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1 pical TRN neurons that could produced strong burst discharge.
2 s contribute to production of high-frequency burst discharge.
3  deficiency, which contributed to arrhythmic burst discharge.
4 lack of methods for specific modification of burst discharge.
5 re well established electrogenic drivers for burst discharge.
6  decreased T-channel availability as well as burst discharges.
7 aptically mediated long-latency epileptiform burst discharges.
8 ) synchronous with the GABAergic interneuron burst discharges.
9 ) generate single, spontaneous, synchronized burst discharges, 2) support activity spread along axes
10 e cells generates repetitive, high-frequency burst discharges, a pattern referred to as "chattering."
11 tegrating synchronous inputs and presynaptic burst discharges, allowing hilar cells to respond over a
12 -voltage fast activity, evolve into rhythmic burst discharges and are followed by a period of suppres
13 tion of the depolarizing envelope underlying burst discharges and attenuated the subsequent afterhype
14 rity of neurons in the dorsal TRN (56%) lack burst discharge, and the remaining neurons (35%) show an
15 ude impaired and arrhythmic action potential burst discharge associated with a deficit in Nav1.6 Na(+
16 rget nuclei display synchronized oscillatory burst discharge at low frequencies, some of which correl
17     Although sensory nerves display rhythmic bursting discharges at theta frequencies during painful
18 rates that synaptically dependent excitatory burst discharges can be evoked from daPC neurons without
19 carotid body generates spontaneous, episodic burst discharges coincident with the onset of disordered
20 in ventral TRN (82%) display a stereotypical burst discharge consisting of a transient, high frequenc
21 onic depolarizations or repetitive, rhythmic burst discharges, either as clonic or spike-wave activit
22          We now report that a single somatic burst discharge evokes large-magnitude calcium responses
23 tion time of input signals and could exhibit bursting discharge.for loosely synchronized inputs, we f
24 ures might reflect a reduction in endogenous burst discharges from that side.
25      Synaptic transmission was optimized for burst discharge >14 Hz and showed considerable short-ter
26 from adult rats, is known to cause prolonged burst discharges (i.e. several seconds vs. tens of milli
27 erneurons, including tonic firing or initial bursting discharge, Ih currents, and islet cell morpholo
28 tion of decreased interictal single neuronal burst discharge in epileptogenic structures stresses the
29 reshold membrane oscillations and rhythmical burst discharge in Mes V neurons from rats ages postnata
30  tonic periods of REM sleep, with occasional burst discharge in phasic REM.
31 voltage-gated Na+ currents in modulating the burst discharge in sensory neurons.
32                A single stimulus could evoke burst discharges in infrapyramidal granule cells but not
33 PD-like locomotor deficits and increased STN burst discharges in normal rats.
34 te blockade of firing in principal cells and burst discharges in putative interneurons.
35 (2)-like receptors inhibit complex EPSCs and burst discharges in the SNR by acting within the STN to
36 microM) to the perfusate elicited repetitive burst discharges in the somatic motor outflow which were
37  channels, play a key role in the genesis of burst discharges in the subthalamic nucleus (STN) and pa
38                                 NMDA induced burst discharges in the sympathetic outflow.
39            We propose that the activation of burst discharges in these cell types is essential for th
40 nerves often display low-frequency, rhythmic bursting discharges in painful conditions.
41                The increased tendency of STN burst discharges may by itself serve as a direct cause o
42             The generation of high-frequency burst discharges may strongly influence the response of
43 amp recordings, SST preferentially inhibited burst discharges mediated by near-threshold corticothala
44 ogenous bursting could be due to the loss of burst discharging neurons as a product of seizure-relate
45                               This decreased burst discharge of nRt neurons during CCK application re
46                         Notably, oscillatory burst discharge of reticular neurons is typical for slee
47 BA(A)- and GABA(B)-receptor antagonists, the burst discharges of immature CA3 pyramidal cells were st
48                                              Burst discharges of thalamic neurons reflected the chang
49  spontaneous activity for stages 39-43 was a bursting discharge pattern in >75% of active neurons (33
50                                              Burst discharges (phasic firing) of dopamine-containing
51 s increased spike rates and the emergence of burst discharges reflecting network hyperexcitability.
52                       The frequency of these burst discharges/rhythmic activity varied between prepar
53 ceptor antagonist DNQX blocked the remaining burst discharges, suggesting that differences in recurre
54 ile mice can generate episodes of repetitive burst discharges that may underlie the pulsatile secreti
55                        TRN neurons that lack burst discharge typically did not produce low threshold
56                                              Burst discharge via Ca(V)3.3 channels induced long-term
57 tic currents (EPSCs), spontaneous EPSCs, and burst discharges were demonstrated in UBCs and granule c
58 d, in deep layer cells only, a short latency burst discharge which could be followed by one or more a
59 is study, we have examined the prevalence of burst discharge within TRN neurons.