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1 aining dopamine neuron firing regularity and burst firing.
2 te single-spike activity rather than rebound burst firing.
3 n/soma but not dendritic excitation impaired burst firing.
4 ncreased the number and the length of phasic burst firing.
5 tion reduced firing rates but did not affect burst firing.
6 attern of dopamine release with nonburst and burst firing.
7 rizing current injections and during rebound burst firing.
8 lease with nonburst stimulation but not with burst firing.
9 ibited half the recorded neurons and blocked burst firing.
10 ons leads to long-lasting increases in their burst firing.
11 of dopamine neurons without altering phasic burst firing.
12 THIP hyperpolarized TC neurons and promoted burst firing.
13 ntial propagation along lateral dendrites by burst firing.
14 c GABA(A)Rs produced longer and more intense burst firing.
15 l firing pattern, promoting action potential burst firing.
16 which in many cells contributes to intrinsic burst firing.
17 ing patterns, such as single-spike and spike-burst firing.
18 that these two currents interact to regulate burst firing.
19 ulation in a pattern mimicking dopamine cell burst firing.
20 ivation of pedunculopontine inputs increased burst firing.
21 ed secondary range and long-duration rebound burst firing.
22 tex operate in two distinct modes, tonic and burst firing.
23 and most neurons did not exhibit changes in burst firing.
24 can boost distal synaptic inputs and promote burst firing.
25 ck, while having no effect on firing rate or burst firing.
26 olarization (AHP) and caused a transition to burst firing.
27 s observed including regular, irregular, and burst firing.
28 rate and reducing the threshold for rebound burst firing.
29 ods and permitting rapid, repetitive, and/or burst firing.
30 polarization amplitude and thereby promoting burst firing.
31 reased firing during singing and song-locked burst firing.
32 nd fully abolished hyperpolarization-induced burst firing.
33 (TRPM2) channels that underlie NMDA-induced burst firing.
34 s (NMDARs) and increasing permissiveness for burst firing.
35 ns, although only a minority (15%) exhibited burst firing.
36 pectively, and abnormal synchronous rhythmic burst firing.
37 lity of synapses to sustain responses during burst firing.
38 M-channels depolarized neurons and increased burst firing.
39 ological observations of dopaminergic neuron burst-firing.
40 howed two minima in all regular-spiking (5), burst-firing (3) and in many fast-spiking cells (17:28).
45 and complex (MS/DB) in vivo exhibit rhythmic burst-firing activity that is phase-locked with the hipp
49 rease was also induced by postsynaptic theta-burst firing alone, yet it was blocked by NMDA receptor
53 hibiting D5R constitutive activity depresses burst firing and alleviates motor impairments in the 6-O
54 inal nociceptive circuits generate intrinsic burst firing and are distinguished by a lower "leak" mem
56 s within human MTL and confirm that neuronal burst firing and enhanced neuronal synchrony observed in
57 polarizations (AHPs); (iv) strongly enhanced burst firing and increased excitability at moderate spik
58 raclopride as well as saline did not reverse burst firing and motor deficits, confirming the selectiv
59 erating low-threshold spikes that facilitate burst firing and neurotransmitter release in neurons.
67 3 function by PIP(2) augmented low-threshold burst firing and spontaneous oscillations; conversely, d
69 dependent behaviors by attenuating DA neuron burst firing and subsequent DA release, without altering
71 neurons that contributes to action potential burst firing and that estradiol regulates I(h) in these
73 be one mechanism by which estrogen augments burst firing and transmitter release in hypothalamic neu
74 T-type) calcium channels are responsible for burst firing and transmitter release in neurons and are
78 ng, we further demonstrated that over 60% of burst-firing and stutter-firing interneurons also expres
79 actions using model neurons in which somatic burst-firing and synaptic plasticity are controlled by c
80 cial for intrinsic excitability and rhythmic burst firing, and PIP(2) serves as a powerful modulator
82 play a key role in neuronal excitability and burst firing, and selective triple T-type calcium channe
87 and nickel also suppressed LTS and neuronal burst firing at concentrations that blocked isolated T c
90 isodes of wakefulness (Aw), no difference in burst firing between epileptic and non-epileptic hippoca
91 CA3 pyramidal neurons (PYRs) exhibit intense burst firing (BF) early in development, concomitant with
92 t, PV interneuron silencing had no effect on burst firing, but instead shifted the spikes' theta phas
93 nt of external calcium by magnesium enhanced burst firing, but it was blocked by cobalt replacement o
94 pin-releasing hormone (GnRH) neurons exhibit burst firing, but the underlying conductances are not kn
95 pha1 receptors increases dopaminergic neuron burst firing by decreasing the calcium-activated potassi
96 cleotide-gated current (I(h)) contributes to burst firing by depolarizing the membrane after a period
97 reclassification also identifies generating burst firing by dopamine neurons as a keystone action.
99 hold for nociceptor excitability and induces burst firing by increasing the amplitude of T-type curre
100 ed Ca(2+) channels also facilitated rhythmic burst firing by triggering intracellular Ca(2+) signalin
103 ctric fish to address how stimulus-dependent burst firing can determine the flow of information in fe
105 = 16) and 28.7 +/- 5.8 ms in regular-spiking/burst-firing cells (n = 6), and the benzodiazepine1-sele
106 drites; a proportion of the fast-spiking and burst-firing cells in addition had basketlike terminals
107 etitive-firing, repetitive/burst and initial-burst-firing cells were reduced to a single-spiking patt
109 lation, but, while causing some increases in burst firing, cells continued to produce tonic spikes ev
110 ngle action potentials continuously, whereas burst firing consists of grouped discharges separated by
111 their intrinsic ability to generate rhythmic burst firing, contributes to the development of sensory
112 l cord raises the possibility that intrinsic burst firing could provide an endogenous drive to the de
113 s using action potential waveforms show that burst firing depends on small net inward currents that f
115 ular pyramidal neurons exhibit low-threshold burst firing driven by a spike afterdepolarization.
117 of the rat spinal cord exhibits oscillatory burst firing during early life, which occurs independent
118 cortical outflow neurons of their patterned burst firing during singing, without changing their spon
119 ionic conductances that underlie all-or-none burst firing elicited in acutely dissociated mouse Purki
120 ACC than PFC, and (iii) hosted neurons with burst firing events that synchronized to distant gamma a
123 However, the tonic firing pattern changed to burst firing exclusively during PTC, and this vlPAG neur
124 burst amplitudes (the number of spikes in a burst), firing frequency within bursts or peak firing ra
125 hat cocaine increases both the pacemaker and burst-firing frequency of rat ventral-midbrain dopaminer
126 together, our data suggest that epileptiform burst firing generated in the CA3 region by activity-dep
130 th an intrinsic ability to generate rhythmic burst-firing have been characterized in lamina I of the
131 lude that OT neurons in males are capable of burst firing highly similar to that seen in lactating ra
132 g DA neurons); mean firing rate; and percent burst firing (i.e., the proportion of action potentials
133 ated acoustically evoked neuronal firing and burst firing, immediately preceding TE, have been observ
134 nd that DA and D2 receptor agonists promoted burst firing in a subset of pyramidal cells, which was r
135 ntly, Ba(2)(+) application unmasked rhythmic burst firing in approximately 42% of nonbursting lamina
136 underlying the expression of high frequency burst firing in awake conditions, I(Twindow) is of criti
137 excitatory synapses but nevertheless induced burst firing in both Fmr1(-/y) and peptide-treated WT sl
138 Because the ADP correlates directly with burst firing in CA1 neurons, R-type calcium channels are
139 n the generation of spontaneous epileptiform burst firing in cornu ammonis (CA) 3 pyramidal neurons i
144 r understanding of the mechanisms underlying burst firing in midbrain dopaminergic neurons and those
145 g OT concentrations from 1 to 100 pm induced burst firing in OT neurons in patch-clamp recordings.
152 re, 5-HT and CP93129 inhibited STN-triggered burst firing in SNr GABA neurons, and CP93129's inhibito
153 the excitatory STN-->SNr projection, reduces burst firing in SNr GABA neurons, and thus may play a cr
154 ncreased the STN-triggered complex EPSCs and burst firing in SNr GABA neurons, demonstrating the effe
155 ctivation of TRPM2 channels is necessary for burst firing in SNr GABAergic neurons and their responsi
160 properties of pulvinar neurons that promote burst firing in the adult may be relevant to the treatme
161 spontaneous regular firing, but also exhibit burst firing in the presence of NMDA or when excitatory
162 ts are involved in generating high frequency burst firing in the subiculum, but the exact nature of t
164 d Ca(2+) spikes that directly correlate with burst firing in these neurons, differential redox regula
166 us (LDTg) is required for glutamate-elicited burst firing in ventral tegmental area DA neurons of ane
170 ng that was similar in frequency and form to burst firing in vivo, (2) the efficacy of glutamatergic
171 rom food-restricted mice exhibited increased burst firing in vivo, an effect that was enhanced by an
172 m Homers enhanced mGluR-induced epileptiform burst firing in wild-type (WT) animals, replicating the
174 abies virus PRV-152 revealed the presence of burst-firing in PRV-infected lamina I neurons, thereby c
175 pendent low-threshold-Ca2+ spikes as well as burst-firing in reticular thalamic neurons at physiologi
177 te Cav3.1-containing T-channels in subicular burst firing, in contrast to several previous reports di
178 ell recordings using KGluc, repetitive theta-burst firing induced AHP plasticity that mimics learning
179 au potential that underlies the epileptiform burst firing induced by metabotropic glutamate receptor
182 tems that modulate dopamine system function: burst firing induces massive synaptic dopamine release,
183 nt injection and were grouped as follows: 1) burst-firing interneurons (n = 13), 2) regular-firing in
184 t in brain slices and converted pathological burst firing into physiological tonic, single-spike firi
187 dels of epilepsy have shown that synchronous burst firing is associated with epileptogenesis, yet the
188 hypothalamic oxytocin (OT) neurons in vivo, burst firing is associated with pulsatile secretion of O
191 asic inhibition generated in response to nRT burst firing is greatly reduced in alpha4(0/0) pairs, su
196 olarizing actions of GABA and GABA-dependent burst-firing may synchronize a rapid release of GABA, NP
197 ealed the capability for autorhythmicity and burst firing, mediated by a T-type Ca(2+) conductance.
198 o switch from repetitive single spiking to a burst-firing mode by constant depolarizing current injec
199 thus enhance the probability to switch into burst-firing mode, which then potentiates GIRK currents
202 ations was of a single spiking rather than a bursting firing nature, and was coherent with extracellu
203 rophysiological types, except for the type I burst-firing neuron, had a main axon that coursed toward
206 trast to continuous firing neurons, 14 of 19 burst firing neurons and 3 of 7 intermittent firing neur
207 ns, four were slow firing neurons, five were burst firing neurons and nine were fast firing neurons.
211 n collaterals of the fast-spiking and type I burst-firing neurons was more extensive than that of the
212 w-firing, fast-spiking, regular-spiking, and burst-firing neurons; previous work has suggested that t
215 are the manifestation of highly synchronized burst firing of a large population of cortical neurons.
217 dings suggest that persistent high-frequency burst firing of cerebellar neurons caused by sodium pump
218 into the vSub decreased the firing rate and burst firing of DA neurons without altering the number o
219 f these neurons during experimentally evoked burst firing of DAergic axons that reproduce the reward-
220 triction also enhanced aspartic acid-induced burst firing of dopamine neurons in an ex vivo brain sli
221 chronic mild food restriction increases the burst firing of dopamine neurons in the substantia nigra
224 Our results support the hypothesis that burst firing of ET cells triggers the release of endocan
226 ental models of Parkinson's disease promotes burst firing of neurons in the subthalamic nucleus (STN)
228 uited in a phasic manner specifically during burst firing of nRT cells and provide sufficient GABA-AR
236 n regulating spike patterning indicates that burst firing of TANs in vivo could arise from direct or
237 logical classification of cells as intrinsic burst firing or regular spiking neurons was correlated w
239 ad Ca2+ influx, large after-depolarizations, burst firing output, and long-term potentiation of perfo
243 bradykinesia is causatively regulated by the burst-firing pattern of the subthalamic nucleus (STN) in
244 eurones with broader spikes and adapting and burst firing patterns activated the broadest IPSPs and r
246 with this finding, both regular-spiking and burst firing patterns were profoundly depressed in the m
247 of MNCs and are necessary for characteristic burst firing patterns which serve to maximize hormone re
249 le neuropeptide secretion is associated with burst firing patterns; however, intracellular signaling
250 "bursty" cells were observed that exhibited burst-firing patterns similar to normal HD cells but wit
251 al-by-trial variations in mean spike rate or burst-firing patterns, and potentially provides a princi
252 type calcium currents, and tonic- or initial bursting firing patterns, and received weak excitatory s
255 o, both the firing rate (tonic activity) and burst firing (phasic activity) of identified midbrain DA
260 s of a cannabinoid agonist known to increase burst firing produce ongoing fluctuations in extracellul
262 channels influence neurotransmitter release, burst firing rate activity, pacing, and critical dampeni
264 esent a seizure-like state in which neuronal burst firing renders animals unresponsive to incoming ta
267 nce in vivo, was arranged such that thalamic burst firing resulted in stimulation of the corticothala
269 ave intrinsic membrane properties that favor burst firing, seen not only during complex spikes elicit
271 e saccades, however, the duration of agonist burst firing significantly affects the control of saccad
273 onto 7/7 oriens-lacunosum moleculare and 5/5 burst firing, sparsely spiny neocortical interneurones d
274 the coupling was strong; they could modulate burst-firing states even when the coupling strength was
275 formed by CA1-region pyramidal neurons onto burst-firing subiculum neurons, presynaptic in vivo knoc
276 s consistent with widespread thalamocortical burst firing such as increased delta oscillations (1-4 H
277 st in characterizing mechanisms that promote burst firing, such as the regulation of NMDA receptor fu
278 neuronal firing and the change from tonic to burst firing suggest that AGS kindling involves increase
279 postsynaptic activity, in the form of theta-burst firing (TBF) of hippocampal CA1 pyramidal neurons,
281 lex EPSCs may contribute to the pathological burst firing that is associated with the symptoms of Par
282 scillations are driven by an unusual form of burst firing that is present in a subset of thalamocorti
283 channels, promoting rhythmic high-frequency burst firing that reduces sensory information transfer.
284 levels of tonic firing were found mixed with burst firing throughout the recordings even under condit
285 se that ICAN is selectively activated during burst firing to boost NMDA currents and allow plateau po
287 ion pattern of action potentials from phasic burst firing to regular tonic firing, hypothetically red
289 ive pharmacological inactivation of dopamine burst firing using the NMDA receptor antagonist, AP-5.
290 Driving GnRH neurons to exhibit simultaneous burst firing was ineffective at altering LH secretion.
292 ent with the established role of I(h) in ETC burst firing, we show that endogenous DA release increas
293 m feedback mechanisms that serve to maintain burst firing when voltage-dependent sodium conductance i
294 dynamic to prevent the prolonged periods of burst firing which can be evoked in brain slice preparat
295 ic rats reveal an age-dependent reduction in burst firing, which likely results in further reductions
296 e mitral cells commonly respond to odours by burst firing with each inhalation cycle, we used bursts
297 acological inhibition of T-channels switched burst firing with lower depolarizing stimuli to regular
298 the two subtypes play a unique function with burst firing, with a somewhat more prominent and possibl
299 In addition, the prevalence of spontaneous burst firing within lamina I was enhanced in the presenc
300 M interneuron silencing powerfully increased burst firing without altering the theta phase of spikes.
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