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 (2R,6R)-HNK
bath application caused a rapid and persistent potentiat
8 o had a more rapid effect: within minutes of
bath application,
E2 acutely increased synaptic strength
9 In slices with sprouting, BDNF
bath application enhanced responses recorded in the inne
10 synaptic transmission, and responses to CRF
bath application in (td)Tomato(+) neurons are similar to
11 izes changes in pCREB levels induced by NMDA
bath application in rat cortical neurons.
12 By contrast,
bath application of (2-aminoethyl)methanethiosulfonate (
13 muscle cells was significantly increased by
bath application of 0.5 microM isoproterenol (isoprenali
14 Bath application of 1 microM GABA increased tonic curren
15 ter excision of an isolated inside-out patch
bath application of 1 mum Ins(1,4,5)P3 increased open ch
16 Bath application of 1-10 micrometer serotonin (5HT), a m
17 Bath application of 1-50 microM troglitazone depolarised
18 Bath application of 10 microM neostigmine, a potent acet
19 With cell-attached recording
bath application of 10 nm ET-1 evoked cation channel cur
20 In Purkinje cells,
bath application of 10, 20 or 100 microM MeHg initially
21 In Purkinje cells,
bath application of 10, 20 or 100 mM MeHg initially incr
22 asynaptic NMDAR-mediated currents induced by
bath application of 100 microM NMDA/10 microM glycine wi
23 In amphotericin whole-cell recordings,
bath application of 2,4-dinitrophenol (DNP, an uncoupler
24 Finally, we demonstrate that both
bath application of 2-arachidonoylglycerol(2-AG) and dep
25 Bath application of 20 microM betaxolol reduced the glut
26 e-cell currents were elicited in response to
bath application of 20 microM NMDA and 50 microM glycine
27 dependent and Ca2+-independent components by
bath application of 200 microM Cd2+, which blocked Ca2+
28 We report that
bath application of 3 mum carbachol (CCh), a muscarinic
29 creased in both TMT and H(2)O mice following
bath application of 300 nM CRF, but only H(2)O mice incr
30 under a similar experimental condition (ie,
bath application of 4-aminopyridine), the initiation of
31 Bath application of 4-ethylphenylamino-1,2-dimethyl-6-me
32 the cytosolic tyrosine kinase pp60c-src, and
bath application of 5 microM insulin, which activates re
33 Bath application of 5 nm nicotine increased the excitabi
34 Bath application of 5-CT inhibits synaptic strength, rel
35 Bath application of 5-HT and injection of 8-OH-DPAT [(+/
36 A single pairing of tetanus in one SN with
bath application of 5-HT evoked long-term (24 hr) increa
37 Bath application of 5-HT(4)R agonists did not affect mot
38 ng of tetanus in the sensory neuron (SN) and
bath application of 5-HT.
39 Bath application of 50 microM (1S,3R)-1-aminocyclopentan
40 Nevertheless,
bath application of 50 microM 4-aminopyridine (4-AP) or
41 cute (15 min) stimulation of OB neurons with
bath application of 50 ng ml(-1) brain-derived neurotrop
42 Bath application of 50-300 nM kainate to an in vitro pre
43 In vitro
bath application of 60 mM ethanol inhibited STP by 35% a
44 Bath application of 7beta-deacetyl-7beta-[gamma-(morphol
45 Bath application of 8-Br-cAMP decreased I(Cl(swell)) by
46 ed by decreased conductances, in response to
bath application of 8-bromo-cAMP but not the membrane-im
47 stimulation-evoked dopamine release and that
bath application of a KOR antagonist provides full rescu
48 ell soma hyperpolarized the interneuron, and
bath application of a lower dose of serotonin (0.1 micro
49 Correspondingly, in vitro
bath application of a mu opioid receptor agonist suppres
50 Bath application of a positive SK channel modulator (1-E
51 es in sIPSCs induced by Ca(2+) uncaging, and
bath application of a selective GluR5-containing recepto
52 P3+ neurons show direct hyperpolarization to
bath application of a selective RXFP3 agonist, RXFP3-A2,
53 amic input synapses to the LA is impaired by
bath application of a specific mGluR5 antagonist, 2-meth
54 ns of external chloride concentration and to
bath application of a stilbene derivative, 4-acetamido-4
55 electrical activity typically observed after
bath application of a stimulatory concentration of gluco
56 n was found to be membrane-delimited because
bath application of ACh did not inhibit GIRK channel act
57 Bath application of actinomycin D, an irreversible RNA s
58 In membrane excitability experiments,
bath application of adenosine and CPA reversibly inhibit
59 Bath application of adenosine or RPIA reversibly inhibit
60 t-hearing onset (P18-20) MNTB neurons during
bath application of agonists and antagonists of nicotini
61 Using extracellular recordings and
bath application of agonists and antagonists, we compare
62 Bath application of alcohol reduced evoked firing in neu
63 Bath application of AMPA also activated astrocytes.
64 E enhances the respiratory motor response to
bath application of AMPA to the brainstem, although it w
65 Bath application of an antisensorin antibody during the
66 Cx36-/- RGCs were significantly inhibited by
bath application of an ionotropic glutamate receptor ant
67 with a postsynaptic Ca2+ chelator but not by
bath application of an NMDA receptor antagonist.
68 evoked inward currents that were blocked by
bath application of an NMDAR antagonist (dl-APV), indica
69 Bath application of anti-TRPC3 and anti-TRPC7 antibodies
70 Bath application of anti-TRPC3 antibodies markedly reduc
71 Bath application of anti-TRPC6 and anti-TRPC1 antibodies
72 Bath application of antibodies to G(alphaq)/G(alpha11) e
73 Typically, multiplex platforms necessitate
bath application of antibody cocktails, increasing proba
74 litude, and decay kinetics were unaltered by
bath application of apamin, suggesting that SK channel b
75 f spontaneous action potentials with a brief
bath application of aziPm that becomes irreversible on p
76 Bath application of Ba(2+) significantly reduced the A-t
77 Bath application of BDNF induced extensive formation of
78 Bath application of bicuculline (a GABA(A) receptor anta
79 alcium chelators in the pipette solution, or
bath application of bicuculline, EPSC enhancement is blo
80 n the bulk of this inhibition was blocked by
bath application of bicuculline, the incidence of platea
81 Furthermore, following
bath application of BK channel blockers for 10 min, etha
82 onized ventral root bursts generated by both
bath application of blockers of inhibitory neurotransmit
83 is effect can be blocked by the simultaneous
bath application of BN 52021 and trans-BTD, PAF receptor
84 % (23 of 35) of OVLT neurons were excited by
bath application of both hypertonic NaCl and AngII.
85 In contrast, the response to
bath application of bradykinin (1 microm, 3 ml) was not
86 Wiwatpanit et al. (2012) showed that
bath application of C-type allatostatin produced either
87 (20 mM BAPTA, without added Ca2+), or by the
bath application of cadmium (100 microM) to block voltag
88 Bath application of cadmium to reduce calcium influx als
89 mbrane-permeant analogue of BAPTA) or by the
bath application of cadmium.
90 ches in the cell-attached configuration, the
bath application of capsaicin evoked single-channel curr
91 to noxious ramp distention of the bowel and
bath application of capsaicin following TNFalpha pre-tre
92 Bath application of capsaicin slowed respiratory motor o
93 tent in vitro gamma oscillations, induced by
bath application of carbachol and kainate (amongst other
94 Bath application of carbachol could overcome the block o
95 cal activation of cholinergic receptors with
bath application of carbachol increased the firing rate
96 cked muscarinic cation currents activated by
bath application of carbachol or intracellular infusion
97 esynaptic potassium channels were blocked by
bath application of channel toxins, and the effect of ka
98 Bath application of CHZ successfully restored the precis
99 Bath application of compound T-588, a neuroprotective ag
100 Furthermore, these findings demonstrate that
bath application of contractile agonists to gastrointest
101 Bath application of corticosterone (100 nm) to prefronta
102 When NMDA receptors were blocked by
bath application of D-2-amino-5-phosphonovaleric acid, L
103 Bath application of DA (0.05-30 microM) produced a rever
104 Bath application of DA had no detectable effect on odora
105 Bath application of DA, 5HT, or Oct enhanced cycle frequ
106 h-clamp experiments from hippocampal slices,
bath application of DHPG induced a depression of synapti
107 Bath application of dioctanoylglycerol (diC8), a diacylg
108 Bath application of dithiothreitol or TPEN (N,N,N',N'-te
109 Bath application of dopamine increased the frequency of
110 Bath application of dopamine or the dopamine D1 agonist
111 Bath application of dopamine significantly enhanced EPSC
112 The evidence implicating PKA has come from
bath application of drugs during LTP induction, an appro
113 Bath application of dynamin inhibitors or anticonvulsant
114 After
bath application of either an excitatory amino acid (AP-
115 Bath application of either BK channel blockers significa
116 Bath application of either the TRPV4 channel blocker HC0
117 Bath application of emetine, a protein synthesis inhibit
118 p recordings from GPe neurons and found that
bath application of ethanol dose-dependently decreased t
119 Bath application of ethanol enhanced the amplitude of mI
120 Bath application of flufenamic acid, Gd3+, La3+ and Ca2+
121 or (H-89), and is mimicked (and occluded) by
bath application of forskolin.
122 Bath application of GABA first decreased the amplitude o
123 Bath application of GABA or muscimol caused an early hyp
124 X), postsynaptic Ca2+ rises triggered by the
bath application of GABA were only moderately depressed
125 Bath application of GABA(A) receptor agonists muscimol (
126 ular layer response was largely resistant to
bath application of GABAA receptor antagonists but was s
127 , and V of all retrohippocampal areas during
bath application of glutamate antagonists.
128 Importantly,
bath application of glutamate to SCN slices rapidly and
129 Although
bath application of GRP or NMB had little or no effect o
130 Bath application of GV-58 alone or in combination with 3
131 arized to near the dark resting potential by
bath application of high K(+) solutions.
132 T1 MF-2 smooth muscle cells responded to the
bath application of histamine or ATP with an increase in
133 Moreover, a
bath application of histamine to acute brain slices inhi
134 Bath application of human PACAP-38 also rescued the curr
135 Bath application of IL-1beta or TNF-alpha led to the rel
136 Pipette or
bath application of insulin evoked a rapid increase in h
137 With cell-attached patch recording,
bath application of isoprenaline produced a pronounced i
138 Bath application of isoproterenol (1 muM), a beta-adrene
139 In contrast,
bath application of K252a prevented the enhancement of s
140 We found that
bath application of kainate (3 microm) profoundly reduce
141 hysiology in hypothalamic slices showed that
bath application of kisspeptin did not affect action pot
142 amic input synapses to the LA is impaired by
bath application of KN-62 in vitro.
143 The effects of l-arginine were blocked by
bath application of l-NAME (20mM).
144 Bath application of lavendustin A, a PTK inhibitor that
145 In cell-attached patches,
bath application of low concentrations of Ang II (1 nM)
146 Bath application of low concentrations of GBZ (25-200 nM
147 gamma-Motoneurons were excited by
bath application of low concentrations of ouabain that s
148 Bath application of metronidazole (Mtz) to fish expressi
149 Bath application of morphine (1 microM) almost completel
150 Bath application of MT-II or alpha-MSH significantly red
151 We found that
bath application of muscarine caused a direct depolariza
152 ls coexpressed with muscarinic M1 receptors,
bath application of muscarinic agonist reduced the maxim
153 ar neurons were less strongly depolarized by
bath application of muscarinic agonists, and uniformly l
154 ACh-induced reduction was also diminished by
bath application of muscimol at the low concentrations t
155 Brief
bath application of N-methyl-D-aspartate (NMDA) to hippo
156 Bath application of NE to the slices resulted in signifi
157 slice preparation can be compensated for by
bath application of neurochemicals known to accelerate t
158 With 250 and 500 nM [Ca2+]i
bath application of NFA (100 microM) increased inward cu
159 Bath application of nicotine during LFS accelerated DP,
160 Bath application of nicotine induced inward currents in
161 Bath application of nicotinic acetylcholine, AMPA, NMDA,
162 external Ca2+, and significantly reduced by
bath application of nifedipine or omega-conotoxin.
163 t was inhibited by intracellular BAPTA or by
bath application of niflumic acid (100 microM), a Ca(2+)
164 rtially inhibited ERK2 activation induced by
bath application of NMDA and strongly suppressed ERK2 ac
165 tion of synaptic and extrasynaptic NMDARs by
bath application of NMDA causes the loss of surface GABA
166 Bath application of NMDA evoked a slow inward current in
167 ation at T840 in the hippocampal CA1 region,
bath application of NMDA induced a strong, protein phosp
168 Bath application of NMDA potently unclustered and dephos
169 Bath application of NMDA produced EPSPs, membrane depola
170 aptic potentiation was produced with a brief
bath application of NMDA to rat hippocampal slices.
171 te (NMDA) subtype of glutamate receptor, and
bath application of NMDA was sufficient to activate PKA.
172 Bath application of NMDA, AMPA, and the D1 agonist SKF38
173 naptic phenotype of chordin null slices, but
bath application of Noggin, another antagonist of BMP si
174 reversal potential to the current evoked by
bath application of noradrenaline (100 microM).
175 Moreover,
bath application of noradrenaline (NA) significantly dep
176 With cell-attached recording,
bath application of noradrenaline, 1-oleoyl-acetyl-sn-gl
177 Bath application of octopamine, 5-HT, and dopamine at co
178 Bath application of orexin-A or orexin-B (30-300 nM) pro
179 Bath application of OXT and an OXTR specific ligand (TGO
180 Bath application of oxytocin (1 and 10 microM) inhibited
181 With inside-out patches,
bath application of PDBu evoked channel currents with si
182 Icat activated by OAG after
bath application of PDBu was not significantly different
183 Bath application of pentylenetetrazole (PTZ) or glutamat
184 Bath application of pituitary adenylate cyclase activati
185 Although
bath application of PKA inhibitor drugs (KT5720, Rp-8CPT
186 Moreover
bath application of PKA inhibitors, H-89, KT5720 and an
187 itation of the pyloric rhythm is mimicked by
bath application of proctolin, its peptide transmitter.
188 nce of striatal LTD, however, was blocked by
bath application of protein translation inhibitors but n
189 of the ryanodine receptor-gated Ca2+ pool by
bath application of ryanodine (10 microM) also blocked t
190 ffusion of BAPTA or heparin into neurones or
bath application of ryanodine suppressed bursting.
191 Bath application of saturating concentrations of proctol
192 n formation away from the Sema3A source, and
bath application of Sema3A to polarized neurons promoted
193 In contrast,
bath application of sensorin accelerated the increase in
194 We found that tetanic stimuli coupled to
bath application of serotonin induced long-term depressi
195 Despite this,
bath application of SIRPalpha's ectodomain increases inh
196 Bath application of SNAP (2mM) or l-arginine (50mM) elic
197 Respiratory rhythm could be restored by
bath application of SP or glutamate transporter blockers
198 Bath application of SR 31742A produced a biphasic effect
199 Bath application of Sub P to brainstem slices for a peri
200 Bath application of substance P (SP; 0.1 to 10 microM) t
201 Bath application of T1E3, an anti-TRPC1 antibody raised
202 Exocytotic frequency evoked by
bath application of tetraethylammonium (1-10 mM) was sig
203 Likewise,
bath application of tetrodotoxin (TTX) reduced the SNR a
204 In addition,
bath application of thapsigargin and ryanodine, and intr
205 Bath application of the 1,2-diacyl-sn-glycerol (DAG) ana
206 In control slices,
bath application of the alpha(1)-agonist phenylephrine (
207 Bath application of the alpha-amino-3-hydroxy-5-methyl-4
208 Bath application of the AMPA receptor antagonist 1-(4-am
209 Bath application of the AMPA receptor antagonist beta-cy
210 In the outer retina,
bath application of the AMPA/KA receptor antagonists 6,7
211 Bath application of the bombesin-like neuropeptides gast
212 Bath application of the Ca(2+) channel antagonist CdCl(2
213 Bath application of the CB1 receptor agonist, WIN 55212-
214 Bath application of the cell-permeant Ca2+ chelator, BAP
215 on-dependent excitability increases, whereas
bath application of the D2 receptor agonist quinpirole i
216 Bath application of the diacylglycerol analogue 1-oleoyl
217 Bath application of the diacylycerol (DAG) analogue 1-oe
218 tes and neurons significantly increase after
bath application of the excitatory amino acid transporte
219 of single spiking activity was unaffected by
bath application of the GABA(A) antagonist picrotoxin (5
220 Bath application of the GABA(A) receptor agonist muscimo
221 Bath application of the GABAA receptor antagonist bicucu
222 er, the complex EPSC was greatly enhanced by
bath application of the GABAA receptor antagonists picro
223 Intriguingly, however, we found that
bath application of the GAT-1 transport blocker NO-711 (
224 Bath application of the kappa opioid receptor agonist U6
225 to induce long-term depression (LTD) during
bath application of the L-channel antagonist nifedipine
226 -cell voltage-clamp recordings revealed that
bath application of the ligand for MrgD, beta-alanine, r
227 Bath application of the MEK1/2 inhibitor U0126 did not a
228 After
bath application of the membrane-permeable cAMP analog a
229 Bath application of the membrane-permeable cAMP analogs
230 Bath application of the membrane-permeable cGMP analogs
231 (L+M)-OFF response in SBCs was eliminated by
bath application of the metabotropic glutamate receptor
232 Bath application of the mixed D1/D5R agonist SKF82958 un
233 Moreover, POA neurons responded to
bath application of the mu-opioid receptor agonist DAMGO
234 Bath application of the N-methyl-D-aspartate (NMDA) rece
235 Bath application of the Na+ channel blocker TTX eliminat
236 The effects of
bath application of the nitric oxide (NO) precursor L-ar
237 Bath application of the NMDA receptor antagonist 3-[2-ca
238 t PF to Purkinje cell synapses is blocked by
bath application of the NMDA receptor antagonist D-2-ami
239 acid (TBOA) and significantly decrease after
bath application of the NMDA receptor antagonist DL-2-am
240 timulation, an effect that was reversed with
bath application of the NMDA receptor partial agonist D-
241 Bath application of the NO donor NOC-18 increased the si
242 Bath application of the NO donor, S-nitroso-N-acetyl-pen
243 Bath application of the nonselective mGluR antagonist, (
244 Bath application of the octopaminergic drugs phentolamin
245 y augmenting projection neuron influence via
bath application of the peptide cotransmitter Cancer bor
246 Similarly,
bath application of the phospholipase C (PLC) inhibitor
247 dialysis of the catalytic subunit of PKA or
bath application of the PKA activator Sp-cAMP significan
248 Bath application of the PKA inhibitor H89 suppressed the
249 In contrast,
bath application of the PKC activator, (-) indolactam V
250 Bath application of the protein kinase C inhibitor chele
251 Bath application of the protein synthesis inhibitor emet
252 Furthermore,
bath application of the reducing agent dithiothreitol in
253 was due in part to an altered redox state as
bath application of the reducing agent, dithiothreitol,
254 Bath application of the selective beta1-adrenoceptor ago
255 Bath application of the selective beta2-adrenoceptor ago
256 agnitude of synaptic suppression elicited by
bath application of the selective CP-AMPAR antagonist na
257 Both Src actions were mostly reversed by
bath application of the Src inhibitors erbstatin (20 mic
258 Bath application of the TRPV1 antagonist capsazepine (10
259 ll dialysis, and was inhibited reversibly by
bath application of the VIP receptor-binding inhibitor L
260 Bath application of thiopental lowered the frequency of
261 nd alpha2-adrenergic receptors (activated by
bath application of transmitters) produced a three- to f
262 tro electrophysiological studies showed that
bath application of TRH caused concentration-dependent m
263 o receptor-mediated GIRK channel inhibition,
bath application of TRH decreased GIRK channel activity
264 Bath application of TRH resulted in a transient cessatio
265 Finally, we show that
bath application of U0126 impairs long-term potentiation
266 Bath application of Val(1)-SIFamide, a peptide whose exp
267 Bath application of various NO donors or CO-containing s
268 Bath application of WAY-100135 raised the ICMS current i
269 Mimicking Zn(2+) release by
bath application of Zn(2+) (50-100 microm) without HFS i
270 ained and the preparation still responded to
bath applications of GABA.
271 Extracellular
bath applications of Pb(2+) significantly reduced curren
272 ons of the Ca(2+) chelator BAPTA (20 mm), or
bath applications of the L-type Ca(2+) channel blocker n
273 The effects of
bath applications of the nitric oxide (NO) donors sodium
274 Bath-application of 5-HT (0.05 mM) caused a significant
275 amatergic hair cell transmission by combined
bath-application of NMDA (7-chloro-kynurenic acid) and A
276 Bath-application of serotonin (30 microm) significantly
277 on, blocking NMDA receptors (NMDARs) through
bath application or intracellular dialysis not only decr
278 Bath-application or local microinjections of glutamaterg
279 In addition, we found that CRF
bath application reduces synaptic drive in CRF1 CeA-LH c
280 he group-selective agonist LY354740 (300 nM,
bath application)
resulted in a reduction of these IPSCs
281 affer collateral-CA1 (SC-CA1) synapse during
bath-application to slices collected from mice, and 2) m
282 ment with the CRF-R1 antagonist CP154526 and
bath application with the CRF-R1 antagonist NBI27914 red