategies on these findings. Hopefully, new imaging techniques such as positron emission tomography (PET) and single photon emission tomography (SPECT) will provide valuable new in vivo data from the earlier course of the disease. Among the transmitter systems changed in Alzheimer disease, the cholinergic system shows the most consistent deficits. Cholinergic muscarinic receptors seem to be preserved in Alzheimer brains while nicotinic receptors show losses. The number of serotonin (both 5-HT1 and 5-HT2) and glutamate receptors are also reduced. Interestingly, kainate receptors increase in number while NMDA receptors are reduced in cortical Alzheimer tissue. Common for all receptor changes in Alzheimer disease is that the changes in number of binding sites are seen while the affinity constant remains unchanged. alpha- and beta-receptors and dopamine receptors are relatively preserved in Alzheimer brains. Among the neuropeptides, losses in receptor sites have been reported for somatostatin and neuropeptide Y (NPY). Interestingly, the number of CRF receptors are increased in cortical areas of Alzheimer brains. Thus, the muscarinic (M1), kainate, and CRF receptors show receptor compensatory reactions probably due to degenerative reactions in Alzheimer disease. Few attempts have been made to visualize neuroreceptors in vivo in Alzheimer patients. The field, however, is in dynamic progress. Reduced numbers of nicotinic receptors have been visualized in the brain of Alzheimer patients by PET and [11C]-nicotine and confirm earlier observations in post-mortem brain tissues. A lower uptake of (R)(+)[11C]nicotine compared to (S)(-)[11C]nicotine in patients with a mild form of dementia might be a possible diagnostic marker. SPECT studies indicate preserved muscarinic receptors in Alzheimer brains. Analysis of neuroreceptor changes in peripheral nonneural tissues have shown a reduction in nicotinic and muscarinic receptors in peripheral lymphocytes obtained from Alzheimer patients.
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PMID:Neuroreceptor changes in Alzheimer disease. 148 17

The development of GABAergic interneurons in feline striate area and extrastriate areas was tracked by single and double labeling immunohistochemistry using antibodies to GABA and to molecular markers which identify subpopulations of GABAergic neurons in adult mammalian neocortex; i.e., neuropeptide Y, somatostatin, and the calcium-binding proteins parvalbumin and calbindin. The density of GABA-ir neurons was relatively constant during development and among visual areas. By contrast, most of the GABA-subpopulations increased in the cortex of visual areas during postnatal development, and thus the proportion of GABA-ir neurons which also expressed another molecular marker increased during development. By the end of the first postnatal month, the neurotransmitter phenotypes of the neocortical GABAergic neurons are mature.
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PMID:Development of subpopulations of GABAergic neurons in cat visual cortical areas. 149 19

The inducible 72 kDa heat shock protein (HSP72) has been shown to be protective in non-neuronal cells and neurons in culture, but its function and the control of its expression in the CNS are poorly understood. Although HSP72 is induced in neurons in vivo by neurotoxic compounds that produce seizures and neuronal damage, it is unknown if its expression is a specific response to excitation per se or to "stressful" or potentially injurious excitation, or if it is a marker or mediator of irreversible injury. We have attempted to identify the nature of the stimulus for HSP72 expression by utilizing focal electrical stimulation that can either excite or destroy postsynaptic cells, depending on the duration of afferent stimulation. Previous studies have demonstrated that intermittent stimulation of the main hippocampal afferent pathway for 24 hr evokes synchronous discharges in dentate granule cells but does not injure them. However, the same stimulation irreversibly destroys three of the four cell populations innervated by the granule cells. The three vulnerable populations are the dentate hilar mossy cells, the somatostatin/neuropeptide Y (NPY)-immunoreactive hilar neurons, and the CA3c pyramidal cells. The fourth and relatively resistant population is the GABA-immunoreactive dentate basket cells. In this study, we have localized HSP72 expression immunocytochemically in the hippocampal dentate gyrus in response to nontoxic durations of potentially neurotoxic afferent stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heat shock protein expression in vulnerable cells of the rat hippocampus as an indicator of excitation-induced neuronal stress. 149 43

Neurons expressing the m1, m2, and m4 muscarinic receptor genes in the adult rat striatum were identified and characterized by using several in situ hybridization and immunohistochemical procedures. Combined in situ hybridization for the simultaneous detection of two mRNAs in the same section or in adjacent sections as well as in situ hybridization and immunohistochemistry on adjacent sections permitted us to identify the neurons containing m1, m2, or m4 receptor mRNA. Our observations demonstrate that m1, m2, and m4 receptor genes are expressed in one or several phenotypically distinct neuronal populations. The m1 receptor gene was the most widely expressed (85% of the striatal neurons). Most cholinergic neurons (80% or more) contain m1, m2, and m4 receptor mRNAs. Almost all the substance P neurons contain m1 and m4 receptor mRNA. All enkephalinergic neurons contained m1 receptor mRNA, but only 39% contained m4 receptor mRNA. Most somatostatin and neurotensin neurons expressed the m1 receptor gene, but only a few (15% and 9%, respectively) contained m4 receptor mRNA. The present study offers anatomical evidence that ACh may act directly in complex ways on the main neuronal populations of the striatum through muscarinic receptors. The m1, m2, and m4 receptors may act as autoreceptors to control ACh release and possibly other parameters of ACh neurons. On the other hand, the m1 and m4 receptors may act as heteroreceptors in cholinoceptive efferent neurons (enkephalin and substance P neurons) and other neurons (somatostatin/neuropeptide Y and neurotensin neurons). The presence of m4 receptor mRNA in only parts of the enkephalin, somatostatin, and neurotensin neuronal populations indicates that muscarinic receptor gene expression contributes to the functional and anatomical heterogeneity of the striatum that may relate to higher order of organization, including patch-matrix compartmentalization. The wide expression of m1 and m4 receptor genes in the striatum suggests that ACh may directly influence neurotransmitter release and synthesis in striatal efferent and intrinsic neurons. Our results imply that the specific pattern of expression of the muscarinic receptor genes mediates direct effects of ACh on activities and functions of chemically and topologically defined striatal neuronal populations. Since the expression of muscarinic receptors occurred in the three main neuronal populations of the striatum, namely ACh, enkephalins, and substance P neurons that also express dopamine receptors, it is highly probable that ACh and dopamine may act together at the single-cell level to influence striatal functions.
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PMID:Phenotypical characterization of the rat striatal neurons expressing muscarinic receptor genes. 152 98

Vibratome sectioning of paraformaldehyde-fixed brains containing a lesion and/or intracerebroventricular grafts and staining of these sections often lead to damage around the site of the lesion and loss of the implants. Various embedding procedures were compared in order to find a method to overcome this problem. The best results were obtained when fixed brain tissue was first embedded under reduced pressure in 10% gelatin at 50 degrees C, and then fixed again, in 4% paraformaldehyde. The method did not affect the immunocytochemical staining for vasopressin, vasoactive intestinal polypeptide, somatostatin, gonadotropin releasing hormone and neuropeptide Y.
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PMID:Gelatin embedding to preserve lesion-damaged hypothalami and intracerebroventricular grafts for vibratome slicing and immunocytochemistry. 152 72

The presence of immunoreactivity to the neuronal phosphoprotein B-50 and the peptides bombesin, calcitonin gene-related peptide, galanin, neurotensin, neuropeptide Y, somatostatin, substance P, and vasoactive intestinal polypeptide was examined in biopsy specimens from the duodenum and rectum of human immunodeficiency virus (HIV)-seropositive and HIV-seronegative male homosexual patients. The distribution of B-50 and the peptides was correlated with HIV serology, number of CD4+ lymphocytes, and the presence of HIV in biopsy culture. There was a very low incidence of enteric pathogens in both groups of patients. It was found that HIV-seropositive patients had a greater incidence of abnormal patterns of immunoreactivity (reduced intensity and/or density of innervation) in enteric nerves and enteroendocrine cells than HIV-seronegative patients. A reduction of substance P immunoreactivity was significantly correlated with reduced CD4+ lymphocyte count and HIV status; a similar trend was also seen for somatostatin and vasoactive intestinal polypeptide. Using B-50 as a marker, it was found that both groups of patients had altered patterns of immunoreactivity in rectal nerves. The findings of this study suggest that some of the clinical symptoms associated with HIV infection may be caused by a specific HIV enteropathy that influences enteric nerve and/or enteroendocrine cell function by altering the density of peptide immunoreactivity.
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PMID:Peptides in the gastrointestinal tract in human immunodeficiency virus infection. The GI/HIV Study Group of the University of Calgary. 153 25

The effects of 1-methyl-4-phenylpyridinium (MPP+) were studied in rat striatum. Using freeze-clamp, microwave, and water-suppressed proton chemical shift magnetic resonance imaging techniques, MPP+ resulted in marked increases in lactate and a depletion of ATP for up to 48 h after the injections. MPP+ produced dose-dependent depletions of dopamine, serotonin, gamma-aminobutyric acid, and substance P that were partially blocked at 1 week by prior decortication or completely blocked by MK-801 at 24 h. The lesions showed relative sparing of somatostatin-neuropeptide Y neurons, consistent with N-methyl-D-aspartate (NMDA) excitotoxicity. MPP+ produces impairment of oxidative phosphorylation in vivo, which may result in membrane depolarization with persistent activation of NMDA receptors and excitotoxic neuronal degeneration. An impairment of energy metabolism may therefore underlie slow excitotoxic neuronal death in neurodegenerative diseases.
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PMID:1-Methyl-4-phenylpyridinium produces excitotoxic lesions in rat striatum as a result of impairment of oxidative metabolism. 156 Feb 46

Cholinergic synaptosomes from rat cerebral cortex were isolated by a magnetic immunoaffinity technique, i.e. immunomagnetophoresis. This subpopulation was extracted and subjected to radioimmunoassay for 4 neuropeptides:neuropeptide Y (NPY); vasoactive intestinal peptide (VIP); substance P (SP); and somatostatin (SRIF). Three of the 4 neuropeptides were enriched in the sorted fraction compared with the mother fraction with respect to the cytosolic marker lactate dehydrogenase (LDH). The most enriched neuropeptide was NPY followed by SP and VIP. Somatostatin was not enriched in the cholinergic synaptosome subpopulation. The presence of NPY has not previously been reported in cortical cholinergic neurones.
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PMID:Neuropeptide content of purified rat brain cholinergic synaptosome subpopulations. 160 51

Chromaffin granules, the secretory organelles of the neuron-like adrenal medullary chromaffin cells, have previously been shown to store and liberate neurotrophic activities that support in vitro survival of several neuron populations including those innervating the adrenal medulla. Molecules resembling fibroblast growth factor and ciliary neurotrophic factor have been identified among these activities. Since chromaffin granules store a variety of neuropeptides and many neuropeptides can have pleiotropic effects on neuronal growth and maintenance we have tested 24 different neuropeptides for their capacities to promote survival of embryonic chick ciliary, dorsal root and sympathetic ganglionic neurons. Peptides tested included several derivatives of proenkephalin (Leu- and met-enkephalin, fragments BAM 22, B, F and E), somatostatin, substance P, neuropeptide Y, neurotensin, VIP, bombesin, secretin, pancreastatin, dynorphin B, dynorphin 1-13, beta-endorphin, alpha-, beta-, and gamma-MSH. Control cultures received saturating concentrations of ciliary neurotrophic or nerve growth factor (CNTF; NGF), or no trophic supplements. At 1 x 10(-5) M leu- and met-enkephalin as well as somatostatin supported sympathetic neurons to the same extent as NGF. At the same concentrations, leu-enkephalin, the proenkephalin fragments BAM 22 and E, and somatostatin maintained about half of the dorsal root ganglionic neurons supported by NGF, but were not effective on ciliary neurons. VIP promoted the survival of approximately 50% of the ciliary and embryonic day 10 dorsal root ganglionic neurons as compared to saturating amounts of CNTF, but required the presence of non-neuronal cells in the cultures to be effective. Neurotensin (1 x 10(-5) M had a small effect on ciliary neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Screening of adrenal medullary neuropeptides for putative neurotrophic effects. 163 76

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.
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PMID:Neurochemical characterization of excitotoxin lesions in the cerebral cortex. 167 Jul 82


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