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1 ially inactivated during a slow up-ramp to a plateau potential.
2 lar firing and was incapable of generating a plateau potential.
3 ca with different propensities to generate a plateau potential.
4 y probenecid promoted the sADP to generate a plateau potential.
5 cation conductance ((CaN)) in generating the plateau potential.
6 ated depolarizing pulses summed to promote a plateau potential.
7 ation current (ICAN) capable of generating a plateau potential.
8 persists after the collapse of the dendritic plateau potential.
9 ight temporal correlation with the dendritic plateau potential.
10  time-locked with the regenerative dendritic plateau potential.
11 R), and no neurons were found that displayed plateau potentials.
12 Both Na(+) and Ca(2+) currents contribute to plateau potentials.
13 nts that predicted the features of simulated plateau potentials.
14 to drive place field formation via dendritic plateau potentials.
15 isinhibition and the production of dendritic plateau potentials.
16 ng neurons and neurons capable of generating plateau potentials.
17 ock of cognitive integration, basal dendrite plateau potentials.
18 ynaptic learning rule dependent on dendritic plateau potentials.
19 iven N-methyl-D-aspartate receptor-dependent plateau potentials.
20 aptic inputs for the generation of dendritic plateau potentials.
21 ursting, mixed mode oscillations, and pseudo-plateau potentials.
22 (CaN) by flufenamate abolished both sADP and plateau potentials.
23 urst firing to boost NMDA currents and allow plateau potentials.
24  by OT stimulation lead to the activation of plateau potentials.
25 ing, high-amplitude depolarizations known as plateau potentials.
26 uration, and spatial compartmentalization of plateau potentials.
27 ion (DDSC) associated with Ca(2+) influx and plateau potentials 10-100 s after BTSP induction.
28 y rescues electrically-evoked basal dendrite plateau potentials after a lifetime of NMDAR compromise.
29                                              Plateau potentials after the antidromic spikes or local
30 l glutamatergic network, which together with plateau potentials, allow amplification of hyperdirect c
31 ure, WT CA1 neurons developed a spike-evoked plateau potential and an increased spike-evoked dendriti
32 t I(to1) plays a crucial role in setting the plateau potential and overall APD, supporting a causativ
33 cally altered, with a significantly elevated plateau potential and prolonged AP duration.
34 63 is required for B50 to elicit the B31/B32 plateau potential and the motor program.
35 Two of these neurons, B51 and B64, generated plateau potentials and a third neuron, B8, exhibited reg
36 partate receptor (NMDAR)-dependent dendritic plateau potentials and accompanying complex spikes at th
37 rofoundly reducing extra spikes, eliminating plateau potentials and allowing temporally stationary, s
38 ough Na(V)1.4 channels is the key trigger of plateau potentials and current through Ca(V)1.1 Ca(2+) c
39 ium channel mediated regulation of dendritic plateau potentials and dendritic excitability underlies
40  with ranolazine prevents the development of plateau potentials and eliminates transient weakness in
41 cantly prolonged the duration of evoked Ca2+ plateau potentials and increased the whole-cell I(Ca) in
42     Additionally, we show that generation of plateau potentials and LTP induction in dorsal CA1 neuro
43 polarizing current steps led to long-lasting plateau potentials and persistent firing (PF), and in tu
44                                  Conversely, plateau potentials and self-sustained discharges are ver
45 ated by 5-HT and NA synapses and have robust plateau potentials and self-sustained discharges.
46 uted distant to the channels responsible for plateau potentials and self-sustained discharges.
47 inal motoneurons is essential for generating plateau potentials and self-sustained discharges.
48 ting conductance and threshold for eliciting plateau potentials and thus increased the occurrences of
49 arized voltage range of the action potential plateau potential, and prolonged action potential durati
50 uency, restitution properties, diastolic and plateau potentials, and drug binding rate constants.
51 iable, contained long-duration supratheshold plateau potentials, and high spike probability, suggesti
52 ge imaging modalities were APs combined with plateau potentials (AP-Plateaus), resembling dendritic C
53 ond the tested values.SIGNIFICANCE STATEMENT Plateau potentials are intrinsic properties of neurons t
54               These data suggest that nigral plateau potentials are mediated by a calcium-activated n
55 ation, distal tuft dendrites readily express plateau potentials as well as local place fields that ar
56                 It is triggered by dendritic plateau potentials associated with somatic burst firing,
57 switched from phasic to continuous firing as plateau potentials became non-inactivating.
58                   The soma was driven into a plateau potential by each of these inputs, during which
59  4-aminopyridine, increased the amplitude of plateau potentials by allowing them to recruit neighbori
60 , calcium transients outlast local dendritic plateau potentials by severalfold.
61                                              Plateau potentials can be elicited in nigral GABAergic n
62  not in Grin1-deficient mice, we ask whether plateau potentials can be restored by an adult intervent
63 g of glutamate and GABA, we demonstrate that plateau potentials can broaden the spatiotemporal window
64 ut triggered in many cases a long excitatory plateau potential capable of triggering repetitive actio
65                                        These plateau potentials coexist in single subthalamic neurons
66                             The incidence of plateau potentials decreased to 39% of neurons by P10-P1
67 ately mirrors the glutamate-evoked dendritic plateau potential (dendritic UP state).
68            This subtle inhibitory control of plateau potential depends on the location and kinetics o
69 nhibiting persistent Na(+) (I (NaP)) blocked plateau potentials, empirically and in simulations.
70 hich higher-order thalamocortically mediated plateau potentials facilitate the fusion of normally seg
71 c of nigral dopamine cells, are converted to plateau potentials following application of apamin, a po
72 ifedipine, in a concentration known to block plateau potential generation, also affects bursting acti
73 e antagonist of L-type Ca2+ channels, blocks plateau potential generation; however, its effects on fi
74 icity driven by dendritic calcium spikes, or plateau potentials, has been reported to underlie place
75 muscarinic agonist oxotremorine restores the plateau potential in B31/B32 and eliminates the necessit
76        Together, our analysis shows that the plateau potential in B31/B32 is not endogenous but condi
77 e blocks the B50-elicited motor program, the plateau potential in B31/B32, and, notably, a slow compo
78 ensity of I(to1) progressively depressed the plateau potential in Kv4.3-infected guinea pig myocytes
79 intrinsic membrane conductance mediating the plateau potential in lateral septal neurons, possibly as
80       Epileptiform bursts with an underlying plateau potential in neurons are a cellular correlate of
81                          The I(CAN)-mediated plateau potential in nigral GABAergic neurons likely aff
82 se in input efficacy, all induced by a large plateau potential in the distal dendrites of CA1 pyramid
83 o reduced the duration and amplitude of Ca2+ plateau potentials in both saline- and cocaine-withdrawn
84                          We demonstrate that plateau potentials in CA1 pyramidal neurons rapidly stre
85  pathways results in the generation of large plateau potentials in distal dendrites of CA1 pyramidal
86 olarization, persistent firing, or prolonged plateau potentials in interneurons and evokes sustained
87 gh activity-dependent feedback inhibition of plateau potentials in magnocellular neurosecretory cells
88 tes phasic bursts by autocrine inhibition of plateau potentials in magnocellular neurosecretory cells
89 interacts with both the graded expression of plateau potentials in motor neurons to generate spasms,
90  molecular layer that generate long-duration plateau potentials in response to excitatory synaptic in
91 ventral CA1 dendrites, however, can generate plateau potentials in response to temporally dispersed e
92 nd nickel all abolished both stimulus-evoked plateau potentials in SGCs and synaptic barrages in down
93 inputs at the distal dendrites could trigger plateau potentials in SPNs.
94 ged glutamate triggered abnormally prolonged plateau potentials in the deafferented neurons when stro
95                       Here, we report silent plateau potentials in these cells.
96 equired for eliciting prolactin-evoked tonic plateau potentials in these neurons that are part of a r
97 ted Ca(2+) channels with Ni(+) prolonged the plateau potential, indicating I (KCa) is important for p
98    When evoked near an existing place field, plateau potentials induced less synaptic potentiation an
99 tive population code, upstream of CA1, while plateau-potential-induced synaptic plasticity in CA1 ena
100                                 However, how plateau potentials interact with subsequent excitatory a
101 pecial class of regenerative events known as plateau potentials introduces the possibility of digital
102          Emerging evidence suggests that the plateau potential is mediated by neuronal canonical tran
103 ce associated with preceding activation of a plateau potential is referred to as 'warm up'.
104                 Furthermore, activation of a plateau potential is thought to manifest itself as a dec
105            This phenomenon, referred to as a plateau potential, is due to the activation of monoamine
106  achieved in the action potential and sets a plateau potential limiting the voltage-dependent activat
107          This behavior is driven by myogenic plateau potentials, long-lasting depolarizations of the
108                The EABs poised below current plateau potential (<=-0.3V) exhibited slower growth but
109 ere we report the presence of a postsynaptic plateau potential mediated by L-type Ca2+ channels using
110 led buccal network neurons and by triggering plateau potential-mediated bursts in B63, can initiate m
111 kers nimodipine and nifedipine abolished the plateau potential observed under control conditions but
112 644 or activation of NMDA receptors enhanced plateau potentials observed under control conditions and
113                                              Plateau potentials observed under control conditions as
114  optically driven spike trains can result in plateau potentials of 10 mV or more, causing incidental
115 recordings reveal transient depolarizations (plateau potentials) of the membrane potential to -25 to
116 ence of its frequency and by the presence of plateau potentials on the falling phase of low threshold
117                              Prolongation of plateau potentials or block of Kv4.2 channels at branch
118 plifying synaptic currents without incurring plateau potentials or self-sustained discharges.
119                              These dendritic plateau potentials produce widespread Ca2+ influx, large
120 ld presynaptic activity and calcium (Ca(2+)) plateau potentials produced a large potentiation with an
121 iated by a fraction of interneurons in which plateau potentials produced large and widespread calcium
122 ity of a CA3PC subtype to generate sustained plateau potentials, providing a state-dependent dendriti
123                                 Blocking the plateau potentials restores the archetypical organizatio
124                 Accordingly, activation of a plateau potential should result in a decrease in the exc
125 s and in particular, the ability to generate plateau potentials, similar to that of STN neurons witho
126                           Characterized by a plateau potential sustained for tens of milliseconds, th
127 tential, indicating I (KCa) is important for plateau potential termination.
128 y distinct in its preferential access to the plateau potential that represents the committed step tow
129   Here we report that the large depolarizing plateau potential that underlies the epileptiform burst
130 ger spike trains, summing IPSPs decayed to a plateau potential that was relatively independent of fir
131 rs voltage-dependent Ca(2+) channel-mediated plateau potentials that are confined to the stimulated d
132 ursts, action potentials are superimposed on plateau potentials that are generated by summation of de
133 neurons, correlated inputs trigger dendritic plateau potentials that drive neuronal plasticity and fi
134 Stronger electrical stimulation evoked small plateau potentials that had significant longer-lasting l
135  suggest astrocytes as a source of dendritic plateau potentials that have been implicated in localize
136 al calcium signals are produced by dendritic plateau potentials that require both vibrissal sensory i
137 However, some neurons exhibit all-or-nothing plateau potentials that, once elicited, can lead to prol
138 reveal characteristic electrical transients (plateau potentials) that trigger and shape dendritic cal
139 endrites rarely express local peri-formation plateau potentials, the timing and extent of their recru
140  receptor activation triggering long-lasting plateau potentials thought to be mediated by both T-type
141 ges that depend on the temporal proximity of plateau potentials to pre-existing place fields.
142 itude of spontaneously occurring depolarized plateau potentials (up events).
143  The circuit autonomously generates rhythmic plateau potentials via IP(3)-mediated Ca(2+) release fro
144                                          The plateau potential was abolished in calcium-free buffer,
145 f VGKCs in regulating the generation of Ca2+ plateau potential was also studied in mPFC neurons.
146 (AP) bursts induced by dendritic Ca(2+)/NMDA plateau potentials, was recently proposed as the main ce
147            These results suggest either that plateau potentials were not engaged (or were rapidly ext
148                 For phrenic motoneurones, no plateau potentials were observed in either state (except
149                  In expiratory motoneurones, plateau potentials were observed in the decerebrates, bu
150 In approximately one-third of these neurons, plateau potentials were observed under control condition
151                      We found that dendritic plateau potentials were produced by an interaction betwe
152                                              Plateau potentials were readily evoked in non-phrenic ce
153     Pharmacological approachesindicated that plateau potentials were triggered by Ca(2+) influx throu
154 ls thus underlie repolarization of dendritic plateau potentials, whereas Kv4.2 channels confine these
155  stunned myocytes demonstrated a decrease in plateau potential without a change in resting membrane p
156 acellular Ca(2+) abolished both sADP and the plateau potential without affecting Ca(2+) spikes.
157 nd BAPTA dialysis, increased the duration of plateau potentials without affecting their amplitude or

 
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