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1                                              Bath application (2 hr) of the actin polymerization inhi
2 ion potential bursting, but not by glutamate bath application activating extrasynaptic NMDA receptors
3       Focal DHPG puffs onto granule cells or bath application after glomerular layer (GL) excision fa
4                                 Importantly, bath application and removal of Mg(2+)-free ATP or a non
5 d-pulse facilitation (PPF) and is blocked by bath application but not blocked by postsynaptic injecti
6                                              Bath application, but not postsynaptic dialysis, of an N
7 o had a more rapid effect: within minutes of bath application, E2 acutely increased synaptic strength
8               In slices with sprouting, BDNF bath application enhanced responses recorded in the inne
9 izes changes in pCREB levels induced by NMDA bath application in rat cortical neurons.
10                                 By contrast, bath application of (2-aminoethyl)methanethiosulfonate (
11  muscle cells was significantly increased by bath application of 0.5 microM isoproterenol (isoprenali
12                                              Bath application of 1 microM GABA increased tonic curren
13 ter excision of an isolated inside-out patch bath application of 1 mum Ins(1,4,5)P3 increased open ch
14                                              Bath application of 1-10 micrometer serotonin (5HT), a m
15                                              Bath application of 1-50 microM troglitazone depolarised
16                                              Bath application of 10 microM neostigmine, a potent acet
17                 With cell-attached recording bath application of 10 nm ET-1 evoked cation channel cur
18                           In Purkinje cells, bath application of 10, 20 or 100 microM MeHg initially
19                           In Purkinje cells, bath application of 10, 20 or 100 mM MeHg initially incr
20 asynaptic NMDAR-mediated currents induced by bath application of 100 microM NMDA/10 microM glycine wi
21       In amphotericin whole-cell recordings, bath application of 2,4-dinitrophenol (DNP, an uncoupler
22            Finally, we demonstrate that both bath application of 2-arachidonoylglycerol(2-AG) and dep
23                                              Bath application of 20 microM betaxolol reduced the glut
24 e-cell currents were elicited in response to bath application of 20 microM NMDA and 50 microM glycine
25 dependent and Ca2+-independent components by bath application of 200 microM Cd2+, which blocked Ca2+
26                               We report that bath application of 3 mum carbachol (CCh), a muscarinic
27  under a similar experimental condition (ie, bath application of 4-aminopyridine), the initiation of
28                                              Bath application of 4-ethylphenylamino-1,2-dimethyl-6-me
29 the cytosolic tyrosine kinase pp60c-src, and bath application of 5 microM insulin, which activates re
30                                              Bath application of 5 nm nicotine increased the excitabi
31                                              Bath application of 5-CT inhibits synaptic strength, rel
32                                              Bath application of 5-HT and injection of 8-OH-DPAT [(+/
33   A single pairing of tetanus in one SN with bath application of 5-HT evoked long-term (24 hr) increa
34                                              Bath application of 5-HT(4)R agonists did not affect mot
35 ng of tetanus in the sensory neuron (SN) and bath application of 5-HT.
36                                              Bath application of 50 microM (1S,3R)-1-aminocyclopentan
37                                Nevertheless, bath application of 50 microM 4-aminopyridine (4-AP) or
38 cute (15 min) stimulation of OB neurons with bath application of 50 ng ml(-1) brain-derived neurotrop
39                                              Bath application of 50-300 nM kainate to an in vitro pre
40                                     In vitro bath application of 60 mM ethanol inhibited STP by 35% a
41                                              Bath application of 7beta-deacetyl-7beta-[gamma-(morphol
42                                              Bath application of 8-Br-cAMP decreased I(Cl(swell)) by
43 ed by decreased conductances, in response to bath application of 8-bromo-cAMP but not the membrane-im
44 stimulation-evoked dopamine release and that bath application of a KOR antagonist provides full rescu
45 ell soma hyperpolarized the interneuron, and bath application of a lower dose of serotonin (0.1 micro
46                    Correspondingly, in vitro bath application of a mu opioid receptor agonist suppres
47                                              Bath application of a positive SK channel modulator (1-E
48 es in sIPSCs induced by Ca(2+) uncaging, and bath application of a selective GluR5-containing recepto
49 amic input synapses to the LA is impaired by bath application of a specific mGluR5 antagonist, 2-meth
50 ns of external chloride concentration and to bath application of a stilbene derivative, 4-acetamido-4
51 electrical activity typically observed after bath application of a stimulatory concentration of gluco
52 n was found to be membrane-delimited because bath application of ACh did not inhibit GIRK channel act
53                                              Bath application of actinomycin D, an irreversible RNA s
54        In membrane excitability experiments, bath application of adenosine and CPA reversibly inhibit
55                                              Bath application of adenosine or RPIA reversibly inhibit
56           Using extracellular recordings and bath application of agonists and antagonists, we compare
57                                              Bath application of alcohol reduced evoked firing in neu
58                                              Bath application of AMPA also activated astrocytes.
59 E enhances the respiratory motor response to bath application of AMPA to the brainstem, although it w
60                                              Bath application of an antisensorin antibody during the
61 Cx36-/- RGCs were significantly inhibited by bath application of an ionotropic glutamate receptor ant
62 with a postsynaptic Ca2+ chelator but not by bath application of an NMDA receptor antagonist.
63  evoked inward currents that were blocked by bath application of an NMDAR antagonist (dl-APV), indica
64                                              Bath application of anti-TRPC3 and anti-TRPC7 antibodies
65                                              Bath application of anti-TRPC3 antibodies markedly reduc
66                                              Bath application of anti-TRPC6 and anti-TRPC1 antibodies
67                                              Bath application of antibodies to G(alphaq)/G(alpha11) e
68   Typically, multiplex platforms necessitate bath application of antibody cocktails, increasing proba
69 litude, and decay kinetics were unaltered by bath application of apamin, suggesting that SK channel b
70                                              Bath application of Ba(2+) significantly reduced the A-t
71                                              Bath application of BDNF induced extensive formation of
72                                              Bath application of bicuculline (a GABA(A) receptor anta
73 alcium chelators in the pipette solution, or bath application of bicuculline, EPSC enhancement is blo
74 n the bulk of this inhibition was blocked by bath application of bicuculline, the incidence of platea
75                       Furthermore, following bath application of BK channel blockers for 10 min, etha
76 onized ventral root bursts generated by both bath application of blockers of inhibitory neurotransmit
77 is effect can be blocked by the simultaneous bath application of BN 52021 and trans-BTD, PAF receptor
78                 In contrast, the response to bath application of bradykinin (1 microm, 3 ml) was not
79         Wiwatpanit et al. (2012) showed that bath application of C-type allatostatin produced either
80 (20 mM BAPTA, without added Ca2+), or by the bath application of cadmium (100 microM) to block voltag
81                                              Bath application of cadmium to reduce calcium influx als
82 mbrane-permeant analogue of BAPTA) or by the bath application of cadmium.
83 ches in the cell-attached configuration, the bath application of capsaicin evoked single-channel curr
84                                              Bath application of capsaicin slowed respiratory motor o
85 tent in vitro gamma oscillations, induced by bath application of carbachol and kainate (amongst other
86                                              Bath application of carbachol could overcome the block o
87 cal activation of cholinergic receptors with bath application of carbachol increased the firing rate
88 cked muscarinic cation currents activated by bath application of carbachol or intracellular infusion
89 esynaptic potassium channels were blocked by bath application of channel toxins, and the effect of ka
90                                              Bath application of CHZ successfully restored the precis
91                                              Bath application of compound T-588, a neuroprotective ag
92 Furthermore, these findings demonstrate that bath application of contractile agonists to gastrointest
93                                              Bath application of corticosterone (100 nm) to prefronta
94          When NMDA receptors were blocked by bath application of D-2-amino-5-phosphonovaleric acid, L
95                                              Bath application of DA (0.05-30 microM) produced a rever
96                                              Bath application of DA had no detectable effect on odora
97                                              Bath application of DA, 5HT, or Oct enhanced cycle frequ
98 h-clamp experiments from hippocampal slices, bath application of DHPG induced a depression of synapti
99                                              Bath application of dioctanoylglycerol (diC8), a diacylg
100                                              Bath application of dithiothreitol or TPEN (N,N,N',N'-te
101                                              Bath application of dopamine increased the frequency of
102                                              Bath application of dopamine or the dopamine D1 agonist
103                                              Bath application of dopamine significantly enhanced EPSC
104   The evidence implicating PKA has come from bath application of drugs during LTP induction, an appro
105                                        After bath application of either an excitatory amino acid (AP-
106                                              Bath application of either BK channel blockers significa
107                                              Bath application of either the TRPV4 channel blocker HC0
108                                              Bath application of emetine, a protein synthesis inhibit
109 p recordings from GPe neurons and found that bath application of ethanol dose-dependently decreased t
110                                              Bath application of ethanol enhanced the amplitude of mI
111                                              Bath application of flufenamic acid, Gd3+, La3+ and Ca2+
112 or (H-89), and is mimicked (and occluded) by bath application of forskolin.
113                                              Bath application of GABA first decreased the amplitude o
114                                              Bath application of GABA or muscimol caused an early hyp
115 X), postsynaptic Ca2+ rises triggered by the bath application of GABA were only moderately depressed
116                                              Bath application of GABA(A) receptor agonists muscimol (
117 ular layer response was largely resistant to bath application of GABAA receptor antagonists but was s
118 , and V of all retrohippocampal areas during bath application of glutamate antagonists.
119                                 Importantly, bath application of glutamate to SCN slices rapidly and
120                                     Although bath application of GRP or NMB had little or no effect o
121 arized to near the dark resting potential by bath application of high K(+) solutions.
122 T1 MF-2 smooth muscle cells responded to the bath application of histamine or ATP with an increase in
123                                  Moreover, a bath application of histamine to acute brain slices inhi
124                                              Bath application of human PACAP-38 also rescued the curr
125                                              Bath application of IL-1beta or TNF-alpha led to the rel
126                                   Pipette or bath application of insulin evoked a rapid increase in h
127          With cell-attached patch recording, bath application of isoprenaline produced a pronounced i
128                                              Bath application of isoproterenol (1 muM), a beta-adrene
129                                 In contrast, bath application of K252a prevented the enhancement of s
130                                We found that bath application of kainate (3 microm) profoundly reduce
131 amic input synapses to the LA is impaired by bath application of KN-62 in vitro.
132    The effects of l-arginine were blocked by bath application of l-NAME (20mM).
133                                              Bath application of lavendustin A, a PTK inhibitor that
134                    In cell-attached patches, bath application of low concentrations of Ang II (1 nM)
135                                              Bath application of low concentrations of GBZ (25-200 nM
136            gamma-Motoneurons were excited by bath application of low concentrations of ouabain that s
137                                              Bath application of morphine (1 microM) almost completel
138                                              Bath application of MT-II or alpha-MSH significantly red
139                                We found that bath application of muscarine caused a direct depolariza
140 ls coexpressed with muscarinic M1 receptors, bath application of muscarinic agonist reduced the maxim
141 ar neurons were less strongly depolarized by bath application of muscarinic agonists, and uniformly l
142 ACh-induced reduction was also diminished by bath application of muscimol at the low concentrations t
143                                        Brief bath application of N-methyl-D-aspartate (NMDA) to hippo
144                                              Bath application of NE to the slices resulted in signifi
145  slice preparation can be compensated for by bath application of neurochemicals known to accelerate t
146                  With 250 and 500 nM [Ca2+]i bath application of NFA (100 microM) increased inward cu
147                                              Bath application of nicotine during LFS accelerated DP,
148                                              Bath application of nicotine induced inward currents in
149                                              Bath application of nicotinic acetylcholine, AMPA, NMDA,
150  external Ca2+, and significantly reduced by bath application of nifedipine or omega-conotoxin.
151 t was inhibited by intracellular BAPTA or by bath application of niflumic acid (100 microM), a Ca(2+)
152 rtially inhibited ERK2 activation induced by bath application of NMDA and strongly suppressed ERK2 ac
153 tion of synaptic and extrasynaptic NMDARs by bath application of NMDA causes the loss of surface GABA
154                                              Bath application of NMDA evoked a slow inward current in
155 ation at T840 in the hippocampal CA1 region, bath application of NMDA induced a strong, protein phosp
156                                              Bath application of NMDA potently unclustered and dephos
157                                              Bath application of NMDA produced EPSPs, membrane depola
158 aptic potentiation was produced with a brief bath application of NMDA to rat hippocampal slices.
159 te (NMDA) subtype of glutamate receptor, and bath application of NMDA was sufficient to activate PKA.
160                                              Bath application of NMDA, AMPA, and the D1 agonist SKF38
161 naptic phenotype of chordin null slices, but bath application of Noggin, another antagonist of BMP si
162  reversal potential to the current evoked by bath application of noradrenaline (100 microM).
163                                    Moreover, bath application of noradrenaline (NA) significantly dep
164                With cell-attached recording, bath application of noradrenaline, 1-oleoyl-acetyl-sn-gl
165                                              Bath application of octopamine, 5-HT, and dopamine at co
166                                              Bath application of orexin-A or orexin-B (30-300 nM) pro
167                                              Bath application of oxytocin (1 and 10 microM) inhibited
168                     With inside-out patches, bath application of PDBu evoked channel currents with si
169                  Icat activated by OAG after bath application of PDBu was not significantly different
170                                              Bath application of pentylenetetrazole (PTZ) or glutamat
171                                              Bath application of pituitary adenylate cyclase activati
172                                     Although bath application of PKA inhibitor drugs (KT5720, Rp-8CPT
173                                     Moreover bath application of PKA inhibitors, H-89, KT5720 and an
174 itation of the pyloric rhythm is mimicked by bath application of proctolin, its peptide transmitter.
175 nce of striatal LTD, however, was blocked by bath application of protein translation inhibitors but n
176 of the ryanodine receptor-gated Ca2+ pool by bath application of ryanodine (10 microM) also blocked t
177 ffusion of BAPTA or heparin into neurones or bath application of ryanodine suppressed bursting.
178                                              Bath application of saturating concentrations of proctol
179 n formation away from the Sema3A source, and bath application of Sema3A to polarized neurons promoted
180                                 In contrast, bath application of sensorin accelerated the increase in
181     We found that tetanic stimuli coupled to bath application of serotonin induced long-term depressi
182                                              Bath application of SNAP (2mM) or l-arginine (50mM) elic
183      Respiratory rhythm could be restored by bath application of SP or glutamate transporter blockers
184                                              Bath application of SR 31742A produced a biphasic effect
185                                              Bath application of Sub P to brainstem slices for a peri
186                                              Bath application of substance P (SP; 0.1 to 10 microM) t
187                                              Bath application of T1E3, an anti-TRPC1 antibody raised
188               Exocytotic frequency evoked by bath application of tetraethylammonium (1-10 mM) was sig
189                                    Likewise, bath application of tetrodotoxin (TTX) reduced the SNR a
190                                 In addition, bath application of thapsigargin and ryanodine, and intr
191                                              Bath application of the 1,2-diacyl-sn-glycerol (DAG) ana
192                           In control slices, bath application of the alpha(1)-agonist phenylephrine (
193                                              Bath application of the alpha-amino-3-hydroxy-5-methyl-4
194                                              Bath application of the AMPA receptor antagonist 1-(4-am
195                                              Bath application of the AMPA receptor antagonist beta-cy
196                         In the outer retina, bath application of the AMPA/KA receptor antagonists 6,7
197                                              Bath application of the bombesin-like neuropeptides gast
198                                              Bath application of the CB1 receptor agonist, WIN 55212-
199                                              Bath application of the cell-permeant Ca2+ chelator, BAP
200 on-dependent excitability increases, whereas bath application of the D2 receptor agonist quinpirole i
201                                              Bath application of the diacylglycerol analogue 1-oleoyl
202                                              Bath application of the diacylycerol (DAG) analogue 1-oe
203 tes and neurons significantly increase after bath application of the excitatory amino acid transporte
204 of single spiking activity was unaffected by bath application of the GABA(A) antagonist picrotoxin (5
205                                              Bath application of the GABA(A) receptor agonist muscimo
206                                              Bath application of the GABAA receptor antagonist bicucu
207 er, the complex EPSC was greatly enhanced by bath application of the GABAA receptor antagonists picro
208         Intriguingly, however, we found that bath application of the GAT-1 transport blocker NO-711 (
209                                              Bath application of the kappa opioid receptor agonist U6
210  to induce long-term depression (LTD) during bath application of the L-channel antagonist nifedipine
211 -cell voltage-clamp recordings revealed that bath application of the ligand for MrgD, beta-alanine, r
212                                              Bath application of the MEK1/2 inhibitor U0126 did not a
213                                        After bath application of the membrane-permeable cAMP analog a
214                                              Bath application of the membrane-permeable cAMP analogs
215                                              Bath application of the membrane-permeable cGMP analogs
216 (L+M)-OFF response in SBCs was eliminated by bath application of the metabotropic glutamate receptor
217           Moreover, POA neurons responded to bath application of the mu-opioid receptor agonist DAMGO
218                                              Bath application of the N-methyl-D-aspartate (NMDA) rece
219                                              Bath application of the Na+ channel blocker TTX eliminat
220                               The effects of bath application of the nitric oxide (NO) precursor L-ar
221                                              Bath application of the NMDA receptor antagonist 3-[2-ca
222 t PF to Purkinje cell synapses is blocked by bath application of the NMDA receptor antagonist D-2-ami
223 acid (TBOA) and significantly decrease after bath application of the NMDA receptor antagonist DL-2-am
224 timulation, an effect that was reversed with bath application of the NMDA receptor partial agonist D-
225                                              Bath application of the NO donor NOC-18 increased the si
226                                              Bath application of the NO donor, S-nitroso-N-acetyl-pen
227                                              Bath application of the nonselective mGluR antagonist, (
228                                              Bath application of the octopaminergic drugs phentolamin
229 y augmenting projection neuron influence via bath application of the peptide cotransmitter Cancer bor
230                                   Similarly, bath application of the phospholipase C (PLC) inhibitor
231  dialysis of the catalytic subunit of PKA or bath application of the PKA activator Sp-cAMP significan
232                                              Bath application of the PKA inhibitor H89 suppressed the
233                                 In contrast, bath application of the PKC activator, (-) indolactam V
234                                              Bath application of the protein kinase C inhibitor chele
235                                              Bath application of the protein synthesis inhibitor emet
236                                 Furthermore, bath application of the reducing agent dithiothreitol in
237 was due in part to an altered redox state as bath application of the reducing agent, dithiothreitol,
238                                              Bath application of the selective beta1-adrenoceptor ago
239                                              Bath application of the selective beta2-adrenoceptor ago
240 agnitude of synaptic suppression elicited by bath application of the selective CP-AMPAR antagonist na
241     Both Src actions were mostly reversed by bath application of the Src inhibitors erbstatin (20 mic
242                                              Bath application of the TRPV1 antagonist capsazepine (10
243 ll dialysis, and was inhibited reversibly by bath application of the VIP receptor-binding inhibitor L
244                                              Bath application of thiopental lowered the frequency of
245 nd alpha2-adrenergic receptors (activated by bath application of transmitters) produced a three- to f
246 tro electrophysiological studies showed that bath application of TRH caused concentration-dependent m
247 o receptor-mediated GIRK channel inhibition, bath application of TRH decreased GIRK channel activity
248                                              Bath application of TRH resulted in a transient cessatio
249                        Finally, we show that bath application of U0126 impairs long-term potentiation
250                                              Bath application of Val(1)-SIFamide, a peptide whose exp
251                                              Bath application of various NO donors or CO-containing s
252                                              Bath application of WAY-100135 raised the ICMS current i
253                  Mimicking Zn(2+) release by bath application of Zn(2+) (50-100 microm) without HFS i
254 ained and the preparation still responded to bath applications of GABA.
255                                Extracellular bath applications of Pb(2+) significantly reduced curren
256 ons of the Ca(2+) chelator BAPTA (20 mm), or bath applications of the L-type Ca(2+) channel blocker n
257                               The effects of bath applications of the nitric oxide (NO) donors sodium
258                                              Bath-application of 5-HT (0.05 mM) caused a significant
259 amatergic hair cell transmission by combined bath-application of NMDA (7-chloro-kynurenic acid) and A
260                                              Bath-application of serotonin (30 microm) significantly
261 on, blocking NMDA receptors (NMDARs) through bath application or intracellular dialysis not only decr
262                                              Bath-application or local microinjections of glutamaterg
263 he group-selective agonist LY354740 (300 nM, bath application) resulted in a reduction of these IPSCs

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