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 aim of the study was to investigate neurochemical changes in a kainic acid (KA; 10 mg/kg, s.c.)-induced spontaneous recurrent seizure model of epilepsy, 6 months after the initial KA-induced seizures. The neuronal markers of cholinergic and gamma-aminobutyric acid (GABA)ergic systems, i.e. choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities, and a marker for neuropeptide, i.e. level of somatostatin, have been investigated. The brain regions investigated were the hippocampus, amygdala/piriform cortex, caudate nucleus, substantia nigra and the frontal, parietal, temporal and occipital cortices. Six months after KA injection, reduced ChAT activity was observed in the amygdala/piriform cortex (47% of control; p<0.001), increased ChAT activity in the hippocampus (119% of control; p<0.01) and normal ChAT activity in the other brain regions. The activity of GAD was significantly increased in all analysed cortical regions (between 146 and 171% of control), in the caudate nucleus (144% of control; p<0.01) and in the substantia nigra (126% of control; p<0.01), whereas in the amygdala/piriform cortex, the GAD activity was moderately lowered. The somatostatin level was significantly increased in all cortical regions (between 162 and 221% of control) as well as in the hippocampus (119% of control), but reduced in the amygdala/piriform cortex (45% of control; p<0.01). Six months after KA injection, the somatostatin:GAD ratio was lowered in the amygdala/piriform cortex (49% of control) and in the caudate nucleus (41% of control), whereas it was normal in the hippocampus and moderately increased in the cortical brain regions. A positive correlation was found between seizure severity and the reduction of both ChAT activities and somatostatin levels in the amygdala/piriform cortex. The results show a specific pattern of changes for cholinergic, GABAergic and somatostatinergic activities in the chronic KA model for epilepsy. The revealed data suggest a functional role for them in the new network that follows spontaneous repetitive seizures.
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PMID:Choline acetyltransferase, glutamic acid decarboxylase and somatostatin in the kainic acid model for chronic temporal lobe epilepsy. 1562 16

We have previously shown that in adult mice with a null mutation in the urokinase-type plasminogen activator receptor (uPAR) gene, maintained on a C57BL/6J/129Sv background, there is a selective loss of GABAergic interneurons in anterior cingulate and parietal cortex, with the parvalbumin-expressing subpopulation preferentially affected. Here, we performed a more detailed anatomical analysis of uPAR(-/-) mutation on the congenic C57BL/6J background. With glutamic acid decarboxylase-67 and gamma-aminobutyric acid (GABA) immunostaining, there is a similar region-selective loss of cortical interneurons in the congenic uPAR(-/-) mice from the earliest age examined (P21). In contrast, the loss of parvalbumin-immunoreactive cells is observed only in adult cortex, and the extent of this loss is less than in the mixed background. Moreover, earlier in development, although there are normal numbers of parvalbumin cells in the uPAR(-/-) cortex, fewer cells coexpress GABA, suggesting that the parvalbumin subpopulation migrates appropriately to the cortex, but does not differentiate normally. Among the other forebrain regions examined, only the adult hippocampus shows a loss of GABAergic interneurons, although the somatostatin, rather than the parvalbumin, subpopulation contributes to this loss. The data suggest that uPAR function is necessary for the normal development of a subpopulation of GABAergic neurons in the telencephalon. It is likely that the late-onset parvalbumin phenotype is due to the effects of an altered local environment on selectively vulnerable neurons and that the extent of this loss is strain dependent. Thus, an interplay between complex genetic factors and the environment may influence the phenotypic impact of the uPAR mutation both pre- and postnatally.
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PMID:Region- and age-specific deficits in gamma-aminobutyric acidergic neuron development in the telencephalon of the uPAR(-/-) mouse. 1602 58

Prevalence of uterine progesterone receptors over estrogen ones, high uterine cAMP level, and low uterine prostaglandin level are necessary conditions of normal pregnancy. In cases of spontaneous and antiprogestin RU486-induced abortions, estrogen receptors prevail over progesterone ones, cAMP level decreases, and prostaglandin concentration in decidual tissue increases. Porcine and bovine beta-lipotropines were the first proteins, whose correct amino acid sequence was first determined in Russia. Several research centers carried out collaborative studies of the nucleotide sequences of human and animal proopiomelanocortin (lipotropin precursor) and prolactin cDNA. Researchers constructed genetic engineering producers of human pre-proinsulin and somatostatin, identified structural genes expressed in pancreatic beta-cells, studied antigenic properties of glutamic acid decarboxylase (GAD), which determine insulin-dependent diabetes, and identified the cholesterase determinant. They revealed mutations in the genes of proopiomelanocortin and melanocortin receptors (MC4-P), which inhibit leptin regulation of appetite and are associated with human obesity.
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PMID:[Molecular and genetic study of the role of hormones, receptors, and enzymes in regulation of reproduction, lipid metabolism, and other human physiological functions]. 1625 Mar 24

Although it is established that neurokinin B is expressed by some neurons in laminae I-III of the rat spinal dorsal horn, little is known about the proportions of cells in these laminae that express neurokinin B, or whether these are excitatory or inhibitory neurons. Neurokinin B is derived from preprotachykinin B, and we have used an antibody against preprotachykinin B to address these issues. We found that preprotachykinin B-immunoreactive neurons were present throughout laminae I-III, constituting 10-11% of the neuronal population in laminae I-II, and 4% of that in lamina III. They formed a prominent band in the ventral half of lamina II (where they made up 16% of the population) and the dorsalmost part of lamina III. The great majority (99%) of preprotachykinin B-immunoreactive axonal boutons contained the vesicular glutamate transporter 2, while none contained glutamic acid decarboxylase. Since most of these boutons are likely to be derived from local preprotachykinin B-expressing cells, these observations suggest that most of the latter are excitatory interneurons. Although 9% of preprotachykinin B-labeled axonal varicosities were substance P-immunoreactive, none contained calcitonin gene-related peptide, which is consistent with reports that neurokinin B is not expressed by primary afferent axons. Many of the preprotachykinin B-immunoreactive cells contained compounds that are present in putative excitatory neurons in laminae I-III: calbindin (84%), protein kinase Cgamma (76%) or somatostatin (31%). However, there was little or no overlap between preprotachykinin B and three other markers associated with excitatory neurons in these laminae: the mu opioid receptor MOR-1, the neurokinin 1 receptor and neurotensin. These results suggest that neurokinin B is expressed by specific populations of excitatory neurons in the superficial dorsal horn. By examining expression of Fos protein in response to intraplantar injection of formaldehyde we provide evidence that many of the preprotachykinin B cells in lamina I and the outer part of lamina II respond to noxious stimulation.
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PMID:Characterization of neurons that express preprotachykinin B in the dorsal horn of the rat spinal cord. 1644 41

The structural organization of the central nervous system is an infrastructure of the modern neuroscience. Especially, anatomical research at the cellular level can serve as a fundamental resource to understand various novel findings from the molecular level to the system level. Of the decade, the importance of rigorous quantitative neuroanatomy is gradually realized, but earlier anatomical reports are usually presented in qualitative terms or quantified with biased methods. This article quantitatively describes the spatial distributions of chemically defined GABAergic neurons in the mouse hippocampus by using unbiased stereological techniques. We focus on the expression of nine major neurochemical markers: glutamic acid decarboxylase 67, three calcium binding proteins (parvalbumin, calretinin, calbindin D28K), four neuropeptides (somatostatin, neuropeptide Y, cholecystokinin, vasoactive intestinal protein) and neuronal nitric oxide synthase. Here we deal with their laminar distributions, numerical densities and the relative ratio to the total GABAergic neurons, with special reference to their differentiation along the dorsoventral axis of the mouse hippocampus. Furthermore, we estimate the absolute numbers of GABAergic neurons contained in a 300-mum-thick hypothetical slice. The present data outline the quantitative aspects of the cellular architecture of hippocampal GABAergic system and also give complementary information to the recent multidisciplinary analyses at the single cell level.
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PMID:Cellular architecture of the mouse hippocampus: a quantitative aspect of chemically defined GABAergic neurons with stereology. 1693 Jul 55

In subjects with schizophrenia, impairments in working memory are associated with dysfunction of the dorsolateral prefrontal cortex (DLPFC). This dysfunction appears to be due, at least in part, to abnormalities in gamma-aminobutyric acid (GABA)-mediated inhibitory circuitry. To test the hypothesis that altered GABA-mediated circuitry in the DLPFC of subjects with schizophrenia reflects expression changes of genes that encode selective presynaptic and postsynaptic components of GABA neurotransmission, we conducted a systematic expression analysis of GABA-related transcripts in the DLPFC of 14 pairs of schizophrenia and age-, sex- and post-mortem interval-matched control subjects using a customized DNA microarray with enhanced sensitivity and specificity. Subjects with schizophrenia exhibited expression deficits in GABA-related transcripts encoding (1) presynaptic regulators of GABA neurotransmission (67 kDa isoform of glutamic acid decarboxylase (GAD(67)) and GABA transporter 1), (2) neuropeptides (somatostatin (SST), neuropeptide Y (NPY) and cholecystokinin (CCK)) and (3) GABA(A) receptor subunits (alpha1, alpha4, beta3, gamma2 and delta). Real-time qPCR and/or in situ hybridization confirmed the deficits for six representative transcripts tested in the same pairs and in an extended cohort, respectively. In contrast, GAD(67), SST and alpha1 subunit mRNA levels, as assessed by in situ hybridization, were not altered in the DLPFC of monkeys chronically exposed to antipsychotic medications. These findings suggest that schizophrenia is associated with alterations in inhibitory inputs from SST/NPY-containing and CCK-containing subpopulations of GABA neurons and in the signaling via certain GABA(A) receptors that mediate synaptic (phasic) or extrasynaptic (tonic) inhibition. In concert with previous findings, these data suggest that working memory dysfunction in schizophrenia is mediated by altered GABA neurotransmission in certain DLPFC microcircuits.
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PMID:Alterations in GABA-related transcriptome in the dorsolateral prefrontal cortex of subjects with schizophrenia. 1747 Dec 87

The distribution and morphological features of calcitonin gene-related peptide (CGRP) positive neurons in the mouse hippocampus were immunohistochemically analyzed, focusing on their differences between mice and rats. In contrast with those in the rat dentate gyrus, the mossy cell somata and their axon terminals in the mouse dentate gyrus were CGRP negative even after intraventricular colchicine injection. In the rat CA1-CA2-CA3 regions, there were two types of CGRP positive neurons, some of the CA3 pyramidal cells and relatively few nonprincipal neurons. In the mouse CA1-CA2-CA3 regions, there were also two types of CGRP positive neurons. The majority were scattered throughout layers and abundant in number when compared with those in the rat hippocampus. They were regarded as nonprincipal neurons by their distribution, structural features and glutamic acid decarboxylase 67 (GAD67) immunoreactivity. The minor group was clustered in the stratum pyramidale of the CA2 region. They extended thick apical dendritic shafts into the stratum radiatum, were GAD67 negative, and thus were regarded as the CA2 pyramidal cells. The CGRP positive nonprincipal neurons were apparently heterogeneous and further characterized immunohistochemically. Although there were significant regional differences in the chemical properties of the CGRP positive nonprincipal neurons, in the whole hippocampus, over 40% of CGRP positive nonprincipal neurons were also positive for parvalbumin, about 15% were positive for somatostatin and about 20% were positive for cholecystokinin, respectively. The present study clearly showed that there were prominent species differences between the mouse and rat hippocampus in the CGRP immunoreactivities.
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PMID:Nonprincipal neurons and CA2 pyramidal cells, but not mossy cells are immunoreactive for calcitonin gene-related peptide in the mouse hippocampus. 1800 45

Aging of the brain is characterized by several neurochemical modifications involving structural proteins, neurotransmitters, neuropeptides and related receptors. Alterations of neurochemical indices of synaptic function have been considered as indicators of age-related impairment of central functions, such as locomotion, memory and sensory performances. Several studies demonstrated that GABA receptors, glutamic acid decarboxylase (GAD65&67), and different subpopulations of GABAergic neurons are markedly decreased in experimental animal brains during aging. Thus, the age-related decline in cognitive functions could be attributable, at least in part, to decrements in GABA inhibitory neurotransmission. In this study, using a passive avoidance test, we show that chronic supplementation of taurine to aged mice significantly ameliorates the age-dependent decline in memory acquisition and retention. We have previously shown that taurine supplementation caused changes in the GABAergic system. These changes include increased levels of the neurotransmitters GABA and glutamate, increased expression of glutamic acid decarboxylase and the neuropeptide somatostatin and increase in the number of somatostatin-positive neurons. These specific alterations of the inhibitory system caused by taurine treatment oppose those naturally occurring in aging, and suggest a protective role of taurine against the normal aging process. Increased understanding of age-related neurochemical changes in the GABAergic system will be important in elucidating the underpinnings of the functional changes of aging. Taurine might help forestall the age-related decline in cognitive functions through alterations of the GABAergic system.
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PMID:Taurine improves learning and retention in aged mice. 1837 59

Understanding the development of cortical interneuron phenotypic diversity is critical because interneuron dysfunction has been implicated in several neurodevelopmental disorders. Here, tyrosine hydroxylase (TH)-immunoreactive neurons in the developing and adult rat cortex were characterized in light of findings regarding interneuron neurochemistry and development. Cortical TH-immunoreactive neurons were first observed 2 weeks postnatally and peaked in number 3 weeks after birth. At subsequent ages, the number of these cell profiles was gradually reduced, and they were seen less frequently in adults. No DNA fragmentation or active caspase 3 was observed in cortical TH cells at any age examined, eliminating cell death as an explanation for the decrease in cell number. Although cortical TH cells reportedly fail to produce subsequent catecholaminergic enzymes, we found that the majority of these cells at all ages contained phosphorylated TH, suggesting that the enzyme may be active and producing L-DOPA as an end-product. Morphological criteria and colocalization of some TH cells with glutamic acid decarboxylase suggest that these cells are interneurons. Previously, parvalbumin, somatostatin, and calretinin were demonstrated in non-overlapping subsets of interneurons. Cortical TH neurons colocalized with calretinin but not with parvalbumin or somatostatin. These findings suggest that the transitory increase in TH cell number is not due to cell death but possibly due to alterations in the amount of detectable TH present in these cells, and that at least some cortical TH-producing interneurons belong to the calretinin-containing subset of interneurons that originate developmentally in the caudal ganglionic eminence.
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PMID:Neurochemical characterization of tyrosine hydroxylase-immunoreactive interneurons in the developing rat cerebral cortex. 1858 6

Age-related impairment of central functions is though to result from alterations of neurochemical indices of synaptic function. These neurochemical modifications involve structural proteins, neurotransmitters, neuropeptides and related receptors. Several studies demonstrated that GABA receptors, glutamic acid decarboxylase (GAD65&67), and different subpopulations of GABAergic neurons are markedly decreased in experimental animal brains during aging. Thus, the age-related decline in cognitive functions could be attributable, at least in part, to decrements in the function of the GABAergic inhibitory neurotransmitter system. In this study we show that chronic supplementation of taurine to aged mice significantly ameliorated the age-dependent decline in memory acquisition and retention, and caused alterations in the GABAergic system. These changes include increased levels of the neurotransmitters GABA and glutamate, increased expression of glutamic acid decarboxylase and the neuropeptide somatostatin and increased in the number of somatostatin-positive neurons. These specific alterations of the inhibitory system caused by taurine treatment oppose those naturally-occurring during aging, and suggest a protective role of taurine in this process. Increased understanding of age-related neurochemical changes in the GABAergic system will be important in elucidating the underpinnings of the functional changes of aging. Taurine might help forestall the age-related decline in cognitive functions through interaction with the GABAergic system.
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PMID:Functional implication of taurine in aging. 1923 50


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