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1 back control of both calcium influx and cell excitability.
2 rizations, indicative of increased intrinsic excitability.
3 zed Daunorubicin is an inhibitor of neuronal excitability.
4 iDANs with appropriate midbrain markers and excitability.
5 sors that couple cell energetics to membrane excitability.
6 regulation of not only pHi, but also cardiac excitability.
7 ynaptic conductance is tuned to postsynaptic excitability.
8 d effects on behavior by regulating neuronal excitability.
9 pe calcium channels in augmenting motoneuron excitability.
10 -permeable GABAA receptor-dependent membrane excitability.
11 ncreasing ERK signaling and pyramidal neuron excitability.
12 role for CaV1.3 L-CDF in regulating neuronal excitability.
13 released opioids directly regulate neuronal excitability.
14 also been linked to a typical cortical hyper-excitability.
15 nd subthreshold and suprathreshold intrinsic excitability.
16 not always give the same change in cortical excitability.
17 rtex indicating a reduction of corticospinal excitability.
18 ivotal importance in the control of neuronal excitability.
19 hannel inactivation, and suppressed neuronal excitability.
20 g neurons, which can increase local neuronal excitability.
21 ons followed by retrograde presynaptic hyper-excitability.
22 c drive but instead show increased intrinsic excitability.
23 ion of ERK and blocked the increase in basal excitability.
24 he influence of excitatory input on neuronal excitability.
25 serted at different phases to probe cortical excitability.
26 nderstood maladaptive modulation of neuronal excitability.
27 lso from cell-autonomous changes in membrane excitability.
28 e key determinants of vascular smooth muscle excitability.
29 of action potentials, indicating an enhanced excitability.
30 nd was essential for estradiol regulation of excitability.
31 neurons predicted minimal change in neuronal excitability.
32 or is a well-known contributor to nociceptor excitability.
33 ents such as muscle contraction and neuronal excitability.
34 lular subtype ratios and increased intrinsic excitability.
35 ic transmission and regulation of electrical excitability.
36 s are mediated by shifts in relative circuit excitability.
37 hances nicotine-induced changes in DA neuron excitability.
38 to a gain of function and increased neuronal excitability.
39 resulted in a gradual reduction in intrinsic excitability.
40 ng membrane potential and levels of cellular excitability.
41 (pHi) are fundamental regulators of neuronal excitability.
42 by linking cellular metabolism with membrane excitability.
43 rons revealed that RPRFamide increases their excitability.
44 s target is capable of altering the target's excitability.
45 lations, coincident with highest hippocampal excitability.
46 ys indicate that mir-92a suppresses neuronal excitability.
47 ip between intracellular Ca(2+) and membrane excitability.
48 nd increasing POMC neuronal firing rates and excitability.
49 he AIS and are essential for tuning neuronal excitability.
50 r unique AIS plasticity to stabilize network excitability.
51 egatively with 1.0 mA anodal tDCS effects on excitability.
52 s during bladder filling stabilizes detrusor excitability.
53 gy of CaCCs and the ionic basis of IO neuron excitability.
54 orks contributed to changes in corticospinal excitability.
55 ays an important role in regulating neuronal excitability.
56 eural tissue exhibit both type I and type II excitability?
57 tudied how estradiol feedback regulates GnRH excitability, a key determinant of neural firing rate us
58 n of the notion that alpha activity reflects excitability across all of cortex and suggest instead th
59 ic cortex (PLC) and assess altered intrinsic excitability after 10 d of operant food self-administrat
60 ations, the difference in surrounding tissue excitability also offers a simple explanation of the cli
61 hat decreased alpha power increases baseline excitability, amplifying the response to both signal and
62 of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhi
63 ntly, Renshaw cells developed with increased excitability and a normal number of cholinergic motor ne
64 KCNQ2 channels alters the intrinsic neuronal excitability and action potential properties of L2/3 pyr
65 dysfunction consisting of enhanced neuronal excitability and altered short-term synaptic plasticity.
66 MNCs from HF rats exhibit increased membrane excitability and an enhanced input-output function, and
67 tified two specific phenotypes: (1) membrane excitability and AP-evoked Ca(2+) entry were impaired at
68 oscillations are thought to reflect cortical excitability and are therefore ascribed an important rol
69 ven the strong correlation between HA neuron excitability and behavioral arousal, we investigated bot
70 mp, GTx had multiple effects: (i) increasing excitability and bursting at moderate spike rates but re
72 that participates in the control of membrane excitability and Ca(2+) signaling events in beta-cells.
73 ctivity in the hippocampus enhances neuronal excitability and cognitive function in young normal mice
74 instead associated with increased intrinsic excitability and decreased HCN channel-mediated IH curre
76 n KCNQ5 mutations, associated with increased excitability and decreased repolarization reserve, lead
77 eal an input-dependent control over neuronal excitability and dendritic complexity in the development
78 an act as autoreceptors to regulate neuronal excitability and dopamine release, but the roles of each
79 de production during G-CSF treatment reduces excitability and G-CSF-induced visceral pain in vivo.
80 ssential roles in the regulation of cellular excitability and have been implicated in neurological an
82 e, that old CA1 pyramidal cells have reduced excitability and increased PERK expression that can be r
83 ding RNA, NEAT1, directly modulates neuronal excitability and is associated with pathological seizure
87 igra, vagal motoneurons do not enhance their excitability and oxidative load in response to chronic m
89 contagious yawning is determined by cortical excitability and physiological inhibition in the primary
90 w a critical role for ERK in maintaining the excitability and plasticity of D2R-MSNs.SIGNIFICANCE STA
91 te that Scn8a plays a vital role in neuronal excitability and provide insight into the mechanism and
92 e homeostatic, including a drop in intrinsic excitability and pruning of excitatory corticostriatal g
94 family are essential for control of cellular excitability and repolarization in a wide range of cell
96 a negative correlation between corticospinal excitability and RT, such that larger motor-evoked poten
97 Kv1.1 substantially contributes to both the excitability and short-term plasticity alterations that
98 Y+ cell types, with differences in intrinsic excitability and short-term plasticity of their inputs.
99 nd substantial derangements in both neuronal excitability and short-term synaptic plasticity-paramete
101 monoamines are important modulators of lOFC excitability and suggest that disruption of this process
102 , Navbeta2 is a critical regulator of axonal excitability and synaptic function in unmyelinated axons
103 s, we identify specific changes in intrinsic excitability and synaptic plasticity in basolateral amyg
105 ce electrophysiology was employed to measure excitability and synaptic transmission in DMS and midbra
106 w in vitro technologies that assess neuronal excitability and the derived synaptic activity within a
108 V) channels are key regulators of myocardial excitability, and Ca(2+)/calmodulin-dependent protein ki
111 n O-GlcNAcylation is a regulator of neuronal excitability, and it represents a promising target for f
113 usly unknown mechanism for the regulation of excitability, and support the hypothesis that Kir2 curre
114 erations in motor function, reduced neuronal excitability, and the inability of medium spiny neurons
115 te that ATP-induced increase and decrease of excitability are caused, respectively, by P2Y1 receptor-
116 find that synaptic excitation and intrinsic excitability are coregulated in individual neurons throu
117 bit selective vulnerability, that changes in excitability are not restricted to this neuronal class a
119 2+) levels, likely owing to altered cellular excitability as a result of BPA-induced Vm hyperpolariza
121 ycine transporters markedly decreased PV+ IN excitability, as assessed by action potential discharge.
122 ous mechanisms that regulate some aspects of excitability, as well as circuit-level mechanisms that a
123 ltered protein translation and brain circuit excitability associated with Gp1 mGluR in neurological d
124 se that these profound changes in mEC neuron excitability associated with the gain-of-function mutati
125 strongly enhanced burst firing and increased excitability at moderate spike rates but reduced spiking
126 haker-like Kv1.1-1.2 channels underlying the excitability brake current IKD Here we studied the role
127 lecular clock drives changes in SCN neuronal excitability, but it is unclear how mutations affecting
128 ated Na(+) channels (Nav ) modulate neuronal excitability, but the roles of the various Nav subtypes
129 els, adrenergic signaling increases dendrite excitability, but the underlying mechanisms remain elusi
130 nels are key factors in controlling membrane excitability, but whether they regulate axon growth rema
131 In principle, 2-AG could modify neuronal excitability by acting directly on ion channels, but suc
132 oinjection of cross-linked 300 kDa increased excitability by depolarizing the resting membrane potent
135 vel mechanism by which neuronal and synaptic excitability can be regulated, and suggest the possibili
136 namic recovery timescale that interacts with excitability captures this dynamic regime and predicts t
137 uisition would be proportional to cerebellar excitability (CBI) changes, whereas later stages of lear
138 strated the absence of ipsilesional cortical excitability change after diabetic strokes, suggesting i
139 t increased MC inhibition involves intrinsic excitability changes in Arc-expressing interneurons.SIGN
140 tive learning, but little is known about the excitability changes that occur specifically on neuronal
141 uced dysfunction of Kv3.4 and the associated excitability changes through upregulation of the native
142 We propose that the blunted cholinergic excitability contributes to the functional mPFC deactiva
143 ngs/varicosities), and dysregulated neuronal excitability (decreased firing at 200-300 pA and increas
146 tent with this notion, broadly enhancing PFC excitability diminishes rule specificity and behavioural
148 etworks where top-down mediated increases in excitability, distributed across excitatory and inhibito
149 t restricted to this neuronal class and that excitability does not increase monotonically with diseas
150 ndings suggest that changes in corticospinal excitability during gross more than fine finger manipula
151 an altered ability to modulate corticospinal excitability during movement preparation when there is a
153 across cellular membranes to regulate muscle excitability, electrolyte movement across epithelia, and
154 ntracortical inhibition, spinal motor neuron excitability (F-waves), index finger abduction force and
156 of synaptic efficacy and intrinsic neuronal excitability for pathways that convey hippocampal and ex
157 These include changes in intrinsic cellular excitability, glutamate release, and glutamate uptake.
159 widespread drug-induced changes in neuronal excitability have been observed, little is known about s
162 sibility that these homeostatic increases in excitability have potential negative functional and stru
164 l phenomenon, in which D2Rs enhance cellular excitability in a manner that depends on synaptic input,
165 solutions accounted for similar GnRH neuron excitability in all groups other than positive feedback
167 ork-wide changes in the brain, affecting the excitability in both nearby and remotely connected regio
168 cross all of cortex and suggest instead that excitability in different regions is reflected in distin
169 expression, decreases Kv current, increases excitability in DRG neurons and leads to spinal cord cen
170 neuronal ensembles, but decreased intrinsic excitability in Fos(-) neurons using distinct cellular m
171 to assess selective alterations of intrinsic excitability in Fos-expressing neuronal ensembles (FosGF
173 lic nucleotide-gated (HCN) channels regulate excitability in neurons, and blocking HCN channel functi
175 at distinct frequencies may reflect cortical excitability in occipital versus posterior parietal cort
176 synchronization coordinates brief periods of excitability in oscillating neuronal populations to opti
177 s a new potential molecular target to reduce excitability in patients with KCNQ2 encephalopathy.
179 represent a state of increased processing or excitability in task-relevant cortical regions, and refl
181 lf-administration led to increased intrinsic excitability in the behaviorally relevant Fos-expressing
182 sodium channel is a critical contributor to excitability in the brain, where pathological loss of fu
183 ibitory synaptic transmission, and intrinsic excitability in the circuits of the central auditory sys
184 ings provide evidence of a dramatic shift in excitability in the dentate gyrus of Pafah1b1(+/-) mice
187 nctional MRI, we show that disrupting neural excitability in the rTPJ reduces behavioral and neural i
188 We find that the daily rhythm in membrane excitability in the ventral SCN (vSCN) was enhanced in a
190 tors on motor neurons increases motor neuron excitability, in part by enhancing subthreshold voltage-
191 nant LGI1 and genetic depletion on intrinsic excitability, in the absence of synaptic input, in hippo
192 , we provide evidence that heightened neural excitability instead reflects a state of biased percepti
193 neurons including the regulation of membrane excitability, intracellular [Ca(2+) ] regulation, and ne
194 teractions that can quickly increase network excitability involve, for example, astrocyte Ca(2+) and
195 alamocortical neurons, we show that membrane excitability is a critical component of dendritic develo
200 Therefore, we propose that changes in neural excitability leave the precision of sensory processing u
201 idual differences in intrinsic corticospinal excitability, local cortical GABA levels, and reaction t
202 ertheless, it remains debated how changes in excitability manifest at the behavioral level in percept
203 Activity-dependent regulation of intrinsic excitability may be a general mechanism for adaptive con
204 ying that enhancing or dampening DG neuronal excitability may cause resistance to or facilitation of
206 triggers transient increases in postsynaptic excitability, occlusion of firing rate potentiation, and
208 ther, our results reveal that changes in the excitabilities of the Mauthner command neuron for escape
209 data indicate that D3 receptors regulate the excitability of a unique, IT prefrontal cell population,
211 Finally, there were no changes in intrinsic excitability of any region in rats exposed to toluene as
212 vel data provide evidence that the intrinsic excitability of appetitive memory-encoding ensembles is
214 In aged animals, a decrease in the intrinsic excitability of CA1 pyramidal neurons is believed to con
219 long been known to dramatically enhance the excitability of cortical neurons, the cellular mechanism
220 inputs to subregions of the SNc regulate the excitability of DA neurons differentially, resulting in
222 ings in brain slices revealed that intrinsic excitability of DG granule neurons was enhanced by adipo
223 extinction of contextual fear and intrinsic excitability of DG granule neurons, implying that enhanc
224 yte-derived ATP differentially modulates the excitability of different types of neurons and efficient
225 nial magnetic stimulation (TMS) to probe the excitability of distinct sets of excitatory inputs to co
228 m commensal bacteria can directly impact the excitability of DRG neurons, through PAR-4 activation.
231 role in food seeking but decreased intrinsic excitability of Fos(-) non-ensembles.SIGNIFICANCE STATEM
232 d that operant self-administration increased excitability of FosGFP(+) neurons and decreased excitabi
237 ory DH interneurons coupled with the reduced excitability of inhibitory DH interneurons post-SCI coul
238 escue was associated with restoration of the excitability of inhibitory interneurons in the hippocamp
240 for 8 weeks), the basal firing rate and the excitability of LHb neurons in brain slices was higher,
242 ration.SIGNIFICANCE STATEMENT The inadequate excitability of motor neurons and their output, the neur
243 brane potentials leads to increased neuronal excitability of neocortical layer 2/3 (L2/3) pyramidal n
244 L) procedure, the present study assessed the excitability of neuronal ensembles in the nucleus accumb
246 physiological data further indicate that the excitability of nonpeptidergic nociceptors is enhanced.
247 in is thought to be driven by changes in the excitability of peripheral nociceptive neurons, but the
248 verall, operant learning increased intrinsic excitability of PLC Fos-expressing neuronal ensembles th
249 t phenomenon, synaptic input can enhance the excitability of prefrontal neurons over timescales on th
250 nal cocaine-induced adaptations in intrinsic excitability of prelimbic (PL) and infralimbic (IL) pyra
251 r correct microbial dysbiosis may affect the excitability of primary afferent neurons, many of which
253 ha oscillations increase the global baseline excitability of sensory systems without affecting percep
255 transition is enabled by an increase in the excitability of the "healthy" surrounding tissue, which
259 We then tested whether the corticospinal excitability of the hand representation under the above
260 hatidylinositol-3,4-bisphosphate predict the excitability of the plasma membrane and modulate the geo
262 ther, our modelling results suggest that the excitability of the tissue surrounding the seizure core
265 l often produced increases in global network excitability or depression of the conditioned pair.
267 suggests that associated changes in neuronal excitability, particularly in developing neurons, may co
268 ment, which suppressed action potential (AP) excitability, particularly when APs occurred at high fre
269 and perceptual sensitivity, by aligning high-excitability phases to events within a stimulus stream.
271 findings show that changes in corticospinal excitability present during power grip compared with fin
274 cerebral blood flow (CBF), and corticospinal excitability, respectively, before and 4 weeks after the
275 erate 'leak' currents that regulate neuronal excitability, respond to lipids, temperature and mechani
276 rontal cortex display higher gain of somatic excitability, responding with a higher number of action
277 alpha oscillations indicate enhanced neural excitability, resulting in improved perceptual acuity.
278 thm may serve as a general index of cortical excitability.SIGNIFICANCE STATEMENT Alpha-band oscillati
279 hold tACS will increase or decrease cortical excitability.SIGNIFICANCE STATEMENT Transcranial alterna
281 nels (CaV1.2) are key regulators of neuronal excitability, synaptic plasticity, and excitation-transc
282 3 (L-type) Ca(2+) channels regulate neuronal excitability, synaptic plasticity, and learning and memo
283 critical mechanism for changes in nociceptor excitability that drive the development of chronic pain.
284 ficant role of Slack in nociceptive neuronal excitability, the AP-2 clathrin-mediated endocytosis tra
285 els effectively reduces growth cone membrane excitability, thereby limiting excessive Ca(2+) influx a
286 m-dependent manner and by dampening neuronal excitability through co-expression of an inwardly rectif
287 antiepileptic drug that suppresses neuronal excitability through the activation of voltage-gated KCN
289 and molecular mechanisms controlling network excitability to assess whether they may be altered in an
290 classes all exhibited increases in intrinsic excitability, transcriptional profiling indicated that t
291 eurons, mutant p.Arg222His channels increase excitability via a depolarisation of resting potential a
292 design, monitoring changes in motor-cortical excitability via transcranial magnetic stimulation up to
293 al neurons; a cocaine-induced increase in PL excitability was decreased by riluzole, and a cocaine-in
296 t with this idea, we found that enhancing MD excitability was sufficient to enhance task performance.
297 lt, loss of GIRK function can enhance neuron excitability, whereas gain of GIRK function can reduce n
298 current would lead to a recovery of neuronal excitability whereby desensitization of the receptor wou
299 cation had heterogeneous effects on neuronal excitability, with both excitation and suppression obser
300 cium channels are key to regulating neuronal excitability, with the range of functional roles enhance
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