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)

The development of somatostatin immunoreactive (SOM-ir) neurons in cat striate and extrastriate cortex was studied to determine whether temporal changes in the morphology, distribution and density of SOM-ir neurons during development would provide clues to the emergence of specific cortical areas. The visual cortical areas examined included areas 17-19 and 7, posteromedial lateral suprasylvian, posterolateral lateral suprasylvian cortex and splenial visual area. We observed that the pattern of SOM-ir neurons in the cortical plate reflects the maturation of the cortical plate. At 1 week of age, SOM-ir neurons were only found in layers V and VI of the developing cortex; by 2 weeks of age, SOM-ir neurons were found in layer IV; and by 3 weeks of age, SOM-ir neurons were located in all layers of the cortex except layer I. SOM-ir neurons in the subplate were much more numerous under lateral cortical areas than under medial areas. This difference decreased over the first 2 postnatal weeks and by the 14th day after birth (P14), the distribution and numbers of SOM-ir neurons in the subplate/white matter had reached the adult pattern. The timing of exuberant SOM expression in the subplate suggests a function in the formation of visual corticocortical connections which begin to develop during the first postnatal week in the kitten.
 ...
PMID:The development of somatostatin immunoreactive neurons in cat visual cortical areas. 809 74

The chemical codings of neurons that project from the small intestine, caecum, proximal colon, distal colon and rectum to the coeliac ganglion of the guinea pig were investigated. The coeliac ganglion was injected with the retrogradely transported dye Fast Blue, and each of the regions was examined 6 days later in wholemounts that had been prepared for immunohistochemical localisation of pairs of antigens. In both the small and large intestines, all intestinofugal neurons were immunoreactive (IR) for choline acetyltransferase (ChAT). In each region of the large intestine, the largest population, representing 50-60% of retrogradely labelled neurons in each region, was immunoreactive for ChAT, bombesin (BN), calbindin (Calb) and nitric oxide synthase (NOS). Most intestinofugal neurons in the small intestine contain bombesin and VIP-IR along with ChAT-IR but none contain either Calb or NOS. Thus, nerve endings of enteric origin in the coeliac ganglion that contain NOS-IR or Calb-IR come from the large intestine and those with bombesin-IR but not NOS-IR are from the small intestine. The gastric wall was injected with Fast Blue in order to label noradrenergic (NA) neurons in the coeliac ganglion and to determine, by localisation of NOS and bombesin-IR, whether they receive inputs from the small and large intestine. Some NA neurons received inputs from the large intestine (and perhaps also from the small intestine) and some received inputs exclusively from the small intestine. Most NA neurons that received intestinofugal inputs had the chemical code NA/-; some were immunoreactive for somatostatin (NA/SOM neurons), but those with IR for neuropeptide Y (NA/NPY) rarely received intestinofugal inputs.
 ...
PMID:Chemical coding of neurons that project from different regions of intestine to the coeliac ganglion of the guinea pig. 878 75

Somatostatin has been reported to have both nociceptive and antinociceptive roles in sensory transmission in the spinal cord. In this study, antisera against SOM (alpha-SOM), a somatostatin antagonist (CYCAM) and a somatostatin agonist (octreotide), were evaluated for their role in thermal and mechanical hyperalgesia in a model of carrageenan-induced inflammatory pain in the rat. Intrathecal administration of alpha-SOM prior to hindpaw inflammation dose-dependently attenuated thermal and mechanical hyperalgesia and the increase in paw size for up to 4 h following injury. Administration of alpha-SOM 3 h following injury had no effect. Intrathecal administration of octreotide or CYCAM prior to or following injection of carrageenan had no effect on any measure. It is suggested that the lack of effect of octreotide and CYCAM resulted from low affinity for the SOM receptor subtypes in the rat spinal cord. The attenuation of hyperalgesia and paw size produced by alpha-SOM may have resulted from attenuation of somatostatin's role in producing a dorsal root reflex that modulates the increase in paw size following injury.
 ...
PMID:Anti-somatostatin antisera, but neither a somatostatin agonist (octreotide) nor antagonist (CYCAM), attenuates hyperalgesia in the rat. 884 65

Recent years have seen an increase in the information concerning the mechanisms of action of brain-gut neuropeptides (cholecystokinin (CCK), vasoactive intestinal peptide (VIP), somatostatin (SS)) on the biliary tract motility. This article is intended to extend our knowledge of the problem and based on our recent studies. Researchers and students interested in an historical overview of the subject, as well as in the information on the physiology and pharmacology of biliary smooth muscle are referred to earlier reviews (Ryan, 1981, 1987). The article focuses on the involvement of cholinergic mechanisms in the action of CCK, SOM and VIP on the gallbladder motility under in vivo and in vitro conditions. Some species differences in the responses of the gallbladder to CCK, VIP and ACh have also been described. Furthermore, new data about the interactions between CCK, SOM and VIP in the regulation of the gallbladder motility are presented.
 ...
PMID:Effects of cholecystokinine on the gallbladder motility: interaction with somatostatin and vasoactive intestinal peptide. 886 69

A variety of cerebral insults induce neuronal damage to the hippocampal formation. The somatostatin-immunoreactive (SOM-ir) neurones in the dentate hilus are particularly vulnerable. In the present study, we demonstrated that augmentation of hippocampal GABAergic inhibition by chronic infusion of gamma-vinyl GABA prevented the delayed seizure-induced damage to hilar SOM-ir neurones. Selective lesions of the cholinergic, serotonergic or noradrenergic pathways to the hippocampus did not attenuate the seizure-induced loss of SOM-ir neurones; rather, the damage was exacerbated by the cholinergic lesion. It is, therefore, the intrahippocampal GABAergic circuitries, rather than the selective subcortical pathways, that are critical for neuroprotection after seizures. Enhanced GABAergic inhibition in the hippocampus prevented damage to hilar SOM-ir neurones, even when started 2 days after status epilepticus. GABAergic agents may thus provide an alternative treatment for delayed neuronal damage caused by cerebral insults.
 ...
PMID:Seizure-induced damage to the hippocampus is prevented by modulation of the GABAergic system. 890 19

Colonic mucosal cells are known to contain several neuropeptides. The distribution of various peptide-containing cells in the colon and their possible modulation by aging and diet are unknown. We quantitated various peptide-containing cells from male Lobund-Wistar rat colon at 2, 22, 28, 30 and 33 months of age using indirect immunohistochemical techniques for several peptides including: neuropeptide Y, peptide YY, somatostatin, and chromogranin A. Four diets, varying in total calories and fat content, were examined. Serum gastrin was quantified by RIA at 2 and 33 months. Only NPY-, PYY- and SOM-positive cells were found in the colon. The number per crypt of neuropeptide Y-positive (0.55 +/- 0.04 at 2 months vs 0.80 +/- 0.22 at 33 months, P = 0.015) and peptide YY-positive cells increased with age. Staining for somatostatin and chromogranin, a marker for all enterochromaffin (EC) cells, revealed no change with aging. Diet did not influence the numbers of any peptide-containing cell. Serum gastrin was not different between the groups. A specific increase in NPY- and PYY-positive cells occurs in the aged rat colon. The extent to which this change may be related to age-related colonic dysmotility seen in elderly humans is worthy of exploration.
 ...
PMID:Neuropeptide Y- and peptide YY-containing colonic cells increase with ageing in male rats. 891 66

NMDA receptors are composed of proteins from two families: NMDAR1, which are required for channel activity, and NMDAR2, which modulate properties of the channels. The mRNA encoding the NMDAR2D subunit has a highly restricted pattern of expression: in the forebrain, it is found in only a small subset of cortical, neostriatal and hippocampal neurons. We have used a quantitative double-label in situ hybridization method to examine the expression of NMDAR2D mRNA in neurochemically defined populations of neurons. In the neostriatum, NMDAR2D was expressed by the interneuron populations marked by preprosomatostatin (SOM), the 67-kDa form of glutamic acid decarboxylase (GAD67), parvalbumin (PARV), and choline acetyltransferase (ChAT) mRNAs but not by the projection neurons expressing beta-preprotachykinin (SP) or preproenkephalin (ENK) mRNAs. In the neocortex, NMDAR2D expression was observed in only a small number of neurons, but these included almost all of the SOM-, GAD67-, and PARV-expressing interneurons. In the hippocampus, NMDAR2D was not present in pyramidal or granule cells, but was abundant in SOM-, GAD67-, and PARV-positive interneurons. NMDAR2D expression appears to be a property shared by interneurons in several regions of the brain. The unique electrophysiological characteristics conveyed by this subunit, which include resistance to blockade by magnesium ion and long channel offset latencies, may be important for the integrative functions of these neurons. NMDAR2D-containing receptor complexes may prove to be important therapeutic targets in human disorders of movement. In addition, the presence of NMDAR2D subunits may contribute to the differential vulnerability of interneurons to excitotoxic injury.
 ...
PMID:Expression of NMDAR2D glutamate receptor subunit mRNA in neurochemically identified interneurons in the rat neostriatum, neocortex and hippocampus. 891 84

In human temporal lobe epilepsy, seizures can begin in the hippocampus, amygdala, or surrounding cortical areas. Histologically, the seizure-induced selective neuronal damage and synaptic reorganization are best documented in the hippocampus. Little information is available about the damage in the other temporal lobe structures or whether the distribution of damage depends on the location of the primary seizure focus. We used an amygdala-kindling model of temporal lobe epilepsy to study whether seizures of amygdaloid origin cause damage to the amygdala and hippocampus. All rats experienced five class 5 generalized seizures. Neuronal damage was assessed by counting the density of GABA-immunoreactive (GABA-ir) and somatostatin-immunoreactive (SOM-ir) neurons in the amygdala and hilus of the dentate gyrus six months after the last seizure. We found that the density of GABA-ir neurons did not differ from that in controls in the contralateral amygdala. The density of SOM-ir neurons was, however, decreased in the lateral (69% of neurons remaining, P < 0.01), basal (67% remaining, P < 0.05), and accessory basal (68% remaining, P < 0.05) nuclei. In the hilus, the densities of GABA-ir and SOM-ir neurons were similar to that in controls. According to our data, a few seizures of amygdaloid origin may cause more severe damage to SOM-ir neurons in the amygdala than in the hilus. Such decrease in SOM-ir neurons which form one subpopulation of GABAergic inhibitory interneurons may increase the local excitability in the amygdala and, therefore, contribute to epileptogenesis.
 ...
PMID:Decrease in somatostatin-immunoreactive neurons in the rat amygdaloid complex in a kindling model of temporal lobe epilepsy. 909 93

In both experimental and human temporal lobe epilepsy, seizures cause loss of hilar somatostatin-immunoreactive (SOM-ir) neurons and sprouting of mossy fibers. To investigate whether in rats these alterations are modulated by hippocampal input projections, we transected the fimbria-fornix or the perforant pathway bilaterally 2 days after seizures induced by systemic administration of kainic acid (9 mg/kg, i.p.). Two months later, the number of SOM-ir neurons in the hilus was counted and mossy fiber sprouting in the supragranular area and in the inner molecular layer was analyzed. In seizured rats with sham-operation, 50% of the hilar SOM-ir neurons were left in the septal end of the hippocampus and only 16% remained in the temporal end. In seizured rats with transection of the fimbria-fornix, the number of hilar SOM-ir neurons in the septal end of the hippocampus did not differ from that in controls (98% of SOM-ir neurons left). However, the temporal end was severely damaged (41% of SOM-ir neurons left). In seizured rats with transection of the perforant pathway, 61% of the hilar SOM-ir neurons were left in the septal end and 51% in the temporal end of the hippocampus. Mossy fiber sprouting was evident throughout the septotemporal axis of the hippocampus in all seizured rats. Our results suggest that in the septal end of the hippocampus the severity of neuronal damage in the hilus is modulated by mechanism(s) that are dependent on the afferent pathways entering the hippocampus via the fimbria-fornix. Transection of the fimbria-fornix, however, does not significantly modulate the severity or the target regions of seizure-induced sprouting of mossy fibers.
 ...
PMID:Seizure-induced damage to somatostatin-immunoreactive neurons in the rat hippocampus is regulated by fimbria-fornix transection. 918 17

Somatostatin and its receptors are widely distributed in the central nervous system and peripheral tissues including those of the gastrointestinal tract (GI tract). The expression patterns of the five known SSTR genes have been analysed in detail by reverse transcription polymerase chain reaction amplifications and in situ hybridizations using tissues dissected from different parts of rat stomach and gut. While SSTR1 mRNA is present at relatively high amounts throughout the gastrointestinal tract, the levels of SSTR2, 3 and 4 mRNAs vary in different regions and SSTR5 mRNA has not been detected. In situ hybridizations revealed the presence of SSTR3 mRNA in enterocytes and in neurons of the myenteric and submucous plexus. These findings are consistent with a role of SSTR3 in the observed somatostatin-mediated inhibition of acetylcholine release from myenteric neurons and of secretomotor neuron activity in the submucous plexus. Sequence analyses of the SSTR1 gene promoter revealed the absence of the canonical TATA and CAAT motifs and the presence of a variety of potential binding sites for transcriptional regulators. Among these are binding sites for GCF, AP-2, AP-4, response elements for somatostatin (SOM-RE), epidermal growth factor (EGF-RE) and cytocines (GAS and NFIL) as well as for tissue-specific factors such as Pit-1 (pituitary) and IDX-1 (pancreatic cells). Mobility shift assays have confirmed that nuclear proteins of pancreatic RIN1046-38 and pituitary GH3 tumour cells bind to oligonucleotides containing the overlapping Pit-1 and IDX-1 binding sites. Thus, the Pit-1/IDX-1 sites may be critical for the activation of the SSTR1 gene in these cell-types.
 ...
PMID:Localization of somatostatin receptor subtype mRNA in the rat gastrointestinal tract and regulation of SSTR1 gene expression. 955 32


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>