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