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1 ., narrower AP half-widths and enlarged fast afterhyperpolarization).
2 ke output by promoting recovery of the spike afterhyperpolarization.
3 potentials, input resistance and the medium afterhyperpolarization.
4 as measured by a decrease in the post-burst afterhyperpolarization.
5 sity relationship and generated a post-train afterhyperpolarization.
6 ttenuated neuronal spiking by increasing the afterhyperpolarization.
7 excitability after each action potential by afterhyperpolarization.
8 the duration and amplitude of the subsequent afterhyperpolarization.
9 ht offset, these cells exhibited a transient afterhyperpolarization.
10 spike-frequency adaptation and the postburst afterhyperpolarization.
11 ials and mediated a large component of their afterhyperpolarization.
12 action potential duration and an increase in afterhyperpolarization.
13 ut is correlated with a decrease in C2 spike afterhyperpolarization.
14 rst discharges and attenuated the subsequent afterhyperpolarization.
15 uded the ability of serotonin to inhibit the afterhyperpolarization.
16 cells by reducing the slow calcium-activated afterhyperpolarization.
17 hich tend to slow firing by producing a deep afterhyperpolarization.
18 by action potentials and affected the spike afterhyperpolarization.
19 spike width but paradoxically increased the afterhyperpolarization.
20 d by real-time manipulation of the postspike afterhyperpolarization.
21 otential and increasing the action potential afterhyperpolarization.
22 ne conductance and the amplitude of the slow afterhyperpolarization.
23 equency adaptation, and did not display slow afterhyperpolarizations.
24 on-elicited AP with no discernible effect on afterhyperpolarizations.
25 requency adaptation, a large 15.6 +/- 1.0 mV afterhyperpolarization, a mean input resistance of 335 +
26 rties (membrane potential, input resistance, afterhyperpolarization, action potential frequency), it
27 tory cellular responses-suppression of spike afterhyperpolarizations, activation of a voltage-depende
28 activated K+ (SK) channels contribute to the afterhyperpolarization, affecting neuronal excitability.
29 activate Ca2+-dependent K+ channels and slow afterhyperpolarizations (AH) lasting approximately 15 se
30 be a reduction in the slow component of the afterhyperpolarization (AHP) and a modest depolarization
31 from single neurons show a depression of the afterhyperpolarization (AHP) and an increase in frequenc
32 nductance channels, abolished the slow spike afterhyperpolarization (AHP) and caused a transition to
33 M) dose-dependently decreased both postburst afterhyperpolarization (AHP) and spike frequency adaptat
34 y, as evidenced by changes in the post-burst afterhyperpolarization (AHP) and spike-frequency accommo
35 of membrane repolarization, the amplitude of afterhyperpolarization (AHP) and the pattern of AP firin
36 between the time course of the motoneurone's afterhyperpolarization (AHP) and the variability in its
37 nal-projecting neurons had larger and longer afterhyperpolarization (AHP) as well as slower frequency
38 tabotropic regulation of the slow and medium afterhyperpolarization (AHP) currents (I(sAHP), I(mAHP))
39 ration (C and Adelta), but not the decreased afterhyperpolarization (AHP) durations (C, Adelta, and A
42 neurons had a long-lasting, sodium-dependent afterhyperpolarization (AHP) following bursts of action
43 showed the amplitude of the Ca2+ -dependent afterhyperpolarization (AHP) following spike trains is s
44 idal neurons via modulation of the postburst afterhyperpolarization (AHP) have been repeatedly demons
45 Using whole-cell recordings, we examined the afterhyperpolarization (AHP) in CA1 pyramidal cells in h
46 Learning-related reductions of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal ne
47 nnel(s) (SK) underlying the apamin-sensitive afterhyperpolarization (AHP) in rat superior cervical ga
48 amplitude of the Ca2+-dependent, K+-mediated afterhyperpolarization (AHP) is related to cognitive dec
49 osite pattern of change, with increased slow afterhyperpolarization (AHP) potential, whereas vulnerab
50 anner, and exhibited a significantly greater afterhyperpolarization (AHP) than did non-bursting POA n
51 ic nucleus (SON) neurons possess a prominent afterhyperpolarization (AHP) that contributes to spike p
52 campal pyramidal neurons is terminated by an afterhyperpolarization (AHP) that displays two main comp
53 (SK channels) contribute to the long lasting afterhyperpolarization (AHP) that follows an action pote
55 id reduction in the size of the long-lasting afterhyperpolarization (AHP) that follows individual the
56 during prolonged discharges and of the slow afterhyperpolarization (AHP) that follows, as occur in v
57 central neurons are followed by a prolonged afterhyperpolarization (AHP) that influences firing freq
58 bstantial decrease in the amplitude of spike afterhyperpolarization (AHP) that was associated with an
59 ately 30%) in the Ca2+-dependent K+-mediated afterhyperpolarization (AHP), because the K+ channel blo
60 hold-crossing neurone model with a postspike afterhyperpolarization (AHP), but absent from those calc
61 ion cells corresponds to a slowly recovering afterhyperpolarization (AHP), but, unlike in cortical ce
62 ability, reflected by an enhanced post-burst afterhyperpolarization (AHP), in CA1 hippocampal pyramid
63 d a persistently reduced BK channel mediated afterhyperpolarization (AHP), repetitive spiking is main
70 endent on the critical interplay between the afterhyperpolarizations (AHPs) and afterdepolarizations
71 s and/or spike-dependent currents that cause afterhyperpolarizations (AHPs) and afterdepolarizations
72 gnificantly larger, longer lasting postburst afterhyperpolarizations (AHPs) and greater spike frequen
74 ptic nucleus (SON) display calcium-dependent afterhyperpolarizations (AHPs) following a train of acti
76 produced long-lasting ( approximately 20 s) afterhyperpolarizations (AHPs) that were insensitive to
78 e membrane potential, reducing the postspike afterhyperpolarization amplitude and decreasing the acti
79 er them more excitable by reducing the spike afterhyperpolarization amplitude and thereby promoting b
80 xcitability manifested as a decreased medium afterhyperpolarization and a longer-lasting afterdepolar
81 A significantly reduces the amplitude of the afterhyperpolarization and increases action potential fr
82 of the potassium current underlying the slow afterhyperpolarization and its modulation has proven elu
83 was higher, whereas the amplitude of medium afterhyperpolarization and M-type K(+) currents were sma
84 ctive L-VSCC agonist Bay K8644 increased the afterhyperpolarization and mimicked the depressive effec
85 ncreased probability of firing after a spike afterhyperpolarization and not directly from subthreshol
86 esurgent sodium current flows at the peak of afterhyperpolarization and persistent sodium current flo
89 impairments at least in part by reducing the afterhyperpolarization and spike-frequency adaptation of
90 d the amplitude of both the action potential afterhyperpolarization and synaptic inputs to motoneuron
91 PS animals expressed larger action potential afterhyperpolarizations and H-current relative to contro
92 Increased excitability (reduced postburst afterhyperpolarizations and reduced spike-frequency adap
94 They have narrower action potentials, deeper afterhyperpolarizations, and make stronger projections t
95 ion potential frequency and the reduction in afterhyperpolarization are occluded by apamin, a small-c
96 l durations are prolonged, the amplitudes of afterhyperpolarizations are reduced, and the responses t
97 embrane depolarization and may contribute to afterhyperpolarization as negative feedback to control n
98 nels increased spike width and decreased the afterhyperpolarization, as expected for loss of an actio
100 g synaptic stimulation, the Ca(2+)-dependent afterhyperpolarization, baseline field potentials, and s
101 e following: (1) that the amplitude of spike afterhyperpolarization be above the GABAA synaptic rever
103 the action potentials and eliminated a slow afterhyperpolarization but had a scarce effect on the fr
104 clamp experiments, NS309 enhanced the medium afterhyperpolarization (but not the slow afterhyperpolar
105 ation and contributes to the medium-duration afterhyperpolarization, but the role of I(M) in control
106 e pharmacological characteristics as the SCG afterhyperpolarization, but to differ from those of homo
107 possibility that serotonin might reduce the afterhyperpolarization by regulating calcium-induced cal
108 members, which contribute to M-currents and afterhyperpolarization conductances in multiple brain ar
109 ate receptor-mediated inhibition of the slow afterhyperpolarization current (I(sAHP)), which is depen
111 we observed that the calcium-activated slow afterhyperpolarization current (IsAHP) was also reduced
112 s clarify key functional aspects of the slow afterhyperpolarization current and its modulation by 5-H
113 e the system; in contrast, activation of the afterhyperpolarization current is unaffected by the incr
114 urons coexpress SK1/SK2 and apamin-sensitive afterhyperpolarization currents are elevated by NMDA and
115 xpresses KCNQ5 channels, the medium and slow afterhyperpolarization currents are significantly reduce
116 strate that KCNQ5 channels contribute to the afterhyperpolarization currents in hippocampus in a cell
119 y through RyRs to generate SK-dependent slow afterhyperpolarizations, demonstrating functional segreg
122 maximum firing frequency, decreased initial afterhyperpolarization duration, and increased total ada
123 on of calcium-induced calcium release to the afterhyperpolarization, enhanced the effect of serotonin
124 action potentials had three components: fast afterhyperpolarization (fAHP), afterdepolarizing potenti
125 e species-independent (e.g., fast and medium afterhyperpolarization, firing frequency, and depolarizi
126 n of Kcnab2 leads to a reduction in the slow afterhyperpolarization following a burst of action poten
127 that K(ATP) channels contribute to the slow afterhyperpolarization following an evoked burst of acti
129 ptic targets of stellate cells, whereas deep afterhyperpolarizations following fusiform cell spike tr
130 fferences in action potential morphology and afterhyperpolarizations, however, emerged when nonadapti
131 endent K(+) current responsible for the slow afterhyperpolarization (I(sAHP)), a prominent regulator
133 potassium channels, which contribute to the afterhyperpolarization in central neurons and other cell
135 ion was tonic cholinergic suppression of the afterhyperpolarization in layer 5 neurons, which was abs
136 creased cytosolic Ca2+ and contribute to the afterhyperpolarization in many excitable cell types.
137 ivated potassium channel-mediated fast spike afterhyperpolarization in neurons in which the M-current
138 otassium channels (SKCa1-3) mediate the slow afterhyperpolarization in neurons, but the molecular ide
140 a(2+)-activated K(+) channels mediate a slow afterhyperpolarization in sensory neurons that was inhib
143 results indicate that serotonin inhibits the afterhyperpolarization in the CA1 region of hippocampus
145 nnels are involved in the generation of slow afterhyperpolarization, in the regulation of firing patt
146 CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrins
150 o CA1 neurons, we demonstrate that postburst afterhyperpolarization is not altered with aging and tha
151 how that, independent of light stimulus, the afterhyperpolarization is significantly greater in type
152 ion potential and decreased the amplitude of afterhyperpolarization led us to ask whether METH alters
155 Single spiking depends on a medium-duration afterhyperpolarization (mAHP) generated by rapid SK curr
156 ntial frequency, as well as a reduced medium afterhyperpolarization (mAHP), a conductance partly medi
157 long been known to contribute to the medium afterhyperpolarization (mAHP), recent evidence indicates
159 etween the medium and slow calcium-dependent afterhyperpolarizations may underlie this firing pattern
160 rates of AP rise and fall with no change in afterhyperpolarization measured to 80 % recovery (AHP80)
163 anism by which use-dependent changes in slow afterhyperpolarizations might regulate electrical firing
164 onent of the SK channels responsible for the afterhyperpolarization of cultured rat SCG neurones.
166 The wide spikes and shallow action potential afterhyperpolarizations of interneurons, compared with t
167 membrane potential (RMP) and do not produce afterhyperpolarization or cumulative inactivation to lim
168 alcium responsible for the generation of the afterhyperpolarization originates from the release of in
170 nd a blunting of the medium component of the afterhyperpolarization potential, a voltage signature of
171 uation, they showed significant reduction of afterhyperpolarization potentials (AHPs) in hippocampal
172 rlies the shortening of the action potential afterhyperpolarization produced by activation of bradyki
173 ng Kv2 current can account for the increased afterhyperpolarization produced by BK inhibition and lik
176 ects of METH on action potential broadening, afterhyperpolarization repression, and spontaneous spike
177 lasting GABAB receptor-mediated IPSP, a slow afterhyperpolarization requiring action potentials but n
178 lie delayed rectifier potassium currents and afterhyperpolarization respectively, are localized in hi
179 ated by a concomitant decrease in the normal afterhyperpolarization response and augmentation of an a
180 e in the amplitude and duration of the spike afterhyperpolarization, resulting in a nonlinear increas
181 ium afterhyperpolarization (but not the slow afterhyperpolarization sAHP) and profoundly affected exc
182 known to be altered by learning are the slow afterhyperpolarization (sAHP) after a burst of action po
183 ause and an increase in the duration of slow afterhyperpolarization (sAHP) after depolarization.
184 g is driven by a delayed and slowly decaying afterhyperpolarization (sAHP) current associated with L-
185 pyramidal neurons, the Ca2+ -dependent slow afterhyperpolarization (sAHP) exhibits an increase with
186 al area CA1 and basolateral amygdala, a slow afterhyperpolarization (sAHP) follows a burst of action
190 ergic signaling in the hippocampus, the slow afterhyperpolarization (sAHP) is an appealing candidate
192 an action potential burst results in a slow afterhyperpolarization (sAHP) that critically regulates
193 yramidal cells of the cortex, express a slow afterhyperpolarization (sAHP) that regulates their firin
194 as correlated with the amplitude of the slow afterhyperpolarization (sAHP), a major mechanism of spik
195 artially underlie the calcium-activated slow afterhyperpolarization (sAHP), a neuronal conductance wh
196 ompanied by AP broadening, an increased slow afterhyperpolarization (sAHP), and faster accumulation o
197 neurons, including the Ca(2+)-dependent slow afterhyperpolarization (sAHP), L-type voltage-gated Ca(2
200 markers, including the increases in the slow afterhyperpolarization, spike accommodation, and [Ca2+]i
201 tic correlation decays slower than the spike afterhyperpolarization, spike bursts can occur during si
206 neuronal excitability by contributing to the afterhyperpolarization that follows an action potential.
207 action potential (AP) and generation of the afterhyperpolarization that follows the AP recorded at t
208 and peripheral nervous system express a slow afterhyperpolarization that is mediated by a slow calciu
209 Many neurons in the nervous systems express afterhyperpolarizations that are mediated by a slow calc
210 arization during repetitive firing, and slow afterhyperpolarizations that distinguished them from non
211 ute to adaptation of firing rate and to slow afterhyperpolarizations that follow repetitive firing.
212 maging reveal that individual SACs have slow afterhyperpolarizations that induce SACs to have variabl
213 y integrate-and-fire neuron model with spike afterhyperpolarization the theory accurately predicts th
214 ameters that vary by cell subtype - the slow afterhyperpolarization, the sag, and the spike frequency
215 ce sodium channel de-inactivation via a fast afterhyperpolarization through BK channel activation.
217 ly in two patterns associated with different afterhyperpolarization timescales, each dictated by a di
218 ramidal neurons by converting the post-burst afterhyperpolarization to an afterdepolarization via a r
219 We discovered an ultraslow, minute-long afterhyperpolarization (usAHP) in network neurons follow
220 or network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase i
221 onent of the current underlying single-spike afterhyperpolarization was sensitive to apamin, phase-lo
225 properties, such as membrane capacitance and afterhyperpolarizations, were flattened in rTg4510 mEC-S
226 ike interval, and decreased the amplitude of afterhyperpolarization, which are consistent with change
227 ivation of INaP affects the action potential afterhyperpolarization, which increases the spontaneous
228 inje cell dendritic excitability produces an afterhyperpolarization, which is hypothesized to release
229 r in duration; 2) their spikes can have dual afterhyperpolarizations with fast and slow components; a
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