1 muscle cells was significantly increased by
bath application of 0.5 microM isoproterenol (isoprenali
2 Bath application of 1 microM GABA increased tonic curren
3 ter excision of an isolated inside-out patch
bath application of 1 mum Ins(1,4,5)P3 increased open ch
4 Bath application of 1-10 micrometer serotonin (5HT), a m
5 Bath application of 1-50 microM troglitazone depolarised
6 Bath application of 10 microM neostigmine, a potent acet
7 With cell-attached recording
bath application of 10 nm ET-1 evoked cation channel cur
8 In Purkinje cells,
bath application of 10, 20 or 100 microM MeHg initially
9 In Purkinje cells,
bath application of 10, 20 or 100 mM MeHg initially incr
10 asynaptic NMDAR-mediated currents induced by
bath application of 100 microM NMDA/10 microM glycine wi
11 In amphotericin whole-cell recordings,
bath application of 2,4-dinitrophenol (DNP, an uncoupler
12 Finally, we demonstrate that both
bath application of 2-arachidonoylglycerol(2-AG) and dep
13 By contrast,
bath application of (
2-aminoethyl)methanethiosulfonate (
14 Bath application of 20 microM betaxolol reduced the glut
15 e-cell currents were elicited in response to
bath application of 20 microM NMDA and 50 microM glycine
16 dependent and Ca2+-independent components by
bath application of 200 microM Cd2+, which blocked Ca2+
17 We report that
bath application of 3 mum carbachol (CCh), a muscarinic
18 creased in both TMT and H(2)O mice following
bath application of 300 nM CRF, but only H(2)O mice incr
19 under a similar experimental condition (ie,
bath application of 4-aminopyridine), the initiation of
20 Bath application of 4-ethylphenylamino-1,2-dimethyl-6-me
21 the cytosolic tyrosine kinase pp60c-src, and
bath application of 5 microM insulin, which activates re
22 Bath application of 5 nm nicotine increased the excitabi
23 Bath application of 5-CT inhibits synaptic strength, rel
24 Bath application of 5-HT and injection of 8-OH-DPAT [(+/
25 A single pairing of tetanus in one SN with
bath application of 5-HT evoked long-term (24 hr) increa
26 Bath application of 5-HT(4)R agonists did not affect mot
27 ng of tetanus in the sensory neuron (SN) and
bath application of 5-HT.
28 Bath-application of 5-HT (0.05 mM) caused a significant
29 Bath application of 50 microM (1S,3R)-1-aminocyclopentan
30 Nevertheless,
bath application of 50 microM 4-aminopyridine (4-AP) or
31 cute (15 min) stimulation of OB neurons with
bath application of 50 ng ml(-1) brain-derived neurotrop
32 Bath application of 50-300 nM kainate to an in vitro pre
33 In vitro
bath application of 60 mM ethanol inhibited STP by 35% a
34 Bath application of 7beta-deacetyl-7beta-[gamma-(morphol
35 Bath application of 8-Br-cAMP decreased I(Cl(swell)) by
36 ed by decreased conductances, in response to
bath application of 8-bromo-cAMP but not the membrane-im
37 stimulation-evoked dopamine release and that
bath application of a KOR antagonist provides full rescu
38 ell soma hyperpolarized the interneuron, and
bath application of a lower dose of serotonin (0.1 micro
39 Correspondingly, in vitro
bath application of a mu opioid receptor agonist suppres
40 Bath application of a positive SK channel modulator (1-E
41 es in sIPSCs induced by Ca(2+) uncaging, and
bath application of a selective GluR5-containing recepto
42 P3+ neurons show direct hyperpolarization to
bath application of a selective RXFP3 agonist, RXFP3-A2,
43 amic input synapses to the LA is impaired by
bath application of a specific mGluR5 antagonist, 2-meth
44 ns of external chloride concentration and to
bath application of a stilbene derivative, 4-acetamido-4
45 electrical activity typically observed after
bath application of a stimulatory concentration of gluco
46 n was found to be membrane-delimited because
bath application of ACh did not inhibit GIRK channel act
47 Bath application of actinomycin D, an irreversible RNA s
48 In membrane excitability experiments,
bath application of adenosine and CPA reversibly inhibit
49 Bath application of adenosine or RPIA reversibly inhibit
50 t-hearing onset (P18-20) MNTB neurons during
bath application of agonists and antagonists of nicotini
51 Using extracellular recordings and
bath application of agonists and antagonists, we compare
52 Bath application of alcohol reduced evoked firing in neu
53 Bath application of AMPA also activated astrocytes.
54 E enhances the respiratory motor response to
bath application of AMPA to the brainstem, although it w
55 Bath application of an antisensorin antibody during the
56 Cx36-/- RGCs were significantly inhibited by
bath application of an ionotropic glutamate receptor ant
57 with a postsynaptic Ca2+ chelator but not by
bath application of an NMDA receptor antagonist.
58 evoked inward currents that were blocked by
bath application of an NMDAR antagonist (dl-APV), indica
59 Bath application of anti-TRPC3 and anti-TRPC7 antibodies
60 Bath application of anti-TRPC3 antibodies markedly reduc
61 Bath application of anti-TRPC6 and anti-TRPC1 antibodies
62 Bath application of antibodies to G(alphaq)/G(alpha11) e
63 Typically, multiplex platforms necessitate
bath application of antibody cocktails, increasing proba
64 litude, and decay kinetics were unaltered by
bath application of apamin, suggesting that SK channel b
65 f spontaneous action potentials with a brief
bath application of aziPm that becomes irreversible on p
66 Bath application of Ba(2+) significantly reduced the A-t
67 Bath application of BDNF induced extensive formation of
68 Bath application of bicuculline (a GABA(A) receptor anta
69 alcium chelators in the pipette solution, or
bath application of bicuculline, EPSC enhancement is blo
70 n the bulk of this inhibition was blocked by
bath application of bicuculline, the incidence of platea
71 Furthermore, following
bath application of BK channel blockers for 10 min, etha
72 onized ventral root bursts generated by both
bath application of blockers of inhibitory neurotransmit
73 is effect can be blocked by the simultaneous
bath application of BN 52021 and trans-BTD, PAF receptor
74 % (23 of 35) of OVLT neurons were excited by
bath application of both hypertonic NaCl and AngII.
75 In contrast, the response to
bath application of bradykinin (1 microm, 3 ml) was not
76 Wiwatpanit et al. (2012) showed that
bath application of C-type allatostatin produced either
77 (20 mM BAPTA, without added Ca2+), or by the
bath application of cadmium (100 microM) to block voltag
78 Bath application of cadmium to reduce calcium influx als
79 mbrane-permeant analogue of BAPTA) or by the
bath application of cadmium.
80 ches in the cell-attached configuration, the
bath application of capsaicin evoked single-channel curr
81 to noxious ramp distention of the bowel and
bath application of capsaicin following TNFalpha pre-tre
82 Bath application of capsaicin slowed respiratory motor o
83 tent in vitro gamma oscillations, induced by
bath application of carbachol and kainate (amongst other
84 Bath application of carbachol could overcome the block o
85 cal activation of cholinergic receptors with
bath application of carbachol increased the firing rate
86 cked muscarinic cation currents activated by
bath application of carbachol or intracellular infusion
87 esynaptic potassium channels were blocked by
bath application of channel toxins, and the effect of ka
88 Bath application of CHZ successfully restored the precis
89 Bath application of compound T-588, a neuroprotective ag
90 Furthermore, these findings demonstrate that
bath application of contractile agonists to gastrointest
91 Bath application of corticosterone (100 nm) to prefronta
92 When NMDA receptors were blocked by
bath application of D-2-amino-5-phosphonovaleric acid, L
93 Bath application of DA (0.05-30 microM) produced a rever
94 Bath application of DA had no detectable effect on odora
95 Bath application of DA, 5HT, or Oct enhanced cycle frequ
96 h-clamp experiments from hippocampal slices,
bath application of DHPG induced a depression of synapti
97 Bath application of dioctanoylglycerol (diC8), a diacylg
98 Bath application of dithiothreitol or TPEN (N,N,N',N'-te
99 Bath application of dopamine increased the frequency of
100 Bath application of dopamine or the dopamine D1 agonist
101 Bath application of dopamine significantly enhanced EPSC
102 The evidence implicating PKA has come from
bath application of drugs during LTP induction, an appro
103 Bath application of dynamin inhibitors or anticonvulsant
104 After
bath application of either an excitatory amino acid (AP-
105 Bath application of either BK channel blockers significa
106 Bath application of either the TRPV4 channel blocker HC0
107 Bath application of emetine, a protein synthesis inhibit
108 p recordings from GPe neurons and found that
bath application of ethanol dose-dependently decreased t
109 Bath application of ethanol enhanced the amplitude of mI
110 Bath application of flufenamic acid, Gd3+, La3+ and Ca2+
111 or (H-89), and is mimicked (and occluded) by
bath application of forskolin.
112 Bath application of GABA first decreased the amplitude o
113 Bath application of GABA or muscimol caused an early hyp
114 X), postsynaptic Ca2+ rises triggered by the
bath application of GABA were only moderately depressed
115 Bath application of GABA(A) receptor agonists muscimol (
116 ained and the preparation still responded to
bath applications of GABA.
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 Bath application of GV-58 alone or in combination with 3
122 arized to near the dark resting potential by
bath application of high K(+) solutions.
123 T1 MF-2 smooth muscle cells responded to the
bath application of histamine or ATP with an increase in
124 Moreover, a
bath application of histamine to acute brain slices inhi
125 Bath application of human PACAP-38 also rescued the curr
126 Bath application of IL-1beta or TNF-alpha led to the rel
127 Pipette or
bath application of insulin evoked a rapid increase in h
128 With cell-attached patch recording,
bath application of isoprenaline produced a pronounced i
129 Bath application of isoproterenol (1 muM), a beta-adrene
130 In contrast,
bath application of K252a prevented the enhancement of s
131 We found that
bath application of kainate (3 microm) profoundly reduce
132 hysiology in hypothalamic slices showed that
bath application of kisspeptin did not affect action pot
133 amic input synapses to the LA is impaired by
bath application of KN-62 in vitro.
134 The effects of l-arginine were blocked by
bath application of l-NAME (20mM).
135 Bath application of lavendustin A, a PTK inhibitor that
136 In cell-attached patches,
bath application of low concentrations of Ang II (1 nM)
137 Bath application of low concentrations of GBZ (25-200 nM
138 gamma-Motoneurons were excited by
bath application of low concentrations of ouabain that s
139 Bath application of metronidazole (Mtz) to fish expressi
140 Bath application of morphine (1 microM) almost completel
141 Bath application of MT-II or alpha-MSH significantly red
142 We found that
bath application of muscarine caused a direct depolariza
143 ls coexpressed with muscarinic M1 receptors,
bath application of muscarinic agonist reduced the maxim
144 ar neurons were less strongly depolarized by
bath application of muscarinic agonists, and uniformly l
145 ACh-induced reduction was also diminished by
bath application of muscimol at the low concentrations t
146 Brief
bath application of N-methyl-D-aspartate (NMDA) to hippo
147 Bath application of NE to the slices resulted in signifi
148 slice preparation can be compensated for by
bath application of neurochemicals known to accelerate t
149 With 250 and 500 nM [Ca2+]i
bath application of NFA (100 microM) increased inward cu
150 Bath application of nicotine during LFS accelerated DP,
151 Bath application of nicotine induced inward currents in
152 Bath application of nicotinic acetylcholine, AMPA, NMDA,
153 external Ca2+, and significantly reduced by
bath application of nifedipine or omega-conotoxin.
154 t was inhibited by intracellular BAPTA or by
bath application of niflumic acid (100 microM), a Ca(2+)
155 rtially inhibited ERK2 activation induced by
bath application of NMDA and strongly suppressed ERK2 ac
156 tion of synaptic and extrasynaptic NMDARs by
bath application of NMDA causes the loss of surface GABA
157 Bath application of NMDA evoked a slow inward current in
158 ation at T840 in the hippocampal CA1 region,
bath application of NMDA induced a strong, protein phosp
159 Bath application of NMDA potently unclustered and dephos
160 Bath application of NMDA produced EPSPs, membrane depola
161 aptic potentiation was produced with a brief
bath application of NMDA to rat hippocampal slices.
162 te (NMDA) subtype of glutamate receptor, and
bath application of NMDA was sufficient to activate PKA.
163 Bath application of NMDA, AMPA, and the D1 agonist SKF38
164 amatergic hair cell transmission by combined
bath-application of NMDA (7-chloro-kynurenic acid) and A
165 naptic phenotype of chordin null slices, but
bath application of Noggin, another antagonist of BMP si
166 reversal potential to the current evoked by
bath application of noradrenaline (100 microM).
167 Moreover,
bath application of noradrenaline (NA) significantly dep
168 With cell-attached recording,
bath application of noradrenaline, 1-oleoyl-acetyl-sn-gl
169 Bath application of octopamine, 5-HT, and dopamine at co
170 Bath application of orexin-A or orexin-B (30-300 nM) pro
171 Bath application of OXT and an OXTR specific ligand (TGO
172 Bath application of oxytocin (1 and 10 microM) inhibited
173 Extracellular
bath applications of Pb(2+) significantly reduced curren
174 With inside-out patches,
bath application of PDBu evoked channel currents with si
175 Icat activated by OAG after
bath application of PDBu was not significantly different
176 Bath application of pentylenetetrazole (PTZ) or glutamat
177 Bath application of pituitary adenylate cyclase activati
178 Although
bath application of PKA inhibitor drugs (KT5720, Rp-8CPT
179 Moreover
bath application of PKA inhibitors, H-89, KT5720 and an
180 itation of the pyloric rhythm is mimicked by
bath application of proctolin, its peptide transmitter.
181 nce of striatal LTD, however, was blocked by
bath application of protein translation inhibitors but n
182 of the ryanodine receptor-gated Ca2+ pool by
bath application of ryanodine (10 microM) also blocked t
183 ffusion of BAPTA or heparin into neurones or
bath application of ryanodine suppressed bursting.
184 Bath application of saturating concentrations of proctol
185 n formation away from the Sema3A source, and
bath application of Sema3A to polarized neurons promoted
186 In contrast,
bath application of sensorin accelerated the increase in
187 We found that tetanic stimuli coupled to
bath application of serotonin induced long-term depressi
188 Bath-application of serotonin (30 microm) significantly
189 Despite this,
bath application of SIRPalpha's ectodomain increases inh
190 Bath application of SNAP (2mM) or l-arginine (50mM) elic
191 Respiratory rhythm could be restored by
bath application of SP or glutamate transporter blockers
192 Bath application of SR 31742A produced a biphasic effect
193 Bath application of Sub P to brainstem slices for a peri
194 Bath application of substance P (SP; 0.1 to 10 microM) t
195 Bath application of T1E3, an anti-TRPC1 antibody raised
196 Exocytotic frequency evoked by
bath application of tetraethylammonium (1-10 mM) was sig
197 Likewise,
bath application of tetrodotoxin (TTX) reduced the SNR a
198 In addition,
bath application of thapsigargin and ryanodine, and intr
199 Bath application of the 1,2-diacyl-sn-glycerol (DAG) ana
200 In control slices,
bath application of the alpha(1)-agonist phenylephrine (
201 Bath application of the alpha-amino-3-hydroxy-5-methyl-4
202 Bath application of the AMPA receptor antagonist 1-(4-am
203 Bath application of the AMPA receptor antagonist beta-cy
204 In the outer retina,
bath application of the AMPA/KA receptor antagonists 6,7
205 Bath application of the bombesin-like neuropeptides gast
206 Bath application of the Ca(2+) channel antagonist CdCl(2
207 Bath application of the CB1 receptor agonist, WIN 55212-
208 Bath application of the cell-permeant Ca2+ chelator, BAP
209 on-dependent excitability increases, whereas
bath application of the D2 receptor agonist quinpirole i
210 Bath application of the diacylglycerol analogue 1-oleoyl
211 Bath application of the diacylycerol (DAG) analogue 1-oe
212 tes and neurons significantly increase after
bath application of the excitatory amino acid transporte
213 of single spiking activity was unaffected by
bath application of the GABA(A) antagonist picrotoxin (5
214 Bath application of the GABA(A) receptor agonist muscimo
215 Bath application of the GABAA receptor antagonist bicucu
216 er, the complex EPSC was greatly enhanced by
bath application of the GABAA receptor antagonists picro
217 Intriguingly, however, we found that
bath application of the GAT-1 transport blocker NO-711 (
218 Bath application of the kappa opioid receptor agonist U6
219 to induce long-term depression (LTD) during
bath application of the L-channel antagonist nifedipine
220 -cell voltage-clamp recordings revealed that
bath application of the ligand for MrgD, beta-alanine, r
221 Bath application of the MEK1/2 inhibitor U0126 did not a
222 After
bath application of the membrane-permeable cAMP analog a
223 Bath application of the membrane-permeable cAMP analogs
224 Bath application of the membrane-permeable cGMP analogs
225 (L+M)-OFF response in SBCs was eliminated by
bath application of the metabotropic glutamate receptor
226 Bath application of the mixed D1/D5R agonist SKF82958 un
227 Moreover, POA neurons responded to
bath application of the mu-opioid receptor agonist DAMGO
228 Bath application of the N-methyl-D-aspartate (NMDA) rece
229 Bath application of the Na+ channel blocker TTX eliminat
230 The effects of
bath application of the nitric oxide (NO) precursor L-ar
231 Bath application of the NMDA receptor antagonist 3-[2-ca
232 t PF to Purkinje cell synapses is blocked by
bath application of the NMDA receptor antagonist D-2-ami
233 acid (TBOA) and significantly decrease after
bath application of the NMDA receptor antagonist DL-2-am
234 timulation, an effect that was reversed with
bath application of the NMDA receptor partial agonist D-
235 Bath application of the NO donor NOC-18 increased the si
236 Bath application of the NO donor, S-nitroso-N-acetyl-pen
237 Bath application of the nonselective mGluR antagonist, (
238 Bath application of the octopaminergic drugs phentolamin
239 y augmenting projection neuron influence via
bath application of the peptide cotransmitter Cancer bor
240 Similarly,
bath application of the phospholipase C (PLC) inhibitor
241 dialysis of the catalytic subunit of PKA or
bath application of the PKA activator Sp-cAMP significan
242 Bath application of the PKA inhibitor H89 suppressed the
243 In contrast,
bath application of the PKC activator, (-) indolactam V
244 Bath application of the protein kinase C inhibitor chele
245 Bath application of the protein synthesis inhibitor emet
246 Furthermore,
bath application of the reducing agent dithiothreitol in
247 was due in part to an altered redox state as
bath application of the reducing agent, dithiothreitol,
248 Bath application of the selective beta1-adrenoceptor ago
249 Bath application of the selective beta2-adrenoceptor ago
250 agnitude of synaptic suppression elicited by
bath application of the selective CP-AMPAR antagonist na
251 Both Src actions were mostly reversed by
bath application of the Src inhibitors erbstatin (20 mic
252 Bath application of the TRPV1 antagonist capsazepine (10
253 ll dialysis, and was inhibited reversibly by
bath application of the VIP receptor-binding inhibitor L
254 ons of the Ca(2+) chelator BAPTA (20 mm), or
bath applications of the L-type Ca(2+) channel blocker n
255 The effects of
bath applications of the nitric oxide (NO) donors sodium
256 Bath application of thiopental lowered the frequency of
257 nd alpha2-adrenergic receptors (activated by
bath application of transmitters) produced a three- to f
258 tro electrophysiological studies showed that
bath application of TRH caused concentration-dependent m
259 o receptor-mediated GIRK channel inhibition,
bath application of TRH decreased GIRK channel activity
260 Bath application of TRH resulted in a transient cessatio
261 Finally, we show that
bath application of U0126 impairs long-term potentiation
262 Bath application of Val(1)-SIFamide, a peptide whose exp
263 Bath application of various NO donors or CO-containing s
264 Bath application of WAY-100135 raised the ICMS current i
265 Mimicking Zn(2+) release by
bath application of Zn(2+) (50-100 microm) without HFS i