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1 ain cholinergic deficits (induced by 192 IgG-saporin).
2 y lesioned with an immunotoxin (IT), 192 IgG-saporin.
3 cortical infusion of the immunotoxin 192 IgG-saporin.
4 ted with the selective cytotoxin substance P-saporin.
5 n composed of basic fibroblast growth factor-saporin.
6 gic neurons in NDB unilaterally with 192-IgG-saporin.
7 oned with the cholinergic immunotoxin 192IgG-saporin.
8 cortical infusion of the immunotoxin 192 IgG-saporin.
9 rebroventricularly with 4 micrograms 192 IgG-saporin.
10 was found in aged rats treated with 192-IgG-saporin.
11 brain with the ribosome-inactivating protein saporin.
12 scular injection of cholera toxin-conjugated saporin.
13 ansported catecholamine immunotoxin, antiDBH-saporin.
14 ced after a ventricular injection of 192 IgG-saporin.
15 VDB) cholinergic neurons produced by 192 IgG-saporin.
16 droxylase antibodies conjugated to the toxin saporin.
17 used with the selective cholinotoxin 192 IgG-saporin (0.005 microgram/0.5 microliter/site) into the f
19 y nerve growth factor receptor conjugated to saporin (192 IgG-saporin), lesioned rats were processed
22 Rats received PBS or the immunotoxin 192IgG-saporin (192Sap) intracerebroventricularly at two doses
23 linked to the ribosome-inactivating protein saporin-6 (rFGF2-SAP) on vascular SMC cytotoxicity and n
25 tibody to DBH coupled by a disulfide bond to saporin (a ribosome inactivating protein), has been show
27 tion of guanidinoneomycin to the plant toxin saporin, a ribosome-inactivating agent, results in prote
28 ng the intraseptal administration of 192-IgG-Saporin, a specific cholinergic neurotoxin, we have foun
30 ith saline or anti-dopamine-beta-hydroxylase-saporin, a toxin that destroys noradrenergic neurons of
31 roventricular anti-dopamine beta-hydroxylase/saporin, a treatment that destroys a majority of noradre
35 -hydroxydopamine (6-OHDA), a toxin devoid of saporin, also damaged NTS catecholamine neurons but did
36 eeks after intraventricular injection of 192-saporin, an immunotoxin directed at the low affinity neu
37 a partial immunolesion to CBFNs with 192 IgG-saporin, an immunotoxin selectively taken up by p75NTR-b
40 e loss of SPR-positive cells, a conjugate of saporin and the more potent and peptidase-resistant SP a
41 tested in combination with a protein toxin, saporin, and a significant reduction in cell viability w
43 electively killed by i.c.v. injection of 192-saporin, and cerebellar Purkinje cells which are killed
44 ection of a retrogradely transported form of saporin, and examined the morphology of contralateral SN
45 rats by bilateral local injection of orexin-saporin, and polysomnography was performed to measure ba
46 to dopamine-beta-hydroxylase conjugated with saporin (anti-DBH-SAP) damages catecholamine neurons in
48 body to the serotonin transporter (SERT) and saporin (anti-SERT-SAP; 1 microm) to kill serotonergic n
50 rtical infusions of the cholinotoxin 192 IgG-saporin, attenuated the beneficial effects of NMDA on dS
51 pressing mu-opioid receptors with dermorphin-saporin, blocked tactile and thermal hypersensitivity, a
54 log [Sar(9), Met(O(2))(11)] Substance P (SSP-saporin) caused negligible nonspecific damage at the inj
57 he neurotoxin saporin (SAP), or the orexin-2-saporin conjugate (OXSAP) in the lateral hypothalamus.
58 region (RTN/Ppy), we injected a substance P-saporin conjugate (SP-SAP; 0.1 pmol in 100 nl) to kill N
60 ere targeted with a single microinjection of saporin conjugated to the mu-opioid agonist dermorphin;
61 fects of the hypocretin-saporin with another saporin conjugated toxin, 192 IgG-saporin, that lesions
63 me inactivation approach through delivery of saporin-conjugated anti-vesicular GABA transporter antib
65 blating microglia in the spinal cord using a saporin-conjugated antibody to Mac1, we demonstrate a ca
66 nally transported catecholamine immunotoxin, saporin-conjugated antiserum to dopamine-beta-hydroxylas
70 cular application of the mitochondrial toxin saporin, coupled to the antibody directed against dopami
78 pressing mu-opioid receptors with dermorphin-saporin did not prevent the onset of SNL-induced tactile
79 ction, we employed the neurotoxin dermorphin-saporin (DS) to selectively lesion VTA GABA neurons prio
80 xylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into
83 cells in vitro when coupled to the cytotoxin saporin either directly or via a secondary antibody.
86 njury in rats pretreated with RVM dermorphin-saporin failed to elicit the expected increase in sensit
87 icacy of [Sar(9), Met(O(2))(11)] Substance P-saporin for producing a selective and spatially extensiv
88 ven GABAergic lesions of the MSDB using GAT1-saporin (GAT1-SAP) and examined on spontaneous explorati
89 he selective cholinergic immunotoxin 192 IgG-saporin have demonstrated that lesions of the cholinergi
90 e medial septum had been destroyed by mu P75-saporin, human MGE-like progenitors, but not ventral spi
92 R agonist dermorphin conjugated to the toxin saporin in the vicinity of ITC neurons caused a 34% redu
93 dermorphin-saporin, but not of dermorphin or saporin, in animals previously undergoing SNL showed a t
98 atment, SNB motoneurons contralateral to the saporin injection were retrogradely labeled with horsera
99 cortical regions was seen 12 weeks after 192-saporin injection with no further change up to 100-week
102 ons of the anti-neuronal immunotoxin 192-IgG saporin into either the hippocampus or the cingulate cor
103 ts of intraparenchymal injections of 192 IgG-saporin into either the MS or NB on the organization of
104 fferents as a result of infusions of 192 IgG-saporin into the basal forebrain show persistent impairm
106 Injection of 100, 237.5 or 375 ng of 192-saporin into the medial septum produced dose-related def
107 ections of the selective immunotoxin 192 IgG-saporin into the medial septum/vertical limb of the diag
113 imics of small oligonucleotide substrates of saporin-L1 are powerful, slow-onset inhibitors when aden
114 We characterized the catalytic properties of saporin-L1 from Saponaria officinalis (soapwort) leaves,
118 The present experiments used the 192IgG-saporin lesion model of AD to evaluate the actions of ga
119 misphere and a 192 immunoglobulin G (192IgG)-saporin lesion of cholinergic neurons in the contralater
121 ceived intracerebroventricular injections of saporin (lesioned) or saline (controls) and were tested
122 ctor receptor conjugated to saporin (192 IgG-saporin), lesioned rats were processed simultaneously wi
123 quently, these results support the use of SP-saporin lesions as a useful technique to study the role
125 f the nBM cholinergic system through 192 IgG-saporin lesions impairs early acquisition of learning se
126 iments, the performance of rats with 192 IgG-saporin lesions of both hippocampal and neocortical chol
135 Others received intrathecal injection of saporin linked to an antibody to the neurotrophin recept
136 the mitotoxin basic fibroblast growth factor-saporin more than 10-fold, thus allowing tumor cell kill
137 d either by microinjecting NPY conjugated to saporin (NPY-SAP) bilaterally into the Arc to kill NPY r
138 ntracerebroventricular injections of 192 IgG-saporin, NPY-immunolabeled neurons in the hilus of the d
139 SI cholinergic lesions, induced with 192 IgG saporin, on behavioral measures of aversive states in ra
142 rmance in this task, the immunotoxin 192 IgG-saporin or its vehicle was infused into the area of the
144 reatment of A549 cells or control cells with saporin or Pseudomonas exotoxin A whose intracellular me
145 wing intraseptal injection of either 192-IgG-saporin or saline, testing began in a battery of behavio
146 activation is not dependent upon reduction (saporin) or only partially dependent upon it (Pseudomona
149 ucleus region was destroyed with substance P-saporin prior to lentivirus injection into the rostral v
150 croinjection of a conjugate of native SP and saporin produced significant nonspecific damage at conce
151 s, although intraseptal injection of 192-IgG-saporin produced similar reductions of ChAT activity, pe
155 septal inputs using the immunotoxin 192 IgG-saporin reduces the number of interneurons containing ne
156 The degree of lesion produced by 192 IgG-saporin relative to controls was compared using three in
157 he selective cholinergic immunotoxin 192 IgG-saporin resulted in a >80% decrease in the number of lar
158 of these neurons by the selective toxin SSP-saporin resulted in a complete disruption of ejaculatory
159 ugation of the sialoside probes to the toxin saporin resulted in toxin uptake and toxin-mediated kill
160 a relatively small concentration of 192 IgG-saporin, resulted in a significant impairment in sustain
161 CD11b and the ribosome-inactivating protein saporin, resulted in reduced microglia staining, reducti
162 l injection of specific cholinotoxin 192-IgG saporin (SAP) +/- intraperitoneal injection of N-[chloro
163 cholaminergic neurons) was done by injecting saporin (SAP) conjugated with a selective NK1R agonist [
164 e produced by bilateral infusions of 192 IgG-saporin (SAP) into the basal forebrain and/or 6-hydroxyd
166 received injections of 100 or 375 ng 192-IgG saporin (SAP) or artificial CSF (C) into the medial sept
168 e, zebrafish Kiss1 peptide was conjugated to saporin (SAP) to selectively inactivate Kiss-R1-expressi
169 forebrain cholinergic neurons by conjugating saporin (SAP), a ribosome-inactivating protein, to a rat
172 ry secretion, we injected DSAP, unconjugated saporin (SAP), or saline bilaterally into the paraventri
173 er phosphate-buffered saline, the neurotoxin saporin (SAP), or the orexin-2-saporin conjugate (OXSAP)
178 iving intrahippocampal injections of 192 IgG-saporin (SAP-HPC), fimbria-fornix lesions (FF), or sham
179 gated soluble DC-HIL receptor with the toxin saporin (SAP; DC-HIL-SAP) and showed it to bind activate
181 aged rats, intraseptal injection of 192-IgG-saporin selectively reduced ChAT activity in the hippoca
183 VM dermorphin-saporin, but not dermorphin or saporin, significantly decreased cells expressing mu-opi
185 We injected (2 x 100 nl) (a) substance P-saporin (SP-SAP; 1 microm) to kill NK1R-expressing neuro
186 arrier impermeable toxin, stable substance P-saporin (SSP-SAP), which ablates cells expressing NK rec
188 igands and the ribosome inactivating protein saporin that specifically target Substance P receptor-ex
189 th another saporin conjugated toxin, 192 IgG-saporin, that lesions only the cholinergic neurons in th
190 ed against dopamine beta hydroxylase (DbetaH-saporin), the analgesic and sedative actions of N(2)O we
191 l immunotoxin was constructed by conjugating saporin, the ribosome-inactivating protein toxin, to an
192 e used cholera toxin B-subunit conjugated to saporin to demyelinate the rat lumbar spinal cord, remov
193 th a single RVM microinjection of dermorphin-saporin to eliminate cells that drive descending facilit
195 tion of sleep drive by administering 192-IgG-saporin to lesion the BF cholinergic neurons and then me
196 ventricular infusions of the immunotoxin OX7-saporin to selectively destroy Purkinje cells throughout
199 ith the cytotoxin, saporin, using either CCK-saporin to target CCK receptor expressing cells, or derm
200 CCK receptor expressing cells, or dermorphin-saporin to target MOR expressing cells, resulted in conc
202 s of the stria terminalis (BNST), vehicle or saporin toxin conjugated to an antibody against dopamine
205 of either phosphate buffer (PBS) or 192 IgG-saporin (Toxin), 3.6 micrograms rat-1, a cholinergic imm
206 hese multivalent ligands with auristatin and saporin toxins are efficiently internalized via hCD22 re
207 gonadally intact saporin-treated males, and saporin-treated males who had been castrated 6 weeks pre
208 ed in normal control males, gonadally intact saporin-treated males, and saporin-treated males who had
210 issues from these DLF-lesioned or dermorphin-saporin-treated SNL rats did not exhibit enhanced capsai
215 d cell lesion in the RVM with the cytotoxin, saporin, using either CCK-saporin to target CCK receptor
217 ance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was interna
218 n selective for cholinergic neurons, 192 IgG-saporin, was examined in rats trained to perform 2 versi
219 ntracerebroventricular injections of 192 IgG-saporin were trained on object discrimination problems a
220 e selective cholinergic immunotoxin, 192-IgG-saporin, were investigated in mature (6-month-old) and a
221 he diagonal band of Broca, made with 192 IgG-saporin, were not impaired in acquiring the same olfacto
223 anding specificity against another biotoxin, saporin, which has mechanism of action similar to ricin.
224 -saporin, which is targeted at Thy1, and 192-saporin, which is targeted at the low affinity neurotrop
226 We contrast the effects of the hypocretin-saporin with another saporin conjugated toxin, 192 IgG-s
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