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1 any neuroprotective effect of brimonidine or somatostatin.
2  cell genes including ghrelin, glucagon, and somatostatin.
3 ily to an increase in cells co-positive with somatostatin.
4 jecting CeA neurons express the neuropeptide somatostatin.
5 zation with glucagon but not with insulin or somatostatin.
6 ssion of crucial delta cell genes, including somatostatin.
7 n through a genetic approach by knocking out somatostatin 1.1 (sst1.1) in zebrafish.
8 performed larger tail bends, indicating that Somatostatin 1.1 inhibits spontaneous locomotion.
9       Altogether our study demonstrates that Somatostatin 1.1 innately contributes to slowing down sp
10           Twenty-nine patients (18 receiving somatostatin, 11 placebo) were included in the final ana
11 : 500 mug), followed by a 2.5 mL/h infusion (somatostatin: 250 mug/h) for 5 days.
12 administered intraoperatively as 5-mL bolus (somatostatin: 500 mug), followed by a 2.5 mL/h infusion
13 fusion, HVPG was lower in patients receiving somatostatin (-81.7% vs -58.8%; P = 0.0084), whereas no
14 fts were associated with increased levels of somatostatin, a GH inhibitor, whereas the deleterious ef
15                                 Baclofen and somatostatin, agonists of Gi-coupled receptors, inhibite
16 ver, the recent approval of the radiolabeled somatostatin analog (177)Lu-DOTATATE has had a significa
17 ne modulation by measuring the effect of the somatostatin analog octreotide on appetitive behavior am
18 four or more BMs per day despite stable-dose somatostatin analog therapy received (1:1:1) placebo, te
19 r, we discuss patient screening, maintenance somatostatin analog therapy requirements, treatment loca
20 ported for other polypeptide tracers such as somatostatin analogs (2.1-2.6 mSv/100 MBq) and are benef
21 received PRRT with (177)Lu- or (90)Y-labeled somatostatin analogs (DOTATATE or DOTATOC).
22                                              Somatostatin analogs (SSAs) are recommended for the firs
23 docrine tumors (NETs) are often treated with somatostatin analogs (SSAs) for control of symptoms and
24                      PET/CT with (68)Ga-DOTA-somatostatin analogs has been tested for therapy monitor
25                                    Synthetic somatostatin analogs have been posed as a potential sour
26 onuclide therapy (PRRT) with (177)Lu-labeled somatostatin analogs in patients with somatostatin recep
27                  PET/CT using (68)Ga-labeled somatostatin analogs is superior to earlier agents, but
28 endocrine neoplasms by using (177)Lu-labeled somatostatin analogs or in the treatment of advanced pro
29 DOTATOC and (68)Ga-DOTATATE are radiolabeled somatostatin analogs used for the diagnosis of somatosta
30 hese modalities through the radiolabeling of somatostatin analogs with various radionuclides has led
31 nity to treat the patient with radiolabelled somatostatin analogs, which successfully controlled the
32 ptor radionuclide therapy using radiolabeled somatostatin analogs.
33                Therefore, coating CTX with a somatostatin analogue such as octreotide (OCT) is benefi
34 ve had disease progression during first-line somatostatin analogue therapy have limited therapeutic o
35 origin, WHO performance status, and previous somatostatin analogue treatment.
36  antitumour efficacy of the combination of a somatostatin analogue with everolimus in lung and thymic
37  the use of statins, but mTOR inhibitors and somatostatin analogues are not recommended.
38 ctive for late dumping syndrome symptoms and somatostatin analogues are preferred for patients who do
39 ce and previous reports on VHL-HB avidity to somatostatin analogues suggested somatostatin receptor (
40                         Medical therapy with somatostatin analogues, cabergoline, and pegvisomant is
41 m evidence for the volume-reducing effect of somatostatin analogues.
42 male participants to a pancreatic clamp with somatostatin and evaluated hepatic glucose and amino aci
43 xpression of other islet hormones, including somatostatin and glucagon.
44 ramidal cells, while concurrently activating somatostatin and inhibiting parvalbumin interneurons.
45                    Cortical distributions of somatostatin and parvalbumin cell gene markers are stron
46    Furthermore, while endogenous activity of somatostatin and parvalbumin neurons was strongly biased
47 onstrate stereotyped negative correlation of somatostatin and parvalbumin transcripts within human an
48  both oligodendrocytes and CINs that express somatostatin and parvalbumin.
49  distinct mono-hormonal insulin+, glucagon+, somatostatin+ and PP+ cells and glucose-responsive synch
50 hway, consisting of inhibition by dynorphin, somatostatin, and corticotropin-releasing hormone-expres
51             However, pancreatic polypeptide, somatostatin, and ghrelin cells also contributed to the
52 on of paracrine factors, such as insulin and somatostatin, and juxtacrine signals between EphA4/7 on
53 rum inhibitory cells containing parvalbumin, somatostatin, and neuropeptide Y also show unique topogr
54 parvalbumin, calretinin, neuropeptide Y, and somatostatin, and the number of interneurons were assess
55    These CeA GABA neurons express dynorphin, somatostatin, and/or corticotropin releasing hormone.
56 are associated with changes in parvalbumin-, somatostatin- and neuropeptide Y-positive interneurons.
57 pacity up to the progenitor stage, but favor somatostatin- and pancreatic polypeptide-positive cells
58 calcium imaging, we recorded hippocampal CA1 somatostatin- and parvalbumin-expressing interneurons as
59 ) expression disperse and differentiate into somatostatin- and parvalbumin-expressing interneurons up
60       This study establishes the efficacy of somatostatin as a liver inflow modulator.
61                    Ten patients responded to somatostatin bolus, with a significant decrease in hepat
62 ampal inhibitory neurons (those that express somatostatin, but not parvalbumin).
63 ssion of IPSCs from dendritically projecting somatostatin cells (SOM-IPSCs).
64 f two neuroprotective drugs (brimonidine and somatostatin) could prevent or arrest retinal neurodysfu
65 tion, which was associated with the relative somatostatin/dopamine-receptors levels, especially sst5
66 rior anatomical experiments in BLA implicate somatostatin expressing (Sst(+)) INs.
67 hat inhibitory synapses from parvalbumin and somatostatin expressing interneurons undergo long-term d
68 ation of p-eIF2alpha in either excitatory or somatostatin-expressing (but not parvalbumin-expressing)
69 the cortex, parvalbumin-expressing (PV+) and somatostatin-expressing (SOM(+)) interneurons, in mice o
70  neurons, and toward non-CRF(+) (CRF(-)) and somatostatin-expressing (SOM(+)) neurons, while fear ext
71 V1 processes head movements is controlled by somatostatin-expressing (SOM) inhibitory neurons, which
72 e, that causal disruption of either PV(+) or somatostatin-expressing (SST(+)) interneuron activity im
73 vement of parvalbumin-expressing (PV(+)) and somatostatin-expressing (SST(+)) interneurons in gamma o
74 nts and reduced firing of dendrite-targeting somatostatin-expressing (SST) GABAergic interneurons.
75  of pyramidal neurons through suppression of somatostatin-expressing (SST) interneurons and, reciproc
76                               In particular, somatostatin-expressing (SST) interneurons selectively i
77 ncy, followed by activation of E neurons and somatostatin-expressing (SST) interneurons.
78      Here we show that, in male rats, 65% of somatostatin-expressing (SST) NTS neurons also express G
79                                              Somatostatin-expressing (SST+) cells form the second lar
80               We found that activity in most somatostatin-expressing and parvalbumin-expressing inter
81  parvalbumin-expressing CA1 interneurons and somatostatin-expressing CA3 interneurons represented spe
82 ns were distributed across cell layers, with somatostatin-expressing cells predominantly in stratum o
83                Pharmacogenetic activation of somatostatin-expressing cells reduced pyramidal neuron h
84                                 By contrast, somatostatin-expressing cells-which reside along the sur
85 ic animals that express Pax4 specifically in somatostatin-expressing cells.
86 le of accessing and manipulating a subset of somatostatin-expressing cortical interneurons with high
87  excitatory PNs compared to parvalbumin- and somatostatin-expressing inhibitory INs.
88                                      Whereas somatostatin-expressing inhibitory neurons are driven by
89          We show that de novo translation in somatostatin-expressing inhibitory neurons in the centro
90                                 In contrast, somatostatin-expressing inhibitory neurons received very
91  via autonomous mechanisms in excitatory and somatostatin-expressing inhibitory neurons.
92           In sharp contrast, layer 5 PNs and somatostatin-expressing INs were gradually and asynchron
93  asynchronous recruitment of layer 5 PNs and somatostatin-expressing INs.
94                                 In contrast, somatostatin-expressing interneuronal activity peaks sig
95 sed transgenic mouse line in which GABAergic somatostatin-expressing interneurons (SOM(pos) INs) are
96  whole-cell recordings demonstrated that DLS somatostatin-expressing interneurons (SST-INs) receive d
97 iles of pyramidal cells and parvalbumin- and somatostatin-expressing interneurons during epileptiform
98 uppression across the population, individual somatostatin-expressing interneurons showed consistent l
99       Here, we provide evidence that, in CA1 somatostatin-expressing interneurons, the alpha5-GABA(A)
100  not known what role, if any, is provided by somatostatin-expressing interneurons, which target the d
101 retinin-positive terminals onto dendrites of somatostatin-expressing interneurons.
102  intense activation of both parvalbumin- and somatostatin-expressing interneurons.
103 t mechanisms from parvalbumin-expressing and somatostatin-expressing interneurons.
104 se of 148 MBq (4.0 mCi) for the detection of somatostatin-expressing NETs.
105                           We also identified somatostatin-expressing neurons in the preBotC and PHOX2
106 e further characterize a novel population of somatostatin-expressing neurons through anatomical and b
107  mediated by GH-releasing hormone (GHRH)- or somatostatin-expressing neurons.
108 ly one-third of putative dendrite-targeting (somatostatin-expressing) interneurons, but only a neglig
109 r translocation and repositioning within the somatostatin gene promoter.
110                                              Somatostatin, ghrelin, and GH-releasing hormones that re
111 ptor or dopamine D(2) receptor was seen with somatostatin, glucagon, or polypeptide Y.
112 ut remained unchanged in the brimonidine and somatostatin groups.
113                                 For example, somatostatin has been previously shown to induce locomot
114     The GETNE-TRASGU (Treated With Analog of Somatostatin in Gastroenteropancreatic and Unknown Prima
115            Here, we investigated the role of somatostatin in innate locomotion through a genetic appr
116 ition of insulin and glucagon secretion with somatostatin infusion and replacement of basal plasma in
117                                              Somatostatin infusion counteracted the decrease in arter
118                                              Somatostatin infusion during LT in patients with CSPH is
119 us motif for maintaining this balance is the somatostatin interneuron (SOM-IN) feedback microcircuit.
120 h SATB1, a transcription factor critical for somatostatin interneuron development, and promoted SATB1
121 s, necessitating high-frequency activity for somatostatin interneuron recruitment.
122          In vivo opto-activation of cortical somatostatin interneurons alleviates motor symptoms in a
123 len Human Brain Atlas expression data reveal somatostatin interneurons and astrocytes to be consisten
124                                              Somatostatin interneurons are likely important to this s
125 hus, layer-specific synaptic properties onto somatostatin interneurons are mediated by both constitut
126 or gain) in models with features typical for somatostatin interneurons but decreased gain in models w
127 duced by DBS or by a stimulation of cortical somatostatin interneurons can restore information proces
128                Therefore, mTORC1 activity in somatostatin interneurons contributes to learning-induce
129 ice), immunohistochemistry revealed that BLA somatostatin interneurons express Y(2)Rs, as do a signif
130 arked deficits in distinct subpopulations of somatostatin interneurons from early postnatal stages of
131 itory input drive from low-threshold-spiking somatostatin interneurons in adulthood, suggesting a cir
132 itutive suppression delays the activation of somatostatin interneurons in circuits, necessitating hig
133 ults demonstrate that activation of cortical somatostatin interneurons may constitute a less invasive
134 cence, consistent with presynaptic Y(2)Rs on somatostatin interneurons mediating the above effects.
135                        Since parvalbumin and somatostatin interneurons preferentially target perisoma
136 duced persistent LTP at excitatory inputs of somatostatin interneurons that depends on type I metabot
137  alpha5 subunit (concentrated on hippocampal somatostatin interneurons).
138        Here, we show that mTORC1 activity in somatostatin interneurons, a major subclass of GABAergic
139 ipal neurons, probably from Y(2)R-expressing somatostatin interneurons, some of which coexpress NPY.
140 essing action potential dynamics typical for somatostatin interneurons.
141 ausing increased survival of parvalbumin and somatostatin interneurons.
142 4 is a key regulator of the specification of somatostatin interneurons.
143 ter-2; SGLT2) or when the action of secreted somatostatin is prevented by somatostatin receptor (SSTR
144  receptor radiotherapy using (177)Lu-labeled somatostatin ligand analogs is a well-established treatm
145 patients allocated to brimonidine (n = 152), somatostatin (n = 145), or placebo (n = 152).
146 anocortin (POMC) subtypes, and an orexigenic somatostatin neuron population.
147 hat the cortex, via cortico-lateral-amygdala somatostatin neurons (CLA-SOM), has a direct inhibitory
148  cognition, and mood-related behaviors, with somatostatin neurons contributing evenly to both behavio
149  and signaling pathways, notably in PYCs and somatostatin neurons, further contribute to behavioral c
150 arily controlled by GH-releasing hormone and somatostatin neurons.
151 PH were randomized double-blindly to receive somatostatin or placebo (2:1).
152                                              Somatostatin or VIP neuron activation also impaired or e
153 omly assigned to one of three arms: placebo, somatostatin, or brimonidine.
154 amidal neurons by optogenetically activating somatostatin- or parvalbumin-positive interneurons, even
155 three subclasses: parvalbumin positive (PV), somatostatin positive (SOM) and serotonin positive neuro
156 ses of interneurons, the parvalbumin and the somatostatin positive cells, tightly control both up-to-
157        We found that TMEM16B is expressed in somatostatin-positive (SOM(+)) GABAergic neurons of the
158 ll excitatory neurons were pyramidal and all somatostatin-positive (SOM(+)) non-fast-spiking interneu
159 urons was not shared with dendrite-targeting somatostatin-positive (SOM+) interneurons.
160                                We focused on somatostatin-positive (SST(+)) GABAergic interneurons be
161                                              Somatostatin-positive (SST(+)) interneurons expressed th
162 , specifically parvalbumin-positive (PV) and somatostatin-positive (SST) inhibitory interneurons.
163   Furthermore, we observed early deficits of somatostatin-positive and Reelin-positive interneurons i
164 tion of engram-forming cells is regulated by somatostatin-positive dendrite-targeting interneurons, w
165 ll stimulation compared with parvalbumin- or somatostatin-positive interneuron stimulation.
166 h parvalbumin-positive interneurons (PV) and somatostatin-positive interneurons (SOM) to pyramidal ne
167 arvalbumin-positive interneurons (PVINs) and somatostatin-positive interneurons (SSTINs) in male prea
168                 In our model, stimulus-tuned somatostatin-positive interneurons develop strong connec
169  had a decreased density of parvalbumin- and somatostatin-positive interneurons in dentate gyrus, but
170 se nucleus incertus (NI) selectively inhibit somatostatin-positive interneurons in the hippocampus, b
171                           The recruitment of somatostatin-positive interneurons is likely fundamental
172 nhibitory synapses formed by parvalbumin- or somatostatin-positive interneurons on pyramidal layer 5
173 rincipal cells as well as of parvalbumin- or somatostatin-positive interneurons to study the effects
174 thmic input to the lateral hypothalamus from somatostatin-positive lateral septum cells evokes food a
175 dendritic synaptic inhibitory loop formed by somatostatin-positive Martinotti cells (MCs) and pyramid
176 s and increased activity of central amygdala somatostatin-positive neurons, putatively projecting to
177 lucagon-producing pancreatic alpha-cells and somatostatin-producing delta-cells become insulin-expres
178                        NET patients received somatostatin radiopeptide therapy with (90)Y-DOTATOC or
179 dionuclide therapy (PRRT) using radiolabeled somatostatin receptor (SSTR) analogs is a common approac
180 have shown enhanced tumor targeting by novel somatostatin receptor (SSTR) antagonists compared with c
181 ion of secreted somatostatin is prevented by somatostatin receptor (SSTR) antagonists.
182  avidity to somatostatin analogues suggested somatostatin receptor (SSTR) expression in VHL-HBs, offe
183 docrine neoplasms (NENs) have long relied on somatostatin receptor (SSTR) expression.
184                              Eligibility for somatostatin receptor (SSTR) radionuclide therapy uses t
185                                              Somatostatin receptor (sstr) scintigraphy for imaging an
186 fficacy, and safety of PRRT in patients with somatostatin receptor (SSTR)-expressing G3 NENs.
187 r available imaging agents for patients with somatostatin receptor (SSTR)-positive neuroendocrine tum
188                                              Somatostatin receptor (SSTR)-targeted peptide receptor r
189 ronal protein gene product 9.5 [PGP9.5], and somatostatin receptor 1 [SSTR1]).
190                                              Somatostatin receptor 2 (SSTR2) is frequently overexpres
191 bles detection of meningioma tissue based on somatostatin receptor 2 expression.
192 led octreotate is an effective treatment for somatostatin receptor 2-expressing neuroendocrine tumors
193  for clinical assessment in the treatment of somatostatin receptor 2-expressing neuroendocrine tumors
194 oval of ubiquitin acceptor residues from the somatostatin receptor 3 (SSTR3) and from the orphan GPCR
195 a TGR5 antagonist alone or concurrently with somatostatin receptor agonists represents a potential th
196  a combination of SBI-115 and pasireotide, a somatostatin receptor analogue.
197  varying glomerular filtration rates, kidney somatostatin receptor densities, tumor volumes, and rele
198                          Hence, TBR reflects somatostatin receptor density more accurately than SUV a
199                                   Imaging of somatostatin receptor expression is an established techn
200 UV) in tumors were suggested as a measure of somatostatin receptor expression.
201 s (27 men) with advanced tumors and enhanced somatostatin receptor expression.
202 flux rate (K(i)), as a representation of the somatostatin receptor expression.
203 umors have been suggested to be a measure of somatostatin receptor expression.
204               In this study, we selected the somatostatin receptor imaging agent DOTATOC as the found
205                                              Somatostatin receptor imaging is a valuable tool in the
206 been posed as a potential source of error in somatostatin receptor imaging through interference with
207 d theoretically lead to misinterpretation of somatostatin receptor imaging with (68)Ga-DOTATATE PET/C
208 found on simultaneous CT or later MR, CT, or somatostatin receptor imaging.
209 r sensory cilia, inhibited enrichment of the somatostatin receptor in primary cilia.
210 e inhibitors to block desensitization of the somatostatin receptor in slices from morphine-treated an
211                                Octreotide, a somatostatin receptor ligand that targets somatotroph ad
212           Pharmacological treatments include somatostatin receptor ligands (such as octreotide, lanre
213                                              Somatostatin receptor PET imaging has had a profound eff
214 brain, preferably with MR, together with the somatostatin receptor scintigraphy (SRS), in each clinic
215            The oncogenic role of the spliced somatostatin receptor sst5TMD4 variant in prostate cance
216 pads for autocrine activation of a GPCR (the somatostatin receptor SSTR5) with its peptide agonist SR
217 is recent in vitro and in vivo evidence that somatostatin receptor subtype 2 (sst2) antagonists are b
218 his concept to a G protein-coupled receptor, somatostatin receptor subtype 2 (SSTR2), in pituitary ce
219 ed with Cu and (64)Cu and tested in vitro in somatostatin receptor subtype 2-overexpressing HEK-293 c
220 ncreased for cells expressing high levels of somatostatin receptor subtype 2.
221 ium-68-labeled DOTATATE ((68)Ga-DOTATATE), a somatostatin receptor subtype-2 (SST2)-binding PET trace
222                                              Somatostatin receptor type 2 (SSTR2) expression and (68)
223  of the potassium conductance induced by the somatostatin receptor was also blocked by compound 101 i
224 important treatment option for patients with somatostatin receptor-2 (SSTR2)-expressing neuroendocrin
225 maging in NOD-SCID mice bearing subcutaneous somatostatin receptor-expressing AR42J tumors.
226 matostatin analogs used for the diagnosis of somatostatin receptor-expressing neuroendocrine tumors (
227 u-DOTATATE is a most effective treatment for somatostatin receptor-expressing neuroendocrine tumors.
228 abeled somatostatin analogs in patients with somatostatin receptor-expressing tumors is often perform
229 E and [(68)Ga]Ga-DOTATATE for PET imaging of somatostatin receptor-expressing tumors, warranting tran
230                         Mice bearing CA20948 somatostatin receptor-positive tumor xenografts were tre
231 eatment approach in inoperable or metastatic somatostatin receptor-positive tumors.
232                            (68)Ga-DOTATOC, a somatostatin receptor-targeted ligand, has been used cli
233 ly, offers the possibility of using a single somatostatin receptor-targeted peptide conjugate as a th
234  95% confidence interval (CI) 1.52-4.77] and somatostatin-receptor imaging (OR 3.681, 95% CI 1.809-7.
235  cPanNENs is increased by the use of EUS and somatostatin-receptor imaging and is higher in specializ
236 rodihydroxyphenylalanine (FDOPA), and (68)Ga somatostatin-receptor ligands in NETs has been expanding
237                            Overexpression of somatostatin receptors (SSTRs) in patients with neuroend
238 orectal cancer, which is reported to express somatostatin receptors (SSTRs).
239                       Targeting dopamine and somatostatin receptors on corticotroph adenomas with cab
240                       The high expression of somatostatin receptors on this neuroendocrine neoplasm o
241 ctable or metastatic; however, expression of somatostatin receptors qualifies it for peptide receptor
242 ses were observed among distinct subtypes of somatostatin+/Reelin+ double-positive cells, including H
243 atal subregions, with additional deficits in somatostatin-related signalling through SSTR2, may contr
244 anism mediated by stimulation of intra-islet somatostatin release.
245 genetic ablation of insulin receptors in the somatostatin-secreting delta-cells, when insulin-induced
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 -secreting delta-cells, when insulin-induced somatostatin secretion is suppressed by dapagliflozin (a
250 e mainly those that express the neuropeptide somatostatin, send projections to the globus pallidus ex
251 islet cells expressing insulin, glucagon, or somatostatin share a lack of methylation at the promoter
252 gies to alter mTORC1 function selectively in somatostatin (SOM) inhibitory interneurons (SOM-INs).
253 ing animals, we show that dendrite-targeting somatostatin (SOM) interneurons are critical for a visua
254                     Excitatory synapses onto somatostatin (SOM) interneurons show robust short-term f
255 associated with activation of CeL-expressing somatostatin (SOM) neurons.
256 d neuropeptides, including parvalbumin (PV), somatostatin (SOM), calretinin (CR), and cholecystokinin
257 eurons expressing either parvalbumin (PV) or somatostatin (SOM), two markers of particular sub-classe
258                        However, targeting of somatostatin (SOM)- and vasoactive intestinal peptide (V
259 tive intestinal peptide (VIP)-expressing and somatostatin (SOM)-expressing inhibitory neurons modulat
260 olecystokinin (CCK+), parvalbumin (PV+), and somatostatin (SOM+) expressing interneurons are prominen
261 ers by targeting either parvalbumin (PV+) or somatostatin (SOM+) interneurons.
262  (TFs) have compensatory roles in repressing somatostatin (SST(+)) interneuron (IN) production in med
263 terations of GABAergic interneurons, notably somatostatin (Sst) as well as parvalbumin (Pvalb), in co
264 pecific activity of medial prefrontal cortex somatostatin (SST) interneurons and that activation of t
265     Here we show that activation of cortical somatostatin (SST) interneurons by Lypd6, an endogenous
266 tivity is shaped by the parvalbumin (PV) and somatostatin (SST) interneurons that inhibit principal e
267 mice and photoactivated parvalbumin (PV) and somatostatin (SST) interneurons to map the timing and st
268 ene is deleted in either parvalbumin (PV) or somatostatin (SST) interneurons, and examined their ASD-
269 files of the inhibitory parvalbumin (PV) and somatostatin (SST) interneurons.
270                         A subset of cortical somatostatin (SST) neurons, the Martinotti cells, gate t
271 interneurons, as well as subtypes expressing somatostatin (Sst) or parvalbumin (Pvalb), but not gluta
272 -cAMP or 3-isobutyl-1-methylxanthine and the somatostatin (SST) receptor 2-5 antagonist H6056.
273                                 Radiolabeled somatostatin (sst) receptor agonists are integral to the
274 linical evidence indicates that radiolabeled somatostatin (sst) receptor antagonists perform better t
275     Medial ganglionic eminence (MGE)-derived somatostatin (SST)+ and parvalbumin (PV)+ cortical inter
276 brain-derived neurotrophic factor (BDNF) and somatostatin (SST), a marker of inhibitory gamma-aminobu
277 reduction of CINs expressing parvalbumin and somatostatin (Sst), and an increased number of MGE-deriv
278 ressing vasoactive intestinal peptide (Vip), somatostatin (Sst), and parvalbumin (Pvalb).
279 nd interneurons expressing parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (V
280               Genes encoding islet hormones [somatostatin (SST), insulin (INS), Glucagon (GCG)], diff
281  such interneuron type is the low-threshold, somatostatin (SST)-expressing cell, which is one of the
282 rgic interneurons include the low-threshold, somatostatin (SST)-expressing cells and the fast-spiking
283 igh levels of Wnt signaling and give rise to somatostatin (SST)-expressing cortical interneurons.
284 ibutions towards strong network-coupling; in Somatostatin (SST)-expressing INs, however, two physiolo
285               Concomitantly, the activity of somatostatin (SST)-expressing interneurons increased and
286 cal inhibitory inputs, particularly those of somatostatin (SST)-expressing interneurons.
287 riods of heightened arousal directly excites somatostatin (SST)-expressing interneurons.
288 e have identified three distinct subtypes of somatostatin (Sst)-expressing neurons in the mouse VTA.
289 tered by the loss of Nf1, without changes in somatostatin (SST)-positive CINs.
290 ibition in layer 1 in vivo, between axons of somatostatin (SST)-positive interneurons and apical tuft
291  of dopamine (tyrosine hydroxylase, TH+) and somatostatin (SST+) neurons in the paraventricular nucle
292 rneurons expressing parvalbumin (PV-INs) and somatostatin (SST-INs) exhibit impaired excitability in
293 hibitory interneurons, parvalbumin- (PV) and somatostatin-(SST) positive interneurons control sound-e
294                   These data reveal that the somatostatin subclass of inhibitory interneurons are dri
295 tion of living HeLa cells overexpressing the somatostatin subtype-2 receptor.
296 lpha(+) inhibitory neurons of parvalbumin or somatostatin subtypes.
297            Approximately 55%, 35% and 63% of somatostatin, thyrotropin-releasing hormone (TRH) and co
298 o gain insight into the contribution of each somatostatin to specific nervous systems circuits and be
299 piny dendrites, and do not typically express somatostatin, VIP, or the muscarinic acetylcholine recep
300                                              Somatostatin was not detected in principal neurons but d

 
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