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