ライフサイエンスコーパス: somatostatin

1 enteroglucagon), pancreatic polypeptide, and somatostatin.

2 d GH-release, a response that was blocked by somatostatin.

3 crine hormone markers insulin, glucagon, and somatostatin.

4 cell genes including ghrelin, glucagon, and somatostatin.

5 of NPY neurons in the AStr also coexpressed somatostatin.

6 of neuropeptide Y, tyrosine hydroxylase, and somatostatin.

7 ily to an increase in cells co-positive with somatostatin.

8 aracentesis, total parenteral nutrition, and somatostatins.

9 emarkably, the cyclic neuroendocrine peptide somatostatin-14 (SST14) was observed to be the most sele

10 blocked by CYN 154806, an antagonist of the somatostatin-2 receptor.

11 Of the six subtypes of SST receptor, somatostatin 2a (sst2a ) is the most prevalent in the VL

12 Baclofen and somatostatin, agonists of Gi-coupled receptors, inhibite

13 n constants (Kd) of the peptide-ligand Delta-somatostatin (AGSKNFFWKTFTSS) binding to hPDI using (19)

14 In the current study, the hybrid labeled somatostatin analog Cy5-DTPA-Tyr(3)-octreotate (DTPA is

15 four or more BMs per day despite stable-dose somatostatin analog therapy received (1:1:1) placebo, te

16 igh uptake of (18)F-FDG with a low uptake of somatostatin analog usually indicates poorly differentia

17 Octreotide, a somatostatin analog, is proposed to reduce the risk of r

18 otable increase in oral bioavailability of a somatostatin analog.

19 PET/CT with (18)F-FDOPA or (68)Ga-DOTATOC, a somatostatin analog.

20 However, PET/CT imaging with novel somatostatin analogs (e.g., (68)Ga-DOTATOC, (68)Ga-DOTAT

21 ATE uptake before treatment with long-acting somatostatin analogs differs from that after treatment.

22 s, is frequently made using the DOTA-derived somatostatin analogs DOTATOC or DOTATATE for PET.

23 Synthetic somatostatin analogs have been posed as a potential sour

24 ession, and disrupted the normal response to somatostatin analogs in PCa cells.

25 uroendocrine tumors (NETs) with radiolabeled somatostatin analogs represent a milestone in the develo

26 DOTATOC and (68)Ga-DOTATATE are radiolabeled somatostatin analogs used for the diagnosis of somatosta

27 F-labeled silicon-fluoride acceptor-modified somatostatin analogs were developed.

28 SiFA- and SiFAlin-derivatized somatostatin analogs were synthesized and radiolabeled u

29 hese modalities through the radiolabeling of somatostatin analogs with various radionuclides has led

30 Preoperative guidance with radiolabeled somatostatin analogs, commonly used for NET diagnosis an

31 ally responsive to certain relatively stable somatostatin analogs, such as octreotide.

32 cinoid syndrome not adequately controlled by somatostatin analogs, treatment with telotristat ethyl w

33 (NETs) can be visualized using radiolabeled somatostatin analogs.

34 ptor radionuclide therapy using radiolabeled somatostatin analogs.

35 acebo-controlled, multinational study of the somatostatin analogue lanreotide in patients with advanc

36 We found that somatostatin analogue octreotide induces apoptosis in VH

37 acy and safety of two different doses of the somatostatin analogue pasireotide long-acting release co

38 oactive molecules, we synthesized COR-005, a somatostatin analogue that is currently in clinical tria

39 ve had disease progression during first-line somatostatin analogue therapy have limited therapeutic o

40 ement of symptomatic, unresectable tumors by somatostatin analogue therapy.

41 our origin, performance status, and previous somatostatin analogue treatment.

42 origin, WHO performance status, and previous somatostatin analogue treatment.

43 antitumour efficacy of the combination of a somatostatin analogue with everolimus in lung and thymic

44 Pasireotide is a novel multireceptor ligand somatostatin analogue, which has been demonstrated to re

45 Somatostatin analogues are commonly used to treat sympto

46 Somatostatin analogues are first line medical treatment

47 Somatostatin analogues are the mainstay of oncologic man

48 1% of tumors and is treated with surgery and somatostatin analogues if not surgically cured.

49 Patient was qualified for treatment with somatostatin analogues in order to stop bile secretion.

50 ce and previous reports on VHL-HB avidity to somatostatin analogues suggested somatostatin receptor (

51 Medical therapy with somatostatin analogues, cabergoline, and pegvisomant is

52 In addition to the use of long-acting somatostatin analogues, targeting the mammalian target o

53 adequately controlled using first-generation somatostatin analogues.

54 Somatostatin and GABA are differentially released to dis

55 xpression of other islet hormones, including somatostatin and glucagon.

56 ibitory interneurons expressing parvalbumin, somatostatin and neuropeptide Y in the dentate gyrus, re

57 The precise connectivity of somatostatin and parvalbumin cortical interneurons is ge

58 Furthermore, while endogenous activity of somatostatin and parvalbumin neurons was strongly biased

59 nterneurons or catecholaminergic fibers with somatostatin and tyrosine hydroxylase (TH) or dopamine b

60 ity and physiological responses to secretin, somatostatin and vascular endothelial growth factor.

61 Numerous NPY(+) /somatostatin(+) and NPY(+) /somatostatin(-) fibers were

62 distinct mono-hormonal insulin+, glucagon+, somatostatin+ and PP+ cells and glucose-responsive synch

63 tide Y (NPY), agouti-related peptide (AGRP), somatostatin, and dopamine.

64 on of paracrine factors, such as insulin and somatostatin, and juxtacrine signals between EphA4/7 on

65 testinal polypeptide, nitric oxide synthase, somatostatin, and vesicular glutamate transporters 1 and

66 Somatostatin- and parvalbumin-expressing (SST(+) and PV(

67 -cell recordings from excitatory neurons and somatostatin- and parvalbumin-positive GABAergic interne

68 We evaluated how optogenetically activating somatostatin- and parvalbumin-positive interneurons subt

69 GABA and somatostatin are colocalized in type 1 cells, and they e

70 Phe residues in Delta-somatostatin are hypothesised as important for recogniti

71 iss1) and energy homeostasis (Pomc, Npy, and Somatostatin) are regulated according to seasons in male

72 assessed the long-term benefits and harm of somatostatin-based radiopeptide therapy in meningioma pa

73 bitory interneurons expressed parvalbumin or somatostatin, but not calbindin or calretinin.

74 ssion of IPSCs from dendritically projecting somatostatin cells (SOM-IPSCs).

75 umans with T2D occurs in both insulin(+) and somatostatin(+) cells.

76 typically basket or chandelier neurons; and somatostatin containing interneurons, which are typicall

77 cell-type dependent: in principal cells and somatostatin-containing (SOM), but not fast-spiking (FS)

78 ls were electrophysiologically distinct from somatostatin-containing cells.

79 ogenous Ucn3 have fewer delta cells, reduced somatostatin content, impaired somatostatin secretion, a

80 Chimeric somatostatin/dopamine compounds such as BIM-23A760, an s

81 tion, which was associated with the relative somatostatin/dopamine-receptors levels, especially sst5

82 connections onto neighboring parvalbumin and somatostatin expressing interneurons.

83 ts are even more powerful at parvalbumin and somatostatin expressing interneurons.

84 ditioning-induced synaptic potentiation onto somatostatin-expressing (SOM(+)) CeL neurons, which has

85 Recent studies indicate that somatostatin-expressing (SOM(+)) neurons in the lateral

86 fined cortical microcircuit: they facilitate somatostatin-expressing (SOM) inhibitory neurons that in

87 rophysiological approach to record and label somatostatin-expressing (Sst) interneurons (GABAergic ne

88 ceptors gated by the spontaneous activity of somatostatin-expressing (Sst) interneurons.

89 in favor of pyramidal neuron hyperactivity: somatostatin-expressing and parvalbumin-expressing inhib

90 We found that activity in most somatostatin-expressing and parvalbumin-expressing inter

91 pressing cells were found in the BNST, while somatostatin-expressing cells and calretinin-expressing

92 ns were distributed across cell layers, with somatostatin-expressing cells predominantly in stratum o

93 Pharmacogenetic activation of somatostatin-expressing cells reduced pyramidal neuron h

94 ic animals that express Pax4 specifically in somatostatin-expressing cells.

95 is negatively correlated with the density of somatostatin-expressing inhibitory interneurons in the v

96 nd selective upregulation in the activity of somatostatin-expressing inhibitory neurons (SOM cells).

97 Learning also reduced the activity of somatostatin-expressing inhibitory neurons (SOM-INs) in

98 Somatostatin-expressing inhibitory neurons (SOM-INs), wh

99 pyramidal cell establishes a synapse onto a somatostatin-expressing interneuron (IN), the synapse re

100 Here we show how somatostatin-expressing interneurons (SOM cells) contrib

101 al inhibition was blocked by inactivation of somatostatin-expressing interneurons (SOM cells), but no

102 the axonal and somatic action potentials of somatostatin-expressing interneurons also depend on BK C

103 When somatostatin-expressing interneurons are inactivated, di

104 ta and axons, including axon collaterals, of somatostatin-expressing interneurons are significantly b

105 We found that fast-spiking and somatostatin-expressing interneurons differed in their e

106 ntials back-propagated into the dendrites of somatostatin-expressing interneurons much more readily t

107 ogenitor division, a loss of PARVALBUMIN and SOMATOSTATIN-expressing interneurons, and defective syna

108 esynaptic GABA release from parvalbumin- and somatostatin-expressing interneurons.

109 for the first time in behaving mice that the somatostatin-expressing neurons in the CeL acquire learn

110 al lateral amygdala (CeL), in particular its somatostatin-expressing neurons, is crucial for both lea

111 We find that in contrast to somatostatin-expressing or vasoactive intestinal polypep

112 in mice that deficiency of the Erbb4 gene in somatostatin-expressing TRN neurons markedly alters beha

113 Somatostatin-expressing-interneurons (SOMIs) in the dent

114 Numerous NPY(+) /somatostatin(+) and NPY(+) /somatostatin(-) fibers were observed, suggesting at leas

115 neurons, those that express parvalbumin and somatostatin, fire action potentials during theta in an

116 Anatomically, the somata of somatostatin immobility-activated neurons were smaller t

117 inhibition, indicated by a greater number of somatostatin-immunoreactive (-ir) cells in the CA1 pyram

118 a common neuropathological abnormality, and somatostatin-immunoreactive axons were exuberant in the

119 cells or activation of parvalbumin- (PV) or somatostatin-immunoreactive interneurons aborted spontan

120 ntromedial hypothalamus and Kiss1, Pomc, and Somatostatin in the arcuate nucleus was observed in jerb

121 hese pituitary cell-types (e.g. GHRH/ghrelin/somatostatin/insulin/IGF-I-receptors/Pit-1).

122 ted at the start of stimulus trains, whereas somatostatin interneuron activation builds during these

123 upon disruption of the early (but not late) somatostatin interneuron network, the synaptic maturatio

124 We also find that parvalbumin(-) and somatostatin(-) interneuron inputs are greatly diminishe

125 However, somatostatin(-) interneuron inputs onto adult-born DGCs

126 ortical pathology, we found that hyperactive somatostatin interneurons disinhibited layer 5 pyramidal

127 Focal ablation of somatostatin interneurons efficiently restored normal ex

128 These results suggest that infragranular somatostatin interneurons exhibit a transient early syna

129 Here, we report that somatostatin interneurons in infragranular layers receiv

130 st-spiking parvalbumin interneurons, but not somatostatin interneurons, preferentially inhibit type A

131 neurons have narrow axons and inhibit nearby somatostatin interneurons, which themselves inhibit pyra

132 tical inputs, yet are strongly innervated by somatostatin interneurons.

133 cation which implies the C-terminus of Delta-somatostatin is a prime recognition region.

134 Decreased somatostatin levels in Hhex-deficient islets cause disru

135 The subset of somatostatin-lineage neurons preserved in VT3(Lbx1)-neur

136 es encoding anorexigenic peptides, POMC, and somatostatin may account for the reduced body weight rep

137 In conclusion, the somatostatin mimic [111In-DOTA]LTT-SS28 specifically loc

138 In this study, we present the somatostatin mimic [DOTA]LTT-SS28 {[(DOTA)Ser1,Leu8,D-Tr

139 anocortin (POMC) subtypes, and an orexigenic somatostatin neuron population.

140 e found that the cortex, via corticostriatal somatostatin neurons (CS-SOM), has a direct inhibitory i

141 ojection neurons-glutamate/GABA co-releasing somatostatin neurons, glutamatergic parvalbumin neurons,

142 dogenous GDNF released from peptidergic CGRP/somatostatin+ nociceptors upon capsaicin stimulation exe

143 In epilepsy, a high and chronic release of somatostatin occurs, which provokes, in both rat and hum

144 Surprisingly, nearly one in five somatostatin or one in seven parvalbumin interneurons we

145 Somatostatin or VIP neuron activation also impaired or e

146 amidal neurons by optogenetically activating somatostatin- or parvalbumin-positive interneurons, even

147 on brain responses to food pictures during a somatostatin pancreatic-pituitary clamp.

148 We analyzed markers of dendritic (somatostatin), perisomatic (parvalbumin), and interneuro

149 ses of interneurons, the parvalbumin and the somatostatin positive cells, tightly control both up-to-

150 c drive present at the DMV is primarily from somatostatin positive GABA (Sst-GABA) DMV neurons.

151 To determine this, we focused on the somatostatin positive GABA (Sst-GABA) interneuron in the

152 matergic, and parvalbumin-positive (PV+) and somatostatin-positive (SOM+) GABAergic neurons - in the

153 By contrast, activation of somatostatin-positive (SOM+) GABAergic neurons promoted

154 ous subtypes, parvalbumin-positive (PV+) and somatostatin-positive (SOM+) neurons.

155 We focused on somatostatin-positive (SST(+)) GABAergic interneurons be

156 inal peptide-positive (VIP+) neurons than to somatostatin-positive (SST+) neurons suggests that disin

157 Optogenetically manipulating somatostatin-positive (Sst+) or parvalbumin-positive (Pv

158 recombinase in either parvalbumin-positive, somatostatin-positive (SST+), or vasoactive intestinal p

159 a specific class of inhibitory interneurons-somatostatin-positive cells-to the generation of slow wa

160 eurons lacking Kv4 (such as parvalbumin- and somatostatin-positive Golgi cells in the cerebellum), co

161 ll stimulation compared with parvalbumin- or somatostatin-positive interneuron stimulation.

162 In contrast, somatostatin-positive interneurons (SOMs) selectively re

163 togenetic control of parvalbumin-positive or somatostatin-positive interneurons and of calmodulin-dep

164 had a decreased density of parvalbumin- and somatostatin-positive interneurons in dentate gyrus, but

165 ession depends on the activity of inhibitory somatostatin-positive interneurons in the superficial la

166 irectional manipulation of GABA release from somatostatin-positive interneurons increased and decreas

167 nhibitory synapses formed by parvalbumin- or somatostatin-positive interneurons on pyramidal layer 5

168 These include a pathway mediated by L5b somatostatin-positive interneurons that specifically tar

169 rincipal cells as well as of parvalbumin- or somatostatin-positive interneurons to study the effects

170 ative cells that express CB, most likely the somatostatin-positive interneurons, are important mediat

171 tal, areas are dominated by input-modulating somatostatin-positive interneurons.

172 thmic input to the lateral hypothalamus from somatostatin-positive lateral septum cells evokes food a

173 ally signaled different task-related events: somatostatin-positive neurons primarily signaled motor a

174 ntial-induced presynaptic Ca(2+) transients (somatostatin-positive synapses).

175 tergic input onto fast spiking (FS), but not somatostatin-positive, non-FS interneurons increases ove

176 ogically relevant cyclic peptides, including somatostatin, proteins, and antibodies, such as a Fab ar

177 NET patients received somatostatin radiopeptide therapy with (90)Y-DOTATOC or

178 ptor radionuclide therapy using radiolabeled somatostatin receptor (SSTR) agonists are successfully u

179 have shown enhanced tumor targeting by novel somatostatin receptor (SSTR) antagonists compared with c

180 Radiolabeled somatostatin receptor (SSTR) antagonists have shown in v

181 avidity to somatostatin analogues suggested somatostatin receptor (SSTR) expression in VHL-HBs, offe

182 Somatostatin receptor (SSTR) imaging is widely used for

183 Somatostatin receptor (sstr) scintigraphy for imaging an

184 sodium iodide symporter (hNIS) and the human somatostatin receptor 2 (hSSR2) in the vaccinia-based OV

185 e gastrin-releasing peptide receptor (GRPR), somatostatin receptor 2 (SSTR2), and chemokine C-X-C mot

186 ntified between mu opioid receptor (MOR) and somatostatin receptor 2 (SSTR2).

187 Meningiomas are known to express somatostatin receptor 2 (SSTR2).

188 bles detection of meningioma tissue based on somatostatin receptor 2 expression.

189 class A G protein-coupled receptors: SSTR2 (somatostatin receptor 2), CHRM2 (cholinergic receptor, m

190 two G protein-coupled receptors (GPCRs)-the somatostatin receptor 3 and rhodopsin.

191 ium enrichment of a chimera of rhodopsin and somatostatin receptor 3, where the dual Ax(S/A)xQ ciliar

192 A somatostatin receptor 5 antagonist, which blunts inhibit

193 a TGR5 antagonist alone or concurrently with somatostatin receptor agonists represents a potential th

194 a combination of SBI-115 and pasireotide, a somatostatin receptor analogue.

195 ming developments in PRRT include the use of somatostatin receptor antagonists and alpha-emitting rad

196 stimulation by paracrine inhibition, because somatostatin receptor blockade potently stimulated gluca

197 Meningiomas express members of the somatostatin receptor family.

198 In this study, we selected the somatostatin receptor imaging agent DOTATOC as the found

199 Somatostatin receptor imaging is a valuable tool in the

200 been posed as a potential source of error in somatostatin receptor imaging through interference with

201 Somatostatin receptor imaging with (68)Ga-DOTATATE PET/C

202 r sensory cilia, inhibited enrichment of the somatostatin receptor in primary cilia.

203 (68)Ga-labeled somatostatin receptor ligand PET imaging has recently be

204 A somatostatin receptor ligand that is easily radiolabeled

205 se delivered by (18)F-FDG- or (68)Ga-labeled somatostatin receptor ligands.

206 eptor-expressing neuroendocrine tumors using somatostatin receptor radioligands.

207 s within the third intracellular loop of the somatostatin receptor replaced the third intracellular l

208 brain, preferably with MR, together with the somatostatin receptor scintigraphy (SRS), in each clinic

209 Tc-hydrazinonicotinamide (HYNIC)-octreotide (somatostatin receptor scintigraphy [SSRS]) SPECT/CT, (68

210 ocol with the commonly used 3-d protocol for somatostatin receptor scintigraphy in patients with gast

211 neoplasm patients undergoing restaging with somatostatin receptor scintigraphy on a modern SPECT/CT

212 The oncogenic role of the spliced somatostatin receptor sst5TMD4 variant in prostate cance

213 The method's application to somatostatin receptor SSTR5 (no experimental structure a

214 is recent in vitro and in vivo evidence that somatostatin receptor subtype 2 (sst2) antagonists are b

215 somatostatin with picomolar affinity for the somatostatin receptor subtype 2 (SSTR2) upregulated in s

216 ormed a screen for drugs that upregulate the somatostatin receptor subtype 2 (sstr2).

217 The somatostatin receptor subtype 2 is expressed on macropha

218 Visualization of somatostatin receptor subtype 2, for oncologic purposes,

219 ed with Cu and (64)Cu and tested in vitro in somatostatin receptor subtype 2-overexpressing HEK-293 c

220 n to have the highest affinity yet found for somatostatin receptor subtype 2.

221 The somatostatin receptor subtype 3 (Sstr3) is selectively t

222 Resected carotid plaques were retrieved for somatostatin receptor subtype-2 (sst2) immunohistochemic

223 ium-68-labeled DOTATATE ((68)Ga-DOTATATE), a somatostatin receptor subtype-2 (SST2)-binding PET trace

224 The somatostatin receptor, which is overexpressed by many ne

225 (68)Ga-DOTATATE for high-quality imaging of somatostatin receptor-bearing tumors.

226 matostatin analogs used for the diagnosis of somatostatin receptor-expressing neuroendocrine tumors (

227 cessfully applied for imaging and therapy of somatostatin receptor-expressing neuroendocrine tumors u

228 T/CT provides information on the location of somatostatin receptor-expressing tumors.

229 r moderately differentiated, nonfunctioning, somatostatin receptor-positive neuroendocrine tumors of

230 They exhibited high binding affinities to somatostatin receptor-positive tumor cells (1.88-14.82 n

231 T patients from a group of 367 patients with somatostatin receptor-positive tumors.

232 (68)Ga-DOTATOC, a somatostatin receptor-targeted ligand, has been used cli

233 We evaluated whether somatostatin receptor-targeted radionuclide therapy with

234 a category of NETs that does not express the somatostatin receptor.

235 ementary argument for replacing SPECT by PET somatostatin-receptor imaging.

236 rodihydroxyphenylalanine (FDOPA), and (68)Ga somatostatin-receptor ligands in NETs has been expanding

237 tate in patients with advanced, progressive, somatostatin-receptor-positive midgut neuroendocrine tum

238 These rare human tumors often express somatostatin receptors (SSTRs) and thus are clinically r

239 r (NOP), MCHR1, both orexin receptors (ORX), somatostatin receptors 1 and 2 (SSTR1, SSTR2), kisspepti

240 Pheochromocytomas/paragangliomas overexpress somatostatin receptors, and recent studies have already

241 l neuroendocrine tumors (NETs) overexpresses somatostatin receptors, especially the sst2 subtype.

242 e of a cocktail of 3 radioligands binding to somatostatin receptors, GLP-1 receptors, and GIP recepto

243 ivate a negative feedback loop that promotes somatostatin release to ensure the timely reduction of i

244 cells, which secrete glucagon, insulin, and somatostatin, respectively, to regulate plasma glucose.

245 ncreas, Hhex is selectively expressed in the somatostatin-secreting delta cell.

246 We found basal glucagon, insulin and somatostatin secretion and respiration from human islets

247 ced mitochondrial metabolism but not lowered somatostatin secretion are crucial in this effect.

248 ctions, and the consequential stimulation of somatostatin secretion inhibits alpha-cell electrical ac

249 h insulin and potentiates glucose-stimulated somatostatin secretion via cognate receptors on delta ce

250 ells, reduced somatostatin content, impaired somatostatin secretion, and exaggerated insulin release,

251 and insulin was also contributed by reduced somatostatin secretion.

252 junction-dependent activation of delta-cells/somatostatin secretion.

253 tified GPR39 as a novel regulator of gastric somatostatin secretion.

254 g the mechanisms of regulation of insulin by somatostatin, serotonin, and melanocortins.

255 islet cells expressing insulin, glucagon, or somatostatin share a lack of methylation at the promoter

256 alretinin (CR) and neuropeptide Y (NPY), and somatostatin (SOM) and glial fibrillary acidic protein (

257 (VIP) interneurons resulted in an increased somatostatin (SOM) interneuron inhibitory drive over lay

258 ing animals, we show that dendrite-targeting somatostatin (SOM) interneurons are critical for a visua

259 erated, we explored how parvalbumin (PV) and somatostatin (SOM) interneurons in CA1 stratum oriens/al

260 Suppressing somatostatin (SOM) neurons enhanced the E and I underlyi

261 pping neocortical IN populations, expressing somatostatin (SOM) or vasoactive intestinal peptide (VIP

262 ure onset rapidly recruits parvalbumin (PV), somatostatin (SOM), and vasoactive intestinal peptitde (

263 ortical inhibitory interneurons that express somatostatin (SOM), because approximately 70% of them ar

264 han 98% of GINs coexpressed the neuropeptide somatostatin (SOM), but only 50% of all SOM + neurons we

265 of interneurons expressing parvalbumin (PV), somatostatin (SOM), or 5HT3a receptors.

266 nd interneurons expressing parvalbumin (PV), somatostatin (SOM), vasoactive intestinal peptide (VIP),

267 ex of behaving mice, we show that spiking of somatostatin (SOM)- and parvalbumin (PV)-expressing inte

268 However, targeting of somatostatin (SOM)- and vasoactive intestinal peptide (V

269 red excitatory input to parvalbumin (PV) and somatostatin (SOM)-expressing interneurons and found dis

270 We found that the neuropeptide somatostatin [somatotropin release inhibiting factor (SR

271 Within the hippocampus, the major somatostatin (SRIF) receptor subtype, the sst2A receptor

272 Somatostatin (SST) and cortistatin (CORT) regulate numer

273 vity of vasoactive intestinal peptide (VIP), somatostatin (SST) and parvalbumin (PV)-positive interne

274 ived interneuron subgroups--those expressing somatostatin (SST) and those expressing parvalbumin (PV)

275 Microinjection of somatostatin (SST) causes site-specific effects on respi

276 Somatostatin (SST) deficits are common pathological feat

277 eleasing hormone (GHRH) for GHRH-neurons and somatostatin (Sst) for Sst-neurons.

278 Growing evidence points to a key role for somatostatin (SST) in schizophrenia (SZ) and bipolar dis

279 ohistology and electrophysiology showed that somatostatin (SST) interneurons in the mPFC express M1-A

280 Since the inhibitory neuropeptide somatostatin (SST) is considered to be a primary oscilla

281 Reduced expression of somatostatin (SST) is reported across chronic brain cond

282 brain-derived neurotrophic factor (BDNF) and somatostatin (SST) mRNAs in the brain decreases progress

283 both vasoactive intestinal peptide (VIP) and somatostatin (SST) neurons.

284 Somatostatin (SST) or agonists of the SST-2 receptor (ss

285 Radiolabeled somatostatin (sst) receptor agonists are integral to the

286 linical evidence indicates that radiolabeled somatostatin (sst) receptor antagonists perform better t

287 nd interneurons expressing parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (V

288 We show that a population of L5b, somatostatin (SST)-positive interneuron receives early t

289 enriched populations of parvalbumin (PV)- or somatostatin (SST)-positive interneurons, which were tra

290 , we report the discovery of a population of somatostatin (Sst)-positive, regular spiking interneuron

291 interneurons that coexpress the neuropeptide somatostatin (SST).

292 tzinger Complex (preBotC) neurons expressing somatostatin (SST).

293 concentrations of Met(5)-enkephalin (ME) and somatostatin (SST; coupling to native SST receptor [SSTR

294 ative number of submucous neurons containing somatostatin tended to be increased (p = 0.062).

295 Importantly, somatostatin treatment fails to decrease Sstr3 ciliary l

296 We further show that somatostatin treatment stimulates beta-arrestin recruitm

297 ilia is dynamic and decreases in response to somatostatin treatment.

298 The somatostatin type 2A receptor (sst2A) is localized on pr

299 protein 3b, Ets variant gene 1, substance P, somatostatin, vasoactive intestinal polypeptide, and par

300 P2045 is a peptide analog of somatostatin with picomolar affinity for the somatostati