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1 ., narrower AP half-widths and enlarged fast afterhyperpolarization).
2 ne conductance and the amplitude of the slow afterhyperpolarization.
3 ke output by promoting recovery of the spike afterhyperpolarization.
4 potentials, input resistance and the medium afterhyperpolarization.
5 as measured by a decrease in the post-burst afterhyperpolarization.
6 by action potentials and affected the spike afterhyperpolarization.
7 sity relationship and generated a post-train afterhyperpolarization.
8 excitability after each action potential by afterhyperpolarization.
9 the duration and amplitude of the subsequent afterhyperpolarization.
10 ht offset, these cells exhibited a transient afterhyperpolarization.
11 spike-frequency adaptation and the postburst afterhyperpolarization.
12 ials and mediated a large component of their afterhyperpolarization.
13 action potential duration and an increase in afterhyperpolarization.
14 ut is correlated with a decrease in C2 spike afterhyperpolarization.
15 rst discharges and attenuated the subsequent afterhyperpolarization.
16 uded the ability of serotonin to inhibit the afterhyperpolarization.
17 cells by reducing the slow calcium-activated afterhyperpolarization.
18 f a modest difference in the duration of the afterhyperpolarization.
19 nabinoid signalling and the action potential afterhyperpolarization.
20 nabinoid signalling and the action potential afterhyperpolarization.
21 ng action potentials and help produce a fast afterhyperpolarization.
22 channel (SK), which mediates the post-spike afterhyperpolarization.
23 -induced suppression of excitation and spike afterhyperpolarization.
24 -induced suppression of excitation and spike afterhyperpolarization.
25 ttenuated neuronal spiking by increasing the afterhyperpolarization.
26 ch may in turn be modulated by the postburst afterhyperpolarization.
27 hich tend to slow firing by producing a deep afterhyperpolarization.
28 spike width but paradoxically increased the afterhyperpolarization.
29 and transiently diminished action potential afterhyperpolarization.
30 d by real-time manipulation of the postspike afterhyperpolarization.
31 potential (AP) threshold and reduced medium afterhyperpolarization.
32 otential and increasing the action potential afterhyperpolarization.
33 equency adaptation, and did not display slow afterhyperpolarizations.
34 ction potential durations and smaller medium afterhyperpolarizations.
35 tion potentials and smaller amplitude medium afterhyperpolarizations.
36 on-elicited AP with no discernible effect on afterhyperpolarizations.
37 requency adaptation, a large 15.6 +/- 1.0 mV afterhyperpolarization, a mean input resistance of 335 +
38 rties (membrane potential, input resistance, afterhyperpolarization, action potential frequency), it
39 tory cellular responses-suppression of spike afterhyperpolarizations, activation of a voltage-depende
40 activated K+ (SK) channels contribute to the afterhyperpolarization, affecting neuronal excitability.
41 activate Ca2+-dependent K+ channels and slow afterhyperpolarizations (AH) lasting approximately 15 se
42 channels, which contribute to a medium-slow afterhyperpolarization (AHP) after spike bursts, regulat
43 be a reduction in the slow component of the afterhyperpolarization (AHP) and a modest depolarization
44 from single neurons show a depression of the afterhyperpolarization (AHP) and an increase in frequenc
45 nductance channels, abolished the slow spike afterhyperpolarization (AHP) and caused a transition to
46 M) dose-dependently decreased both postburst afterhyperpolarization (AHP) and spike frequency adaptat
47 y, as evidenced by changes in the post-burst afterhyperpolarization (AHP) and spike-frequency accommo
48 of membrane repolarization, the amplitude of afterhyperpolarization (AHP) and the pattern of AP firin
49 between the time course of the motoneurone's afterhyperpolarization (AHP) and the variability in its
50 nal-projecting neurons had larger and longer afterhyperpolarization (AHP) as well as slower frequency
51 tabotropic regulation of the slow and medium afterhyperpolarization (AHP) currents (I(sAHP), I(mAHP))
52 ration (C and Adelta), but not the decreased afterhyperpolarization (AHP) durations (C, Adelta, and A
55 neurons had a long-lasting, sodium-dependent afterhyperpolarization (AHP) following bursts of action
56 showed the amplitude of the Ca2+ -dependent afterhyperpolarization (AHP) following spike trains is s
57 idal neurons via modulation of the postburst afterhyperpolarization (AHP) have been repeatedly demons
58 Using whole-cell recordings, we examined the afterhyperpolarization (AHP) in CA1 pyramidal cells in h
59 Learning-related reductions of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal ne
60 nnel(s) (SK) underlying the apamin-sensitive afterhyperpolarization (AHP) in rat superior cervical ga
61 amplitude of the Ca2+-dependent, K+-mediated afterhyperpolarization (AHP) is related to cognitive dec
62 osite pattern of change, with increased slow afterhyperpolarization (AHP) potential, whereas vulnerab
63 anner, and exhibited a significantly greater afterhyperpolarization (AHP) than did non-bursting POA n
64 ic nucleus (SON) neurons possess a prominent afterhyperpolarization (AHP) that contributes to spike p
65 campal pyramidal neurons is terminated by an afterhyperpolarization (AHP) that displays two main comp
66 (SK channels) contribute to the long lasting afterhyperpolarization (AHP) that follows an action pote
68 id reduction in the size of the long-lasting afterhyperpolarization (AHP) that follows individual the
69 during prolonged discharges and of the slow afterhyperpolarization (AHP) that follows, as occur in v
70 central neurons are followed by a prolonged afterhyperpolarization (AHP) that influences firing freq
71 bstantial decrease in the amplitude of spike afterhyperpolarization (AHP) that was associated with an
72 ately 30%) in the Ca2+-dependent K+-mediated afterhyperpolarization (AHP), because the K+ channel blo
73 hold-crossing neurone model with a postspike afterhyperpolarization (AHP), but absent from those calc
74 ion cells corresponds to a slowly recovering afterhyperpolarization (AHP), but, unlike in cortical ce
75 ability, reflected by an enhanced post-burst afterhyperpolarization (AHP), in CA1 hippocampal pyramid
76 d a persistently reduced BK channel mediated afterhyperpolarization (AHP), repetitive spiking is main
77 ion channels responsible for IO neuron spike afterhyperpolarization (AHP)-a result that appears to ha
87 endent on the critical interplay between the afterhyperpolarizations (AHPs) and afterdepolarizations
88 s and/or spike-dependent currents that cause afterhyperpolarizations (AHPs) and afterdepolarizations
89 gnificantly larger, longer lasting postburst afterhyperpolarizations (AHPs) and greater spike frequen
90 pothalamic supraoptic nucleus (SON) generate afterhyperpolarizations (AHPs) during spiking to slow fi
92 ptic nucleus (SON) display calcium-dependent afterhyperpolarizations (AHPs) following a train of acti
94 produced long-lasting ( approximately 20 s) afterhyperpolarizations (AHPs) that were insensitive to
98 e membrane potential, reducing the postspike afterhyperpolarization amplitude and decreasing the acti
99 er them more excitable by reducing the spike afterhyperpolarization amplitude and thereby promoting b
100 ctopic neurons are less excitable (increased afterhyperpolarization amplitude, decreased sag, lower f
102 potential repolarization, larger post-burst afterhyperpolarization and a functional enhancement of C
103 xcitability manifested as a decreased medium afterhyperpolarization and a longer-lasting afterdepolar
104 output due to an increase in the inter-spike afterhyperpolarization and a reduction in spike half-wid
105 esulted from a reduction in action potential afterhyperpolarization and alterations in the maximal ra
106 Kv1.1-induced increase in the fast phase of afterhyperpolarization and coincident decreased distal s
107 ns BK current flows primarily after the fast afterhyperpolarization and helps to prevent a later afte
108 le-cell recording pipette reduced the medium afterhyperpolarization and increased action potential ou
109 A significantly reduces the amplitude of the afterhyperpolarization and increases action potential fr
110 of the potassium current underlying the slow afterhyperpolarization and its modulation has proven elu
111 was higher, whereas the amplitude of medium afterhyperpolarization and M-type K(+) currents were sma
112 ctive L-VSCC agonist Bay K8644 increased the afterhyperpolarization and mimicked the depressive effec
113 ncreased probability of firing after a spike afterhyperpolarization and not directly from subthreshol
114 esurgent sodium current flows at the peak of afterhyperpolarization and persistent sodium current flo
117 impairments at least in part by reducing the afterhyperpolarization and spike-frequency adaptation of
118 d the amplitude of both the action potential afterhyperpolarization and synaptic inputs to motoneuron
119 rd currents, M-type potassium currents, slow afterhyperpolarization and T-type calcium currents, whic
120 PS animals expressed larger action potential afterhyperpolarizations and H-current relative to contro
121 Increased excitability (reduced postburst afterhyperpolarizations and reduced spike-frequency adap
122 ening of action potentials, reduction of the afterhyperpolarization, and increased propensity to ente
124 They have narrower action potentials, deeper afterhyperpolarizations, and make stronger projections t
125 ion potential frequency and the reduction in afterhyperpolarization are occluded by apamin, a small-c
126 l durations are prolonged, the amplitudes of afterhyperpolarizations are reduced, and the responses t
127 embrane depolarization and may contribute to afterhyperpolarization as negative feedback to control n
129 nels increased spike width and decreased the afterhyperpolarization, as expected for loss of an actio
130 currents, M-type potassium currents and slow afterhyperpolarization, as well as corresponding ion cha
132 g synaptic stimulation, the Ca(2+)-dependent afterhyperpolarization, baseline field potentials, and s
133 e following: (1) that the amplitude of spike afterhyperpolarization be above the GABAA synaptic rever
135 e effect on action potential width or a fast afterhyperpolarization but converted a medium afterhyper
136 the action potentials and eliminated a slow afterhyperpolarization but had a scarce effect on the fr
137 clamp experiments, NS309 enhanced the medium afterhyperpolarization (but not the slow afterhyperpolar
138 ation and contributes to the medium-duration afterhyperpolarization, but the role of I(M) in control
139 e pharmacological characteristics as the SCG afterhyperpolarization, but to differ from those of homo
140 possibility that serotonin might reduce the afterhyperpolarization by regulating calcium-induced cal
141 members, which contribute to M-currents and afterhyperpolarization conductances in multiple brain ar
142 ate receptor-mediated inhibition of the slow afterhyperpolarization current (I(sAHP)), which is depen
144 we observed that the calcium-activated slow afterhyperpolarization current (IsAHP) was also reduced
145 s clarify key functional aspects of the slow afterhyperpolarization current and its modulation by 5-H
146 e the system; in contrast, activation of the afterhyperpolarization current is unaffected by the incr
147 CNN1, decreased total potassium currents and afterhyperpolarization currents and increased excitabili
148 urons coexpress SK1/SK2 and apamin-sensitive afterhyperpolarization currents are elevated by NMDA and
149 xpresses KCNQ5 channels, the medium and slow afterhyperpolarization currents are significantly reduce
150 strate that KCNQ5 channels contribute to the afterhyperpolarization currents in hippocampus in a cell
153 y through RyRs to generate SK-dependent slow afterhyperpolarizations, demonstrating functional segreg
154 ys to compensate for this loss of a critical afterhyperpolarization-dependent control of neuronal exc
156 unit size (amplitude) and firing behaviour (afterhyperpolarization duration and muscle fibre conduct
157 interval, firing pattern, MU potential area, afterhyperpolarization duration and muscle fibre conduct
159 maximum firing frequency, decreased initial afterhyperpolarization duration, and increased total ada
162 on of calcium-induced calcium release to the afterhyperpolarization, enhanced the effect of serotonin
163 action potentials had three components: fast afterhyperpolarization (fAHP), afterdepolarizing potenti
164 e species-independent (e.g., fast and medium afterhyperpolarization, firing frequency, and depolarizi
165 n of Kcnab2 leads to a reduction in the slow afterhyperpolarization following a burst of action poten
166 that K(ATP) channels contribute to the slow afterhyperpolarization following an evoked burst of acti
168 ptic targets of stellate cells, whereas deep afterhyperpolarizations following fusiform cell spike tr
169 fferences in action potential morphology and afterhyperpolarizations, however, emerged when nonadapti
170 endent K(+) current responsible for the slow afterhyperpolarization (I(sAHP)), a prominent regulator
172 potassium channels, which contribute to the afterhyperpolarization in central neurons and other cell
175 ion was tonic cholinergic suppression of the afterhyperpolarization in layer 5 neurons, which was abs
176 creased cytosolic Ca2+ and contribute to the afterhyperpolarization in many excitable cell types.
178 ivated potassium channel-mediated fast spike afterhyperpolarization in neurons in which the M-current
179 otassium channels (SKCa1-3) mediate the slow afterhyperpolarization in neurons, but the molecular ide
181 a(2+)-activated K(+) channels mediate a slow afterhyperpolarization in sensory neurons that was inhib
184 results indicate that serotonin inhibits the afterhyperpolarization in the CA1 region of hippocampus
186 nnels are involved in the generation of slow afterhyperpolarization, in the regulation of firing patt
187 CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrins
191 o CA1 neurons, we demonstrate that postburst afterhyperpolarization is not altered with aging and tha
192 how that, independent of light stimulus, the afterhyperpolarization is significantly greater in type
193 ion potential and decreased the amplitude of afterhyperpolarization led us to ask whether METH alters
196 depression of the medium and slow post-spike afterhyperpolarization (mAHP and sAHP), increasing the e
197 Single spiking depends on a medium-duration afterhyperpolarization (mAHP) generated by rapid SK curr
198 ntial frequency, as well as a reduced medium afterhyperpolarization (mAHP), a conductance partly medi
199 d a reduction of the amplitude of the medium afterhyperpolarization (mAHP), but not the fast AHP (fAH
200 Furthermore, the amplitude of the medium afterhyperpolarization (mAHP), mediated by SK channels,
201 long been known to contribute to the medium afterhyperpolarization (mAHP), recent evidence indicates
203 etween the medium and slow calcium-dependent afterhyperpolarizations may underlie this firing pattern
204 rates of AP rise and fall with no change in afterhyperpolarization measured to 80 % recovery (AHP80)
207 anism by which use-dependent changes in slow afterhyperpolarizations might regulate electrical firing
208 onent of the SK channels responsible for the afterhyperpolarization of cultured rat SCG neurones.
210 The wide spikes and shallow action potential afterhyperpolarizations of interneurons, compared with t
211 membrane potential (RMP) and do not produce afterhyperpolarization or cumulative inactivation to lim
212 alcium responsible for the generation of the afterhyperpolarization originates from the release of in
215 nd a blunting of the medium component of the afterhyperpolarization potential, a voltage signature of
216 uation, they showed significant reduction of afterhyperpolarization potentials (AHPs) in hippocampal
217 rlies the shortening of the action potential afterhyperpolarization produced by activation of bradyki
218 ng Kv2 current can account for the increased afterhyperpolarization produced by BK inhibition and lik
221 ects of METH on action potential broadening, afterhyperpolarization repression, and spontaneous spike
222 lasting GABAB receptor-mediated IPSP, a slow afterhyperpolarization requiring action potentials but n
223 lie delayed rectifier potassium currents and afterhyperpolarization respectively, are localized in hi
224 ated by a concomitant decrease in the normal afterhyperpolarization response and augmentation of an a
225 e in the amplitude and duration of the spike afterhyperpolarization, resulting in a nonlinear increas
226 ium afterhyperpolarization (but not the slow afterhyperpolarization sAHP) and profoundly affected exc
227 known to be altered by learning are the slow afterhyperpolarization (sAHP) after a burst of action po
228 ause and an increase in the duration of slow afterhyperpolarization (sAHP) after depolarization.
229 g is driven by a delayed and slowly decaying afterhyperpolarization (sAHP) current associated with L-
230 pyramidal neurons, the Ca2+ -dependent slow afterhyperpolarization (sAHP) exhibits an increase with
231 al area CA1 and basolateral amygdala, a slow afterhyperpolarization (sAHP) follows a burst of action
235 ergic signaling in the hippocampus, the slow afterhyperpolarization (sAHP) is an appealing candidate
237 an action potential burst results in a slow afterhyperpolarization (sAHP) that critically regulates
238 yramidal cells of the cortex, express a slow afterhyperpolarization (sAHP) that regulates their firin
239 as correlated with the amplitude of the slow afterhyperpolarization (sAHP), a major mechanism of spik
240 artially underlie the calcium-activated slow afterhyperpolarization (sAHP), a neuronal conductance wh
241 ompanied by AP broadening, an increased slow afterhyperpolarization (sAHP), and faster accumulation o
242 neurons, including the Ca(2+)-dependent slow afterhyperpolarization (sAHP), L-type voltage-gated Ca(2
243 s negatively related to the size of the slow afterhyperpolarization (sAHP), which is reduced in the e
245 rent, decreases rheobase, reduces the medium afterhyperpolarization, shortens spike duration and decr
247 markers, including the increases in the slow afterhyperpolarization, spike accommodation, and [Ca2+]i
248 tic correlation decays slower than the spike afterhyperpolarization, spike bursts can occur during si
250 esent with a higher prevalence of ultra slow afterhyperpolarization than slow alpha motoneurons that
254 neuronal excitability by contributing to the afterhyperpolarization that follows an action potential.
255 entials and to increase the amplitude of the afterhyperpolarization that follows each action potentia
256 action potential (AP) and generation of the afterhyperpolarization that follows the AP recorded at t
257 and peripheral nervous system express a slow afterhyperpolarization that is mediated by a slow calciu
258 Many neurons in the nervous systems express afterhyperpolarizations that are mediated by a slow calc
259 arization during repetitive firing, and slow afterhyperpolarizations that distinguished them from non
260 ute to adaptation of firing rate and to slow afterhyperpolarizations that follow repetitive firing.
261 maging reveal that individual SACs have slow afterhyperpolarizations that induce SACs to have variabl
262 y integrate-and-fire neuron model with spike afterhyperpolarization the theory accurately predicts th
263 ameters that vary by cell subtype - the slow afterhyperpolarization, the sag, and the spike frequency
264 ce sodium channel de-inactivation via a fast afterhyperpolarization through BK channel activation.
266 ly in two patterns associated with different afterhyperpolarization timescales, each dictated by a di
267 fterhyperpolarization but converted a medium afterhyperpolarization to an afterdepolarization and cou
268 ramidal neurons by converting the post-burst afterhyperpolarization to an afterdepolarization via a r
269 We discovered an ultraslow, minute-long afterhyperpolarization (usAHP) in network neurons follow
270 or network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase i
271 (+) pumps produces a post-activity ultraslow afterhyperpolarization (usAHP) up to ~10 mV in amplitude
272 onent of the current underlying single-spike afterhyperpolarization was sensitive to apamin, phase-lo
276 properties, such as membrane capacitance and afterhyperpolarizations, were flattened in rTg4510 mEC-S
277 ike interval, and decreased the amplitude of afterhyperpolarization, which are consistent with change
278 ivation of INaP affects the action potential afterhyperpolarization, which increases the spontaneous
279 inje cell dendritic excitability produces an afterhyperpolarization, which is hypothesized to release
280 exhibited a sodium pump-mediated ultra-slow afterhyperpolarization, which was absent in slow alpha m
281 r in duration; 2) their spikes can have dual afterhyperpolarizations with fast and slow components; a